Effects of pindolol on the cardiovascular response to tracheal intubation. Treatment of stress response to laryngoscopy and intubation with fentanyl. Effects of adenosine triphosphate on the cardiovascular response to tracheal intubation. Evaluation of esmolol in controlling increases in heart rate and blood pressure during endotracheal intubation in patients undergoing carotid endarterectomy. Effects of intravenous lidocaine and/or esmolol on hemodynamic responses to laryngoscopy and intubation: a double-blind, controlled clinical trial. Effects of labetalol on perioperative stress markers and isoflurane requirements. The use of esmolol, nicardipine, or their combination to blunt hemodynamic changes after laryngoscopy and tracheal intubation. Does alfentanil preserve left ventricular pump function during rapid sequence induction of anaesthesia? Optimal dose of nicardipine for maintenance of hemodynamic stability after tracheal intubation and skin incision. QT interval of the ECG, heart rate and arterial pressure during anaesthetic induction: comparative effects of alfentanil and esmolol. Does urapidil attenuate the blood pressure response to tracheal intubation for general anaesthesia? Modification of the haemodynamic responses to induction of anaesthesia and tracheal intubation with alfentanil, esmolol and their combination. Cardiovascular responses caused by the combination of lidocaine and vecuronium in the induction of general anaesthesia. Effect of pre-operative metoprolol on cardiovascular and catecholamine response and bleeding during hysterectomy. Attenuation of pulse rate & blood pressure-response to laryngoscopy & intubation with verapamil. The effect of various administration routes of lidocaine on hemodynamics and ECG rhythm during endotracheal intubation. Effect of labetalol or lidocaine on the hemodynamic response to intubation: a controlled randomized double-blind study. Circulatory responses to laryngoscopy: the comparative effects of placebo, fentanyl and esmolol. Nifedipine versus fentanyl to prevent the pressor response to tracheal intubation. Haemodynamic responses to laryngoscopy and tracheal intubation in geriatric patients: effects of fentanyl, lidocaine and thiopentone. A comparison of different doses of gabapentin to attenuate the haemodynamic response to laryngoscopy and tracheal intubation in normotensive patients. Partial attenuation of hemodynamic responses to rapid sequence induction and intubation with labetalol. Topical nitroglycerin prevents the pressor response to tracheal intubation and sternotomy in patients undergoing coronary artery bypass graft surgery. Intratracheal aerosolized etidocaine to attenuate cardiovascular and cough responses to laryngoscopy and intubation. The effect of intraoperative use of esmolol and nicardipine on recovery after ambulatory surgery. Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent. Partial attenuation of the cardiovascular responses to tracheal intubation with oral manidipine. Circulatory responses to laryngoscopy and endotracheal intubation in patients with and without cardiovascular disease. Effect of prophylactic practolol. Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation. Effects of alfentanil on the pressor and catecholamine responses to tracheal intubation. Protection by fentanyl against cardiac dysrhythmias during induction of anaesthesia. Intravenous chloroprocaine attenuates hemodynamic changes associated with direct laryngoscopy and tracheal intubation. Esmolol attenuates hemodynamic responses during fentanyl-pancuronium anesthesia for aortocoronary bypass surgery. Lidocaine: the optimal timing of intravenous administration in attenuation of increase of intraocular pressure during tracheal intubation. Lidocaine inhalation attenuates the circulatory response to laryngoscopy and endotracheal intubation. Nifedipine prevents the pressor response to laryngoscopy and tracheal intubation in patients with coronary artery disease. Failure of intravenous nitroglycerin to prevent intraoperative myocardial ischemia during fentanyl-pancuronium anesthesia. Attenuation of the cardiovascular and catecholamine responses to tracheal intubation with oral guanabenz. Effects of intratracheal lidocaine on circulatory responses to tracheal intubation. Attenuation of the pressor response to direct laryngoscopy and tracheal Intubation: oral clonidine vs. oral gabapentin premedication. Cardiovascular effects of intravenous clonidine. Partial attenuation of the pressor response to intubation by clonidine. Attenuation of the pressor response to tracheal intubation with oral nitrendipine. Partial attenuation of the cardiovascular responses to tracheal intubation with oral nisoldipine. The preoperative use of gabapentin, dexamethasone, and their combination in varicocele surgery: a randomized controlled trial. The safety and efficacy of esmolol during myocardial revascularization. Small-dose fentanyl: optimal time of injection for blunting the circulatory responses to tracheal intubation. Comparison of two bolus doses of esmolol for attenuation of haemodynamic response to tracheal intubation. Attenuation of hypertensive response to tracheal intubation with nitroglycerin. Nebulized bupivacaine attenuates the heart rate response following tracheal intubation. Effect of nicardipine on the cardiovascular response to tracheal intubation. The effect of diltiazem on the cardiovascular response to tracheal intubation. Efficacy of oropharyngeal lidocaine instillation on hemodynamic responses to orotracheal intubation. Haemodynamic effects of pretreatment with metoprolol in hypertensive patients undergoing surgery. Effect of oral gabapentin on the intraocular pressure and haemodynamic responses induced by tracheal intubation. Comparative effects of lidocaine, esmolol, and nitroglycerin in modifying the hemodynamic response to laryngoscopy and intubation. The prevention of hypertension at intubation. A controlled study of intravenous hydrallazine on patients undergoing intracranial surgery. Treatment of hypertension following endotracheal intubation. A study comparing the efficacy of labetalol, practolol and placebo. The effect of sufentanil on the cardiovascular responses to tracheal intubation. The effect of magnesium sulphate on hemodynamics and its efficacy in attenuating the response to endotracheal intubation in patients with coronary artery disease. Alfentanil obtunds the cardiovascular and sympathoadrenal responses to suxamethonium-facilitated laryngoscopy and intubation. The effect of nitroglycerin on response to tracheal intubation. Assessment by radionuclide angiography. Reducing the haemodynamic responses to laryngoscopy and intubation. A comparison of alfentanil with fentanyl. Bolus doses of esmolol for the prevention of perioperative hypertension and tachycardia. Gabapentin reduces cardiovascular responses to laryngoscopy and tracheal intubation. Induction using fentanyl to suppress the intubation response in the cardiac patient: what is the optimal dose?
Laryngoscopy and tracheal intubation often cause hypertension, tachycardia and arrhythmias, which may be exaggerated during rapid-sequence induction of anaesthesia. We have studied the efficacy of pindolol in attenuating the cardiovascular responses to laryngoscopy and intubation in patients receiving pindolol 2 micrograms kg-1 or 4 micrograms kg-1 3 min before induction of anaesthesia in a double-blind design. The data were compared with those in a control group receiving saline. Each group consisted of 10 patients undergoing elective surgery. Anaesthesia was induced with thiopentone 5 mg kg-1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. Patients receiving saline showed a significant increase in mean arterial pressure and heart rate associated with tracheal intubation. These increases after tracheal intubation were reduced in pindolol 4 micrograms kg-1 treated patients compared with those in the control group (P less than 0.05). Pindolol 2 micrograms kg-1 attenuated tachycardia in response to intubation but did not affect hypertension. These data suggest that a bolus injection of pindolol 4 micrograms kg-1 is a simple, practical and effective method for attenuating cardiovascular responses to laryngoscopy and tracheal intubation. The cardiovascular response to laryngoscopy and intubation was investigated in lightly anaesthetised patients admitted to hospital for elective intracranial surgery. One group of patients was given fentanyl 5 microgram/kg body weight before induction with thiopentone and suxamethonium. The other group served as controls. Fentanyl treatment caused a significant attenuation of the blood pressure and pulse response to laryngoscopy and intubation. Different techniques for induction of anaesthesia are discussed in relation to the demands of neuroanaesthesia. Laryngoscopy and tracheal intubation often cause hypertension and tachycardia, which may be exaggerated during rapid-sequence induction of anaesthesia. The efficacy of adenosine triphosphate (ATP) in attenuating this response was studied in patients receiving ATP 0.05 mg kg-1 or 0.1 mg kg-1 simultaneously with the start of laryngoscopy. These data were compared with those for a control group receiving saline. Each group consisted of 10 patients undergoing elective surgery. Anaesthesia was induced with thiopentone 5 mg kg-1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg-1 i.v. During anaesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increase after tracheal intubation were reduced in ATP-treated patients compared with those of the control group (P less than 0.05). The data suggest that a bolus injection of ATP is a simple, practical and effective method for attenuating the hypertensive response to laryngoscopy and tracheal intubation. nan To evaluate the efficacy of intravenous lidocaine and two doses of esmolol for attenuating the cardiovascular responses to laryngoscopy and intubation, and to assess whether a combination of both drugs is more effective than either drug alone.
                Randomized, prospective, double-blind, placebo-controlled study.
                University hospital.
                90 ASA status I and II normotensive women scheduled for elective gynecologic procedures with general anesthesia.
                Induction of anesthesia was standardized for all patients. The first group received lidocaine 1.5 mg/kg (Group LID); the second and third groups received esmolol 1 mg/kg and 2 mg/kg, respectively (Groups E1 and E2, respectively); the fourth group received lidocaine 1.5 mg/kg and esmolol 1 mg/kg (Group LID-E1); the fifth group received lidocaine 1.5 mg/kg and esmolol 2 mg/kg (Group LID-E2); the sixth group received saline as a placebo (Group PLAC).
                Systolic blood pressure and heart rate (HR) were recorded before induction, before injection of the first test drug, immediately before laryngoscopy, and 1, 2, and 5 minutes following intubation. Duration of laryngoscopy was recorded. Only patients receiving placebo had increased HR values after intubation compared with baseline values (p < 0.05). The proportion of patients with a maximum HR exceeding 90 beats/min was significantly higher in the placebo group (8 of 15 patients) than in both esmolol groups (E1 2 of 15; E2 2 of 15) (p < 0.05). Systolic blood pressure values after tracheal intubation did not differ among groups except for those receiving the combinations of lidocaine and esmolol, and they had significantly lower blood pressure (BP) values compared with placebo (p < 0.05).
                Esmolol 1 to 2 mg/kg is reliably effective in attenuating HR response to tracheal intubation. Neither of the two doses of esmolol tested nor that of lidocaine affected the BP response. Only the combination of lidocaine and esmolol attenuated both HR and BP responses to tracheal intubation. We have studied the effect of labetalol on anaesthetic requirements, cardiac and humoral responses in 16 healthy women during elective abdominal surgery. The experimental group (n = 8) received increments of i.v. labetalol 0.15-0.3 mg kg-1 to reduce mean arterial pressure (MAP) by 15% from values obtained before anaesthesia. All patients received thiopentone 6 mg kg-1 and anaesthesia was maintained with isoflurane and nitrous oxide. In the placebo group, tracheal intubation provoked a 33% increase in heart rate (HR) and a 52% increase in MAP (P less than 0.001 vs baseline for both). In contrast, pretreatment with labetalol resulted in a 7.3% increase in HR and a 21.3% increase in MAP (P less than 0.05 vs baseline for MAP). Two patients treated with labetalol had a reduction in MAP to 50-60 mm Hg during surgery. After tracheal extubation, the labetalol group had a significantly slower HR than the placebo group (P less than 0.05). The cardiovascular response to tracheal intubation was associated with an increase in plasma noradrenaline concentration in both groups. Labetalol did not affect isoflurane requirements, plasma concentrations of adrenaline, cortisol and aldosterone or arterial PO2, but prevented the decrease in plasma concentration of potassium which occurred in placebo treated patients (P less than 0.05) in early recovery. We conclude that preanaesthetic administration of labetalol attenuated the perioperative hypertensive and tachycardic responses, but was accompanied by intraoperative hypotension when given in doses greater than 0.5 mg kg-1, despite an increase in plasma noradrenaline concentrations. Laryngoscopy and tracheal intubation (LTI) often provoke an undesirable increase in blood pressure (BP) and/or heart rate (HR). We tested the premise that nicardipine (NIC) and esmolol (ESM) in combination (COMB) would oppose both. Adult surgical patients received pretreatment (randomized) with IV bolus NIC 30 microg/kg (n = 31), ESM 1.0 mg/kg (n = 34), or COMB (one-half dose each, n = 32). Peak BP and HR after LTI were compared with controls (CONT; n = 35) with no pretreatment. Anesthetic induction was standardized: IV thiopental (5-7 mg/kg), fentanyl (1-2 microg/kg), and succinylcholine (1.5 mg/kg). Systolic (S), diastolic (D), and mean (M) BP and HR awake before pretreatment (baseline) were similar in all test groups. No patient was treated for hypotension, bradycardia, or tachycardia after pretreatment or anesthetic induction. Peak HR after LTI was increased versus baseline in CONT and all test groups, but did not differ from CONT among the test groups. Peak SBP and DBP increased versus baseline in CONT, and with ESM and NIC, but not COMB. Peak SBP, DBP, and MBP were increased with ESM versus COMB, and peak DBP with ESM versus NIC. Compared with no pretreatment before the IV induction of general anesthesia, the peak increase in BP after LTI is best blunted by the combination of nicardipine and ESM, compared with either drug alone. No single drug or combination in the doses tested opposed increased HR.
                Compared with no pretreatment before the IV induction of general anesthesia, the peak increase in blood pressure after laryngoscopy and tracheal intubation is best blunted by the combination of nicardipine and esmolol, compared with either drug alone. No single drug or combination in the doses tested opposed increased heart rate. A double-blind, randomised trial was conducted in 24 patients without cardiopulmonary disorders (20-43 years), to assess the effect of an intravenous bolus of alfentanil on the circulatory and catecholamine responses to rapid sequence induction of general anaesthesia. Induction included injection of thiopentone 5 mg/kg and suxamethonium 1.5 mg/kg in rapid succession, followed by laryngoscopy and intubation. Half of the patients received alfentanil 100 micrograms/kg immediately before thiopentone. The other half received saline. Blood pressure, heart rate, and plasma catecholamine concentrations were measured repeatedly, together with left ventricular ejection fraction assessed by radionuclide angiocardiography. The responses following laryngoscopy and intubation were completely different in the saline vs. the alfentanil group: rate pressure product +76% vs. -32%, mean arterial blood pressure +46% vs. -25%, heart +46% vs. no change, noradrenaline +117% vs. -25%, adrenaline +50% vs. -53%, and left ventricular ejection fraction -32% vs. no change. In conclusion, during rapid sequence induction of anaesthesia with thiopentone and suxamethonium, an intravenous bolus of alfentanil 100 micrograms/kg 1 min before laryngoscopy and intubation completely prevents hypertension, tachycardia, decrease in left ventricular ejection fraction, and activation of plasma catecholamines, though at the expense of moderate hypotension. To determine the optimal dose of nicardipine (N) for maintenance of hemodynamic stability during the postinduction period, we designed a randomized, double-blind, placebo-controlled, dose-ranging study using four different doses of N administered after a standardized anesthetic induction sequence. A total of 106 patients were assigned to one of the following treatment groups: saline (control), N 0.5 mg (N0.5), N 1 mg (N1), N 2 mg (N2), and N 4 mg (N4). The study medication was administered intravenously (I.V.) in 2.5 mL of saline over 30 s 2 min before laryngoscopy. Mean arterial pressure (MAP) and heart rate (HR) were recorded at 1-min intervals for 15 min after tracheal intubation and for 5 min after skin incision. After intubation, the peak MAP values differed from the preinduction baseline MAP values by 21% +/- 20%, 9% +/- 12%, 1% +/- 13%, -10% +/- 12%, and -15% +/- 13% (mean +/- SD) in the control, N0.5, N1, N2, and N4 groups, respectively. However, the percent change in the pre- to postintubation MAP values (37% to 47%) was similar in all five groups. The highest postintubation HR values were recorded in the N4 group (P < 0.05 versus the other groups). However, the increases in MAP values after skin incision were the least in the N4 group. In conclusion, N1 I.V., administered 2 min before laryngoscopy provides optimal control of arterial blood pressure during the postinduction period. Implications: Acute increases in blood pressure during anesthesia are undesirable in patients with preexisting cardiovascular diseases. This double-blind study found that the calcium-channel blocker, nicardipine, 1 mg intravenously 2 min before tracheal intubation maintained hemodynamic stability during the intraoperative period. In a double-blind study the effect of esmolol and alfentanil on the QT interval of the ECG corrected by the heart rate (QTc), heart rate and arterial pressure during anaesthetic induction was studied in 59 oxycodone- and atropine-premedicated ASA class I-(II) patients with a mean age of 26 yr (range 15-50 yr). The patients were randomly allocated to one of the four groups: saline, esmolol 2 mg.kg-1, esmolol 3 mg.kg-1 or alfentanil 0.03 mg.kg-1. Both doses of esmolol prevented the prolongation of the QTc interval after thiopental and suxamethonium, but not after laryngoscopy and intubation. Alfentanil prevented the prolongation of the QTc interval following thiopental, suxamethonium and laryngoscopy but not after intubation. Esmolol did not prevent the increase in the heart rate and arterial pressure in response to laryngoscopy and intubation. No cardiovascular responses to laryngoscopy and intubation occurred in the patients treated with alfentanil. No cardiac arrhythmias occurred in the esmolol 3 mg.kg-1 group, whereas the frequency of ventricular ectopic beats was 40% in the saline group and 13-20% in the other groups. nan The purpose of this double-blind randomized work was to study the effect of alfentanil and esmolol and their half-dose combination on the increases of heart rate and arterial pressure and on the prolongation of the QTc interval of the ECG occurring during anaesthetic induction. Sixty ASA class I-II patient with mean age ranging from 26 to 32 yr among the groups. Patients were allocated to one of four equal groups to receive saline, esmolol 2 mg.kg-1, alfentanil 0.03 mg.kg-1 and alfentanil 0.015 mg.kg-1+esmolol 1 mg.kg-1. Anaesthesia was induced with thiopentone. Succinylcholine was used to facilitate tracheal intubation. Haemodynamic variables were measured non-invasively and the QTc interval with the aid of a microcomputer. Comparisons between the groups were performed using two-way analysis of variance with repeated measures. Both alfentanil and alfentanil-esmolol prevented the increase of heart rate and arterial pressure caused by intubation whereas esmolol prevented only the increase of the heart rate. None of the treatments prevented prolongation of the QTc interval after intubation and only alfentanil prevented that after succinylcholine. The present results suggest that in the prevention of the haemodynamic responses to tracheal intubation, the half-dose combination of alfentanil and esmolol is as effective as alfentanil and superior to esmolol. The combination is preferable to relatively large doses of either drug in circumstances where side effects, such as respiratory depression due to alfentanil or bradycardia due to both drugs should be minimized. Fentanyl, vecuronium and enflurane may cause bradyarrhythmias during anaesthesia. Lidocaine administered before endotracheal intubation may interact synergistically with these agents. In this randomized and double-blind study, lidocaine 1 mg kg-1 (24 patients) or saline (20 patients) was given, immediately after glycopyrrolate 5 micrograms kg-1, fentanyl 1.5 micrograms ml-1 and thiopentone 3-5 mg kg-1, together with vecuronium 0.1 mg kg-1 as a rapid i.v. injection to healthy (ASA 1) surgical patients. Enflurane 0.8% was included in the inhaled gases 10 min and enflurane 1.6% 25 min after lidocaine administration. The plasma concentrations of lidocaine rose to a mean level of 3.1 micrograms ml-1 (maximum 7.1 micrograms ml-1) which may affect the electrical conduction at various sites in the heart. There were no statistically significant differences in arterial blood pressures or heart rates during anaesthesia between the groups. The incidence of junctional rhythm was 7/24 patients in the lidocaine group and 5/20 patients in the saline group. Three patients in the lidocaine group, and two patients in the control group developed junctional rhythm immediately after intubation. The plasma concentrations of vecuronium were unaffected by lidocaine. The ratio of the unbound lidocaine to plasma protein bound lidocaine was at the expected level and did not differ significantly 2 and 10 min after the injection. The effect of a pre-operative dose of metoprolol on the catecholamine and cardiovascular responses to tracheal intubation and surgery, cardiac complications and intra-operative blood loss, were studied in patients undergoing elective hysterectomy during general anaesthesia. The study was double-blind and placebo controlled. The patients received metoprolol 100 mg or placebo orally 1-25 h before anaesthesia. In patients given metoprolol, heart rate and mean arterial pressure were lower during the first 45 min of anaesthesia. Plasma adrenaline and noradrenaline concentrations increased in both groups in response to tracheal intubation and surgery, but were higher after metoprolol. The incidence of arrhythmias was less after metoprolol. The mean operative blood loss was greater in the placebo group (486 +/- 170 ml (SEM) compared to 231 +/- 43 ml (SEM) after metoprolol). We conclude that oral premedication with metoprolol attenuates the hypertensive response to tracheal intubation and reduces both arrhythmias and operative blood loss. nan Observations of arterial blood pressure, heart rate and cardiac rhythm during endotracheal intubation and within a five minute period thereafter were made in 80 patients randomly assigned into four groups. The aim was to study the cardiovascular changes following endotracheal intubation using a standard anesthesia technique and to compare the efficacy of lidocaine in controlling cardiovascular changes using different administration techniques. Anesthesia was induced with thiopentone and succinylcholine followed by endotracheal intubation. In group A, the control group, no lidocaine was given. In groups B, C, and D, lidocaine as laryngotracheal spray, transtracheal injection or intravenous injection in a dosage of 1 mg/kg BW was administered prior to endotracheal intubation. In the control group, laryngoscopy and endotracheal intubation caused a significant rise in blood pressure and heart rate with a high percentage (60%) of cardiac dysrhythmias including serious types. In the lidocaine groups, we observed significantly lower values of blood pressure and cardiac dysrhythmias as compared to the control group. Only 20-25% of the cases showed sinus tachycardia. No significant differences were noticed between the lidocaine groups. We conclude from our study that those patients who had received lidocaine prior to endotracheal intubation showed minimal cardiovascular changes. Lidocaine should therefore routinely be used prior to endotracheal intubation. Labetalol, a combined alpha 1- and nonselective beta-adrenergic blocking drug, was compared to lidocaine or saline to minimize the hypertensive and tachycardic response to intubation in a controlled randomized double-blind study in patients undergoing surgical procedures under general anesthesia. Forty adult patients were divided into four groups of 10 each: placebo (saline), lidocaine 100 mg, labetalol 5 mg, or labetalol 10 mg. The double-blind preparation was administered as an IV bolus just prior to induction and 2 min before the stimulus of laryngoscopy and intubation. Heart rate and blood pressure were measured at 1-min intervals for 2 min prior to induction of anesthesia and through 6 min following induction of anesthesia. Labetalol 10 mg prevented a rise in heart rate after intubation compared to patients who received placebo, lidocaine 100 mg, or labetalol 5 mg. The hypertensive response to intubation was similar in all four groups. Labetalol 10 mg IV just prior to induction of anesthesia is a safe and cost-effective means of preventing tachycardia but not hypertension in response to laryngoscopy and intubation. The circulatory response to a 30-second laryngoscopy followed by orotracheal intubation was recorded in 60 patients of ASA physical status III or IV undergoing a variety of non-cardiac surgical procedures. Patients were randomly allocated to either the placebo, esmolol (500 micrograms.kg-1.min-1 X 6 minutes, followed by 300 micrograms.kg-1.min-1 X 9 minutes), or fentanyl (0.8 microgram.kg-1.min-1 X 10 minutes) group, and the observer was blinded to the infusion administered. Esmolol blunted the heart rate (HR) response, while fentanyl decreased it below the baseline and maintained it there, in spite of laryngoscopy. Similarly, fentanyl decreased the systolic (SBP), mean (MBP) and diastolic blood pressures (DBP) significantly below the baseline, while these pressures were either retained at or elevated slightly above control in the esmolol group. In these doses, the HR response to laryngoscopy was more effectively blocked by fentanyl, while esmolol better retained perfusion pressure. There were no complications or ischaemic electrocardiographic changes in any patient. Thirty six patients, ASA I or II, undergoing surgery that required tracheal intubation, were allocated randomly into three groups of twelve. Before induction of anesthesia, they received either saline, nifedipine sublingual 10 mg or fentanyl 1.5 micrograms.kg-1 i.v. Heart rate, systolic blood pressure, diastolic blood pressure and mean blood pressure (MAP) were recorded automatically every minute for 5 minutes before induction of anesthesia, and for 5 minutes after intubation. Nifedipine was better than fentanyl in blocking the pressor response to intubation. The fentanyl dose was too small to abolish this response completely. The increase in HR and blood pressure were most evident in the control group, followed by fentanyl, and the least increase was seen with nifedipine. The haemodynamic responses to laryngoscopy and intubation after induction of anaesthesia with thiopentone alone or in combination with 1.5 mg.kg-1 lidocaine and/or 1.5 or 3.0 microgram.kg-1 fentanyl were measured in 150 patients over 64 years of age to determine whether lidocaine, fentanyl or both lidocaine and fentanyl attenuated the pressor response. Fentanyl reduced the rises in systolic, diastolic and mean arterial pressures, heart rate, and rate pressure product and lidocaine decreased the rises in arterial blood pressure and rate pressure product (P less than 0.05). Fentanyl decreased the incidence of marked fluctuations in haemodynamic variables, often seen in geriatric patients (P less than 0.05). The haemodynamic effects of lidocaine and fentanyl were independent of each other. Complications occurred in all groups. Lidocaine-treated patients had fewer cardiac dysrhythmias (P less than 0.05) and 34 per cent of them had tinnitus. Fentanyl-treated patients had a higher incidence of hypotension (P less than 0.05). Respiratory depression developed in only one per cent of the fentanyl-treated patients. Both lidocaine and fentanyl are recommended adjuncts to induction of anaesthesia with thiopentone in geriatric patients. Laryngoscopy and intubation evokes a transient but marked sympathetic response manifesting as increase in heart rate, blood pressure & arrhythmias. We conducted a study to compare the effect of different doses of gabapentin on hemodynamics associated with laryngoscopy and intubation. PATIENTS #ENTITYSTARTX00026;
                Ninety normotensive patients (ASA I and II) between 20-60 years undergoing elective surgery requiring intubation were randomly allocated into three groups of 30 patients each. Group I received oral placebo, Group II received 600 mg of gabapentin and Group III received1000 mg of gabapentin, with sip of water 1 h prior to surgery in the operation theatre. Patients were premedicated with Glycopyrrolate, midazolam and fentanyl and induction was done with thiopentone sodium and succinylcholine. Heart rate, systolic, diastolic and mean arterial pressure were recorded at baseline, 0, 1, 3, 5 and 10 min after intubation.
                MAP and HR were significantly increased in patients receiving placebo and 600 mg gabapentin after laryngoscopy and intubation compared to baseline value and Group III. Significant decrease in MAP was seen just after intubation, 1, 3, 5 and 10 min after (P < 0.001, P < 0.001, P < 0.05, P < 0.05 and P < 0.05 respectively) in Group III compared to Groups I and II. HR was significantly decreased within 10 min of intubation (P<0.001)) in Group III compared to Groups I and II.
                Gabapentin1000 mg given 1 h before operation significantly attenuated the haemodynamic response to laryngoscopy and intubation in normotensive patients. The effectiveness of labetalol (a combination nonselective beta and alpha-1-adrenergic receptor antagonist) in modifying hemodynamic responses associated with rapid sequence induction and tracheal intubation was evaluated. In a double-blind study, 24 ASA physical status I or II male patients scheduled for elective surgery were given either IV labetalol, 0.25 mg/kg (n = 8) or 0.75 mg/kg (n = 8), or a saline placebo (n = 8). Five minutes later, patients were given oxygen by mask and IV vecuronium, 0.01 mg/kg. Ten minutes after giving labetalol or placebo, cricoid pressure was applied and anesthesia was induced with IV sodium thiopental (4 mg/kg) and succinylcholine (1.5 mg/kg) 1 minute prior to intubation. The mean duration of laryngoscopy was 17 +/- 3 seconds. Prior to induction, the 0.25 mg/kg and 0.75 mg/kg doses of labetalol significantly (p less than 0.05) reduced mean arterial pressure by 4.4 +/- 1.9 and by 8.6 +/- 2.0 mmHg, respectively, but did not significantly alter heart rate or cardiac output. The 0.75 mg/kg dose of labetalol also significantly (p less than 0.05) decreased total peripheral resistance by 10.1 +/- 3.0%. Within 30 seconds after intubation, patients in all three groups exhibited increases in heart rate, mean arterial pressure, total peripheral resistance, and rate pressure product and a decrease in stroke volume. However, patients in the 0.25 and 0.75 mg/kg labetalol groups, compared to those in the placebo group, had significantly lower increases in peak heart rate (33 +/- 2 and 27 +/- 3 vs. 44 +/- 7 beats/minute), peak mean arterial pressure (38 +/- 6 and 38 +/- 7 vs. 58 +/- 7 mmHg), and peak rate pressure product (7,726 +/- 260 and 7,215 +/- 300 vs. 14,023 +/- 250 units). The results show that these doses of labetalol significantly blunt, but do not completely block, autonomic responses to rapid sequence induction and intubation. Thirty adult patients who underwent coronary artery bypass graft surgery were allocated randomly to one of two equal groups to receive either 2% nitroglycerin, or a placebo ointment, applied topically over an area of 5 cm by 10 cm, in a double-blind manner, 1 h before induction of anaesthesia. Premedication consisted of oral diazepam 5-10 mg, intramuscular morphine 0.2 mg.kg-1 and promethazine 0.4 mg.kg-1. Anaesthesia was induced with morphine 0.15-0.2 mg.kg-1 and thiopentone 3-5 mg.kg-1. Laryngoscopy and tracheal intubation were facilitated by suxamethonium 1.5 mg.kg-1, and pancuronium 0.1 mg.kg-1 was used for subsequent muscle relaxation. Anaesthesia was maintained with 0.5% halothane and 40% oxygen in nitrous oxide. A significant increase in blood pressure occurred during and after laryngoscopy and tracheal intubation, and following midline sternotomy in the control group. These changes were absent in patients pretreated with topical nitroglycerin. The nitroglycerin group also maintained a lower rate-pressure product than the control group. We conclude that topical nitroglycerin is a simple and useful pretreatment to prevent the pressor response to tracheal intubation and midline sternotomy in patients undergoing coronary artery bypass graft surgery. Forty-five ASA I or II patients scheduled for elective surgery were randomized into one of three groups. Patients in Group 1 (n = 15) received no intratracheal aerosol at laryngoscopy. Patients in Group 2 (n = 15) and Group 3(n = 15) received 50 mg and 75 mg, respectively, of intratracheal aerosolized etidocaine at laryngoscopy. Cardiovascular and respiratory responses were observed at laryngoscopy and intubation and for the first ten minutes following laryngoscopy and intubation (with anesthesia provided by IV thiopental and nitrous oxide [70%] in oxygen). The magnitude and duration of blood pressure and heart rate increases caused by laryngoscopy and intubation were significantly less in the etidocaine-treated patients than in the controls (P less than .05). The incidence of coughing after intubation also was decreased significantly in the etidocaine-treated patients (P less than .05). Etidocaine did not, however, decrease the incidence of arrhythmias after intubation. There is controversy regarding the optimal technique for maintaining hemodynamic stability during anesthesia. We designed this prospective, randomized, double-blinded study to test the hypothesis that the technique used for maintaining hemodynamic stability during general anesthesia can influence recovery after ambulatory surgery. Forty-five healthy consenting women undergoing gynecologic laparoscopy procedures were randomly assigned to 1 of 3 treatment groups: Group 1 (control, n = 15) received normal saline 5 mL and 1 mL, followed by a saline infusion at a rate of 0.005 mL x kg(-1) x min(-1); Group 2 (n = 15) received esmolol 50 mg and saline 1 mL, followed by an esmolol infusion 5 microg x kg(-1) x min(-1); and Group 3 (n = 15) received esmolol 50 mg and nicardipine 1 mg, followed by an esmolol infusion 5 microg x kg(-1) x min(-1). The study drugs were administered after the induction of anesthesia with fentanyl 1.5 microg/kg, and propofol 2 mg/kg I.V. Tracheal intubation was facilitated with vecuronium 0.12 mg/kg I.V. Anesthesia was initially maintained with desflurane 2% end-tidal and N(2)O 67% in oxygen in all 3 groups. During surgery, the mean arterial blood pressure (MAP) was maintained within +/-15% of the baseline value by varying the study drug infusion rate and the inspired concentration of desflurane. In addition to MAP and heart rate values, electroencephalogram bispectral index values were recorded throughout the perioperative period. Recovery times and postoperative side effects were assessed. Compared with the control group, adjunctive use of esmolol and nicardipine attenuated the increase in heart rate (in Group 2) and MAP (in Group 3) after tracheal intubation. Furthermore, the use of an esmolol infusion as an adjunct to desflurane to control the acute autonomic responses during the maintenance period significantly decreased emergence times (4 +/- 2 versus 7 +/- 4 min), decreased the need for postoperative opioid analgesics (43% versus 80%), and reduced the time to discharge (209 +/- 89 versus 269 +/- 100 min). We conclude that the adjunctive use of esmolol alone or in combination with nicardipine during the induction of anesthesia reduced the hemodynamic response to tracheal intubation. Furthermore, use of an esmolol infusion as an adjuvant to desflurane-N(2)O anesthesia for controlling the acute hemodynamic responses during the maintenance period improved the recovery profile after outpatient laparoscopic surgery.
                The adjunctive use of the beta-adrenergic blocker esmolol to control the acute sympathetic responses during desflurane-based anesthesia provided a more rapid awakening from anesthesia, reduced the postoperative opioid analgesic requirement, and decreased the time to discharge home after ambulatory laparoscopic surgery. In a non-double-blind, prospective, randomized study, the intra-operative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beta-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication. Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beta-adrenergic blocking agent had normal preoperative electrocardiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a beta-adrenergic blocking agent (P less than 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk. We conducted a placebo-controlled, randomized, and double-blinded study to evaluate the efficacy of manidipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation. Thirty normotensive patients (ASA physical status 1) undergoing elective surgery were allocated to one of three groups (n = 10 for each); placebo, 5 mg manidipine, and 10 mg manidipine groups. These tablets were orally administered 3 h before induction of anaesthesia. Anaesthesia was induced with thiopentone 5 mg.kg-1 iv, and tracheal intubation was facilitated with vecuronium 0.2 mg.kg-1. Laryngoscopy lasting 30 sec was attempted 2 min after induction of anaesthesia. Patients receiving placebo showed a significant increase in systolic and diastolic blood pressure associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving manidipine 10 mg compared with patients receiving placebo or manidipine 5 mg (P < 0.05). Oral administration of manidipine 10 mg before induction of anaesthesia is a simple and effective method for attenuating pressor response to laryngoscopy and tracheal intubation. We stressed that the potential beneficial effect of a reduced haemodynamic reaction to intubation might be obtained at the expense of hypotension later on. The effect of small intravenous doses of practolol (0.2 mg/kg body weight) on the circulatory response to laryngoscopy and endotracheal intubation, when administered with atropine (0.01 mg/kg b.w.) prior to anaesthesia was studied in 39 patients with and without cardiovascular disease. Practolol diminished significantly the rise of mean arterial pressure and pulse rate affected by laryngoscopy and endotracheal intubation when performed under thiopentone-succinylcholine anaesthesia. Arrhythmias were also less frequent through the statistical significance could not be ascertained in this small series. The small practolol dose used had no adverse circulatory effects. It is suggested that the administration of a small prophylactic dose of practolol is useful in preventing the excessive cardiovascular response due to laryngoscopy and endotracheal intubation. We have compared the efficacy of three calcium channel blockers, nicardipine, diltiazem and verapamil, in attenuating the cardiovascular responses to laryngoscopy and intubation in 60 normotensive patients (ASA I) undergoing rapid sequence induction of anaesthesia with thiopentone and fentanyl. We also examined whether or not these blockers inhibited catecholamine release induced by intubation. The patients were allocated to one of four groups (n = 15 for each): saline (control), nicardipine 30 micrograms kg-1, diltiazem 0.2 mg kg-1 or verapamil 0.1 mg kg-1. Verapamil and the three other drugs were administered 45 s and 60 s before the start of direct laryngoscopy, respectively, in a double-dummy design. Anaesthesia was induced with thiopentone 4 mg kg-1 i.v. and fentanyl 2 micrograms kg-1 i.v. Tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. During anaesthesia, ventilation was assisted or controlled with 1% isoflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after administration of thiopentone and vecuronium. Patients receiving saline exhibited significant increases in systolic and diastolic arterial pressures (AP), heart rate (HR) and plasma concentrations of catecholamines associated with tracheal intubation. The increase in AP was attenuated in patients treated with any calcium channel blocker. The greatest effect was elicited by verapamil, which attenuated the increase in HR, although nicardipine seemed to enhance tachycardia. All three drugs failed to suppress the increase in plasma catecholamine concentrations in response to tracheal intubation. These findings suggest that bolus injection of verapamil 0.1 mg kg-1 was a more effective method of controlling hypertension and tachycardia associated with intubation than diltiazem 0.2 mg kg-1 or nicardipine 30 micrograms kg-1, and that these prophylactic effects were not caused by inhibition of the catecholamine response. The effects of alfentanil (given during induction of anaesthesia) on the haemodynamic and catecholamine responses to tracheal intubation were studied in 44 adult patients who received alfentanil 10 micrograms kg-1 or 40 micrograms kg-1, or saline placebo. Alfentanil 10 micrograms kg-1 and 40 micrograms kg-1 prevented any increase in heart rate and arterial pressure after tracheal intubation. Alfentanil 40 micrograms kg-1 produced profound hypotension and bradycardia. The use of alfentanil in both doses was associated with a decrease in plasma adrenaline concentrations after tracheal intubation. The effect of fentanyl on electrocardiographic changes during anaesthetic induction was studied in 113 adults and 77 children. The adults were pretreated with fentanyl 1, 2 or 3 micrograms kg-1 and the children received fentanyl 1 or 2 micrograms kg-1 as pretreatment. The control groups received no pretreatment. Two minutes after the pretreatment, thiopentone 5 mg kg-1 was injected followed by succinylcholine 1.5 mg kg-1 before laryngoscopy and intubation. In control adults, ventricular ectopic beats (VEB) occurred in 26% of the patients whereas fentanyl in all doses totally prevented them. In children, the incidence of VEB was 22% in the control group whereas both doses of fentanyl prevented the occurrence of VEB. In any doses, fentanyl did not prevent the prolongation of QT interval after succinylcholine. We compared the effects of an IV administration of chloroprocaine and lidocaine on circulatory responses associated with endotracheal intubation. Thirty patients were randomly allocated to receive normal saline (placebo), lidocaine (1.5 mg/kg), or preservative-free chloroprocaine (4.5 mg/kg) 45 s before endotracheal intubation. Blood pressures and heart rate and rhythm were recorded before laryngoscopy and at 0.5, 1, 1.5, 2, 3, and 5 min after intubation. Blood samples were analyzed for catecholamine and chloroprocaine concentrations. Chloroprocaine reduced increases in blood pressure in response to intubation when compared with patients receiving normal saline and lidocaine. Systolic blood pressures at 0.5 and 1 min after intubation were significantly lower in the chloroprocaine group when compared with both the control and lidocaine groups (P < 0.05). Diastolic and mean blood pressures were significantly lower in the chloroprocaine group at all time points until 5 min after intubation (P < 0.05). Chloroprocaine and, to a lesser degree, lidocaine, produced marked attenuation of intubation-induced increases in plasma concentration of epinephrine and norepinephrine. Plasma concentrations of norepinephrine were significantly smaller in the chloroprocaine group at 0.5, 1, and 1.5 min, and plasma concentrations of epinephrine were significantly smaller at 0.5 after intubation when compared with control and lidocaine groups (P < 0.05). Measurable concentrations of chloroprocaine were recorded in plasma samples for 2 min after its administration. No adverse chloroprocaine effects (i.e., circulatory disturbances, venous irritation) were detected. The IV administration of chloroprocaine effectively blunted cardiovascular response produced by laryngoscopy and endotracheal intubation, and this effect was more pronounced when compared with IV lidocaine. We evaluated the effects of esmolol, a short acting (t1/2 beta = 9 min) beta-blocker on hemodynamics during noxious stimulation associated with aortocoronary bypass surgery. Group E (n = 10) and P (n = 10) patients had their morning dose of beta- or calcium blockers withheld except for nifedipine, and were given infusions of esmolol (E) or placebo (P) beginning prior to anesthetic induction and continuing until mediastinal dissection. Group S (n = 10) patients received their usual medication the morning of surgery and received neither esmolol nor placebo. All patients received fentanyl infusions for anesthesia and pancuronium for relaxation. Esmolol patients had no changes in heart rate throughout the study. In contrast, significant increases in heart rate occurred during induction, intubation, and surgical stimulation in Groups P and S. Esmolol patients had a statistically significant but transient increase in pulmonary capillary wedge pressure (PCWP) after intubation, which did not require treatment. There were no significant changes in PCWP in Group S and a decrease in PCWP in Group P patients. We conclude that esmolol was effective in attenuating potentially deleterious responses to noxious stimulation during fentanyl-pancuronium anesthesia. This study was designed to examine the optimal timing of intravenous lidocaine in attenuation of increase of intraocular pressure in response to laryngoscopy and tracheal intubation during induction of anesthesia.
                One hundred and thirty five adult patients of ASA class I, aged between 20-35 years, undergoing surgical procedures irrelevant to ophthalmology were enrolled for study. Patients were randomly assigned to one of five groups. In group II, III, IV and V the patients received intravenous injection of lidocaine (2 mg/kg), 1, 3, 5, 10 min before tracheal intubation, respectively. Group I in which patients did not receive lidocaine served as the control group.
                In patients of groups I, IV and V, the intraocular pressure increased significantly after intubation, whereas in those of groups II and III, the intraocular pressure did not. All patients in the five groups showed concomitantly a surge of blood pressure, but the magnitude of increase was smallest in group III in comparison with the other groups. The values of systolic and diastolic pressures 1 min after intubation were significantly less in groups III and IV than in the control group.
                In healthy patients aged between 20 and 35 the most optimal time of administration of intravenous lidocaine to attenuate the increase of intraocular pressure seemed to be the space between 1 to 3 min before laryngoscopy and tracheal intubation. To evaluate the effect of lidocaine inhalation on the circulatory response to direct laryngoscopy and endotracheal intubation.
                Prospective, randomized study.
                Operating theater at a public hospital.
                Eighty patients (ASA physical status I and II ages 25 to 45 years) scheduled for major abdominal surgery.
                In the first stage, 40 patients were randomly assigned to receive inhalation of either lidocaine 40 mg or a 0.9% solution of sodium chloride (placebo). In the second stage, the next 20 consecutive patients received inhalation of lidocaine 120 mg, and another 20 consecutive patients received intravenous (IV) lidocaine 1 mg/kg.
                Mean arterial pressure rose significantly in the i.v. lidocaine group (21.2 mmHg; p < 0.05), the saline inhalation group (29.2 mmHg; p < 0.05), and the lidocaine 40 mg inhalation group (22.9 mmHg; p < 0.05), but not in the lidocaine 120 mg inhalation group (10.1 mmHg). The heart rate (HR) response to intubation with lidocaine inhalation was dose dependent. In the saline inhalation group, HR increased by 15.6 beats per minute (bpm) (p < 0.05); in the lidocaine 40 mg inhalation group, HR increased by 9.1 bpm (p < 0.05); and in the lidocaine 120 mg inhalation group, HR increased by only 3.1 bpm.
                Inhalation of lidocaine 120 mg prior to induction of anesthesia is an effective, safe, and convenient method to attenuate the circulatory response to laryngoscopy and endotracheal intubation. The efficacy of sublingual nifedipine, administered one minute before anaesthetic induction, in order to minimise the pressor response to laryngoscopy and tracheal intubation was studied in a group of 15 patients who underwent coronary artery bypass surgery. Another group of 15 similar patients served as control. Premedication consisted of oral diazepam 5-10 mg, intramuscular morphine 0.2 mg/kg and promethazine 0.4 mg/kg. Anaesthesia was induced with morphine 0.1-0.15 mg/kg and thiopentone 3-5 mg/kg. Laryngoscopy and tracheal intubation were facilitated with suxamethonium 1.5 mg/kg. A significant increase in blood pressure occurred during and after laryngoscopy and tracheal intubation in the control group. This increase was absent in the patients pretreated with nifedipine. The nifedipine group also maintained a lower rate-pressure-product than the control group during the period of study. It is concluded that nifedipine 10 mg is a useful pretreatment to prevent the pressor response to laryngoscopy and tracheal intubation in patients with coronary artery disease. Twenty patients undergoing coronary artery bypass grafting under fentanyl-pancuronium anesthesia were studied. Continuous electrocardiographic (ECG) recording by a Holter Monitor was utilized to determine the incidence of ECG changes of myocardial ischemia during the precardiopulmonary bypass period and to determine the efficacy of an intravenous nitroglycerin (iv NTG) infusion for preventing ischemic ECG changes. Patients in Group 1 (n = 9) received a 0.5 microgram . kg-1 . min-1 iv NTG infusion 20 min prior to induction of anesthesia and throughout the study. Patients in Group 2 (n = 11) received placebo. A randomized double-blind protocol was employed. Anesthesia was induced with fentanyl 3 micrograms . kg-1 . min-1. After fentanyl 25 micrograms/kg and pancuronium 0.1 microgram/kg, the trachea was intubated. After fentanyl 50 micrograms/kg surgery commenced. Prior to induction of anesthesia, iv NTG caused significant decreases in mean arterial pressure and pulmonary capillary wedge pressure, whereas placebo had no effect. However, subsequent to induction of anesthesia, hemodynamics in the two groups were identical. Fifty per cent of patients developed ECG changes of myocardial ischemia during the period from induction of anesthesia to commencement of cardiopulmonary bypass. The incidence of ischemic ECG changes was virtually identical in Group 1 (5/9) and Group 2 (5/11). Ischemic ECG changes were associated with increases in heart rate, mean arterial pressure, and rate pressure product, and decreases in the endocardial viability ratio (DPTI/SPTI). Increases in pulmonary capillary wedge pressure were not associated with myocardial ischemia. Fentanyl-pancuronium anesthesia, as administered in this study, was associated with a high incidence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS) We conducted a randomized, placebo-controlled, and double-blind study to evaluate the efficacy of oral guanabenz, an alpha 2-adrenergic agonist, in attenuating the cardiovascular and catecholamine responses to laryngoscopy and tracheal intubation in 30 normotensive (ASA physical status 1) patients undergoing elective surgery. They were allocated to one of three groups (n = 10 for each): placebo, 4 mg, or 6 mg of guanabenz groups. These tablets were administered 2 h before the induction of anesthesia. Anesthesia was induced with thiopental 5.0 mg/kg intravenously (IV), and tracheal intubation was facilitated by the administration of vecuronium, 0.2 mg/kg IV. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after the administration of thiopental and vecuronium. Patients receiving placebo showed a significant increase in mean arterial blood pressure, heart rate, and plasma catecholamine concentrations in response to tracheal intubation. These changes were significantly smaller in patients receiving either dose of guanabenz (P < 0.05). Oral administration of guanabenz before induction of anesthesia is a simple and effective method for attenuating the pressor and tachycardic responses to laryngoscopy and tracheal intubation with the drug acting at least partly via inhibition of the increases in plasma catecholamines concentrations. nan We carried out this study to compare the efficacy of oral gabapentin and clonidine premedication for controlling the pressor responses to laryngoscopy and tracheal intubation.
                In this double-blind clinical trial, ninety-six patients were randomly allocated to one of three groups according to the agents to be used before the induction of anaesthesia: Group P (n = 32) received oral placebo, Group G (n = 32) received 800 mg of gabapentin, and Group C (n = 32) received 0.3 mg of clonidine 90 minutes prior to surgery. Systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), heart rate (HR) and rate pressure product (RPP) were measured at baseline (3 min before induction), just before laryngoscopy, and postintubation (at 1, 3, 5, 10 and 15 min after starting laryngoscopy). Statistical analysis of data was done with repeated measure ANOVA and chi-square test.
                HR and RPP significantly decreased in Group G and Group C at 5, 10, and 15 minutes after tracheal intubation compared with those just before laryngoscopy (p < 0.05). No significant difference was noted between Group G and Group C considering these variables. SAP, DAP, MAP and RPP at 1, 3, 5, 10, and 15 minutes after intubation were significantly lower in Group G compared with Group P (p < 0.05). There was no significant difference between Group C and Group P in this regard.
                The present study demonstrated that premedication with oral gabapentin 800 mg or clonidine 0.3 mg similarly blunted the hyperdynamic response after laryngoscopy and intubation. The effect of clonidine on the pressor and heart rate response to tracheal intubation was studied in a placebo-controlled, randomised, double-blind trial. Thirty patients were pretreated with either clonidine 1.25 micrograms/kg, or clonidine 0.625 microgram/kg or an equivalent volume of normal saline, given intravenously 15 minutes before induction of anaesthesia. The attenuation of the pressor response to intubation of both clonidine groups was statistically significant compared to the saline group. Neither dose of clonidine completely abolished the increase in either heart rate or blood pressure. There was no difference in attenuation between the clonidine treatments; this indicated that the lower dose may be the more appropriate. The effect of nitrendipine on the cardiovascular responses to tracheal intubation was studied in a placebo-controlled, randomised, double-blind trial. Thirty patients (ASA physical status 1) undergoing elective surgery received either 5 or 10 mg nitrendipine, or a placebo orally 3 h before induction of anaesthesia (n = 10 for each group). Anaesthesia was induced with sodium thiopentone 5 mg/kg i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg/kg i.v. Patients receiving the placebo showed a significant increase in the mean arterial pressure and the rate-pressure product in response to tracheal intubation. These increases following intubation were reduced in nitrendipine-treated patients compared with the placebo group (P < 0.05). Oral administration of nitrendipine (5 or 10 mg, 3 h before induction of anaesthesia) was able to attenuate the hypertensive response to tracheal intubation in ASA 1 patients under light anaesthesia. We propose this pharmacological technique with supplementary doses of opioids and/or benzodiazepines for the management of patients with hypertension or coronary artery disease. To evaluate the efficacy and safety of nisoldipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation.
                Randomized, double-blind, placebo-controlled study.
                Induction of anesthesia for elective surgery at a university hospital.
                Thirty normotensive patients (ASA physical status I) undergoing elective surgery were assigned to one of three groups; placebo, nisoldipine 5 mg, or nisoldipine 10 mg. Each group consisted of ten patients.
                Either 5 mg of nisoldipine, 10 mg of nisoldipine, or a placebo was administered orally 2 hours before induction of anesthesia. Anesthesia was induced with thiopental sodium 5 mg/kg intravenously, and tracheal intubation was facilitated with vecuronium 0.2 mg/kg. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 seconds was attempted 2 minutes after administration of thiopental sodium and vecuronium.
                Patients receiving the placebo showed a significant increase in mean arterial pressure associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving nisoldipine 10 mg compared with patients receiving the placebo (p less than 0.05).
                Oral administration of nisoldipine before induction of anesthesia is a simple, practical, and safe method for attenuating pressor response to laryngoscopy and tracheal intubation. We investigated the effects of gabapentin and dexamethasone given together or separately 1 h before the start of surgery on laryngoscopy, tracheal intubation, intraoperative hemodynamics, opioid consumption, and postoperative pain in patients undergoing varicocele operations.
                Patients were randomly divided into four double-blind groups: group C (control, n = 20) received placebo, group G (gabapentin, n = 20) received 800 mg gabapentin, group D (dexamethasone, n = 20) received 8 mg dexamethasone, group GD (gabapentin plus dexamethasone) received both 800 mg gabapentin and 8 mg dexamethasone IV 1 h before the start of surgery. Standard induction and maintenance of anesthesia were accomplished and continued by propofol and remifentanil infusion. Heart rate and arterial blood pressure were recorded before induction and after intubation. Intraoperative total remifentanil consumption was recorded. Hemodynamic variables and visual analog scale were recorded for 24 h. Side effects were noted.
                Hemodynamics at 1, 3, 5, and 10 min after tracheal intubation, total remifentanil consumption during surgery, postoperative visual analog scale scores at 30 min, 1, 2, 4, 6, and 12 h, and postoperative nausea and vomiting were found to be significantly lower in group GD than in group G and group D (P < 0.05 for both), and substantially lower when compared with group C (P < 0.001). All values in group C were also higher than in groups G and D (P < 0.05).
                Gabapentin and dexamethasone administered together an hour before varicocele surgery results in less laryngeal and tracheal intubation response, improves postoperative analgesia, and prevents postoperative nausea and vomiting better than individual administration of each drug. The safety and efficacy of esmolol during high-dose fentanyl anesthesia were studied in 37 patients undergoing coronary artery bypass grafting (CABG). The anesthetic management consisted of fentanyl 75 micrograms/kg, pancuronium 0.15 mg/kg, and O2. To assess the safety of esmolol, it was administered in a double-blind manner to 17 anesthetized patients prior to surgical incision. Infusion of the drug was increased in stepwise fashion to obtain administration rates between 100 and 300 micrograms X kg-1 X min-1. Esmolol produced small but significant increases in pulmonary capillary wedge pressure (PCWP) (8.3 +/- 1.7 to 13.2 +/- 2.0 mmHg) when compared with placebo (10.9 +/- 1.0 to 12.1 +/- 0.6 mmHg) (P less than 0.05). For the other studied parameters (heart rate, mean arterial pressure, central venous pressure, cardiac index, stroke index, left ventricular stroke work index, systemic vascular resistance, and peripheral vascular resistance), no significant differences were observed between esmolol and placebo. To evaluate the efficacy of esmolol, 20 patients were randomly assigned to an esmolol group (n = 11) or a placebo group (n = 9). The study medication was infused from 5 min before induction through initiation of cardiopulmonary bypass. Infusion of esmolol at 200 micrograms X kg-1 X min-1 prevented tachycardia in response to intubation. In the esmolol group the heart rate increased from 63.4 +/- 2.7 to 67.6 +/- 2.9 beats/min after intubation, while in the placebo group it increased from 61.4 +/- 4.3 to 72.4 +/- 3.4 beats/min (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS) This study was designed to examine the optimal time of injection of a small dose of fentanyl during anesthetic induction to attenuate circulatory responses to laryngoscopy and tracheal intubation. One hundred seventy patients were randomly assigned to one of five groups. In Groups II, III, IV, and V, patients received fentanyl (2 microg/kg) 1, 3, 5, or 10 min before tracheal intubation, respectively. Group I patients did not receive fentanyl and served as the control group. In Groups III and IV, blood pressures were not increased, except diastolic pressure in Group III, significantly postintubation compared with preinduction values; but Groups I, II, and V showed a significant increase (P < 0.05). The 1-min postintubation values of systolic, diastolic, and mean arterial pressure in Groups III and IV were less than those in the control group (P < 0.05). Increases of heart rate in Group IV were less (P < 0.05) than those in the control group, but significant differences were not observed in Groups II, III, and V. The number of patients with tachycardia and dysrhythmia was significantly smaller in Group IV than in the control group (P < 0.05). We conclude that the most effective time to administer fentanyl to protect circulatory responses to laryngoscopy and tracheal intubation is 5 min before tracheal intubation.
                Fentanyl is often used to reduce the hemodynamic response to tracheal intubation. However, large doses may cause unwanted side effects. Administration of fentanyl at the optimal time reduces the dose required. Our results indicate that optimal injection time of fentanyl for intubation is 5 min before intubation. This prospective study was designed to compare the effectiveness of esmolol (either 100 mg or 200 mg) with a placebo in blunting the haemodynamic response to laryngoscopy and intubation. Seventy-five patients of ASA I or II scheduled for routine-surgery were selected and entered into a placebo-controlled study. Patients were randomly allocated to receive placebo, 100 mg or 200 mg of esmolol IV as part of an anaesthetic induction technique. There were no significant differences in the demographic distribution of the patients in the study. There was no statistical difference in the baseline heart rate (HR) and systolic blood pressure (SBP) between the three groups. One minute after the administration of the drug (prior to intubation) the differences in HR between the placebo group and both the 100 mg and 200 mg groups were significant (p < 0.05), and also at 1 min and 2 min following intubation for the 200 mg group (p < 0.05). In the 200 mg group there was a significant decrease, compared with placebo, in SBP at 1 min (p < 0.05) and at 2 min (p < 0.05) after intubation. In this study, adequate haemodynamic control following was obtained with the administration of 200 mg of esmolol. To evaluate the efficacy and safety of intravenous (IV) nitroglycerin in attenuating the hypertensive response to laryngoscopy and intubation as a new application of the drug.
                Controlled, randomized, double-blind study.
                University hospital.
                Thirty normotensive patients (ASA physical status I) undergoing elective surgery were divided into three groups of ten patients each.
                Anesthesia was induced with thiopental sodium 5 mg/kg i.v., and tracheal intubation was facilitated with vecuronium 0.2 mg/kg i.v. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Either 1.5 micrograms/kg of nitroglycerin, 2.5 micrograms/kg of nitroglycerin, or saline (control) was administered IV simultaneously with the start of laryngoscopy (lasting 30 seconds), which was attempted 2 minutes after administration of thiopental sodium and vecuronium.
                Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in nitroglycerin-treated patients compared with those in the control group (p < 0.05).
                A single, rapid IV dose of nitroglycerin is a simple, practical, effective, and safe method to attenuate the hypertensive response to laryngoscopy and tracheal intubation. To determine whether nebulized bupivacaine attenuates the acute hemodynamic response to laryngoscopy and intubation.
                Prospective, randomized, placebo-controlled study.
                Operating room at a university medical center.
                40 health ASA physical status I and II patients scheduled for minor surgical procedures.
                Patients were randomized to receive 4 ml of a nebulized solution of either saline (n = 20) or 0.75% bupivacaine (n = 20) 15 minutes before induction of anesthesia. On completion of the aerosol treatment, fentanyl 1.5 micrograms/kg was given intravenously (i.v.), and 3 minutes later anesthesia was induced with thiopental sodium 5 mg/kg i.v. and succinylcholine 1.5 mg/kg i.v.. Laryngoscopy was begun 60 seconds after induction, and the trachea was intubated at 90 seconds. Anesthesia was maintained with 50% nitrous oxide in oxygen following intubation, and 1% isoflurane was administered at 180 seconds.
                Heart rate (HR) and blood pressure were recorded automatically every 30 seconds for 5 minutes. Bupivacaine significantly attenuated HR (p < 0.05) but not the hypertensive response to laryngoscopy and intubation.
                Nebulized 0.75% bupivacaine was only partially effective in blunting the hemodynamic response to tracheal intubation. We studied the cardiovascular responses to laryngoscopy and intubation in 30 patients who received nicardipine 15 micrograms kg-1 or 30 micrograms kg-1, or saline placebo 60 s before the start of laryngoscopy. Anaesthesia was induced with thiamylal 5 mg kg-1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. Patients receiving saline showed a significant increase in mean arterial pressure (MAP) and rate-pressure product (RPP) associated with tracheal intubation. The increases in MAP and RPP following tracheal intubation were reduced in both groups of patients who received nicardipine. The efficacy of diltiazem in the attenuation of the cardiovascular response to laryngoscopy and tracheal intubation was studied in patients who received 0.2 or 0.3 mg/kg diltiazem 60 seconds before the start of laryngoscopy. These data were compared with a control group who received saline. Each group consisted of 10 patients who had elective surgery. Patients who received saline showed a significant increase in mean arterial pressure and rate pressure product associated with tracheal intubation. These increases after tracheal intubation were reduced in diltiazem-treated patients compared with those of the control group (p less than 0.05). The data suggest that a bolus injection of diltiazem is a simple, practical and effective method to attenuate the hypertensive response to laryngoscopy and tracheal intubation. To determine whether oropharyngeal instillation of lidocaine after anesthetic induction modifies the hemodynamic response to intubation.
                Prospective, randomized, double-blind, placebo-controlled study.
                Operating room of a university hospital.
                56 ASA physical status I and II adult patients scheduled for elective surgery requiring orotracheal intubation and general anesthesia.
                Patients were randomized to receive oropharyngeal instillation with either 5 mL 2% lidocaine (n = 28, lidocaine group) or 5 mL normal saline (n = 28, control group) 45 seconds after anesthetic induction bolus. Orotracheal intubation was attempted three minutes later.
                Systolic (SBP), diastolic (DBP), mean arterial pressure (MAP), and heart rate (HR) were recorded at baseline, just before intubation, and for three minutes postintubation at one-minute intervals. Occurrence of adverse events such as arrhythmias, ischemic changes in electrocardiography, and bronchospasm after intubation were also documented.
                All postintubation values of SBP, DBP, MAP, and HR were significantly lower in the lidocaine group than the control group (P < 0.01). In both groups, postintubation HRs were significantly higher than baseline values (P < 0.05). More patients (P < 0.001) became hypertensive postintubation in the control group (14/28, 50%) than the lidocaine group (2/28, 7%).
                Oropharyngeal instillation of lidocaine for three minutes before intubation attenuates the cardiovascular responses to intubation. Thirty hypertensive patients scheduled for cholecystectomy or hernia repair under general anaesthesia with thiopentone-fentanyl-nitrous oxide-pancuronium were divided into two groups of 15. One group received metoprolol tablets 200 mg in a slow release form, once daily for at least 2 weeks including the morning of surgery. In addition, metoprolol 15 mg was injected i.v. shortly before the induction of anaesthesia. The other group received placebo tablets and saline. Two patients in the treatment group and one patient in the placebo group were subsequently excluded, because of complications during treatment. Metoprolol significantly reduced arterial pressure both during undisturbed anaesthesia, during intubation and after extubation. A similar tendency was observed also during surgery, although it was not quite significant (P = 0.055). However, metoprolol had no effect on variations in systemic vascular resistance. Mean pulmonary arterial pressures during anaesthesia and surgery were significantly greater in the control, than in the metoprolol, group. Central venous pressure (CVP) and pulmonary arterial occlusion pressure (PAOP) increased significantly in both groups in response to the surgical stimulus. There was no significant difference between the groups in PAOP and CVP. One patient in the metoprolol group had marked bradycardia (minimum heart rate 26 beat min-1) after neostigmine and atropine; otherwise metoprolol pretreatment was tolerated well. Laryngoscopy and tracheal intubation may cause undesirable increases in blood pressure, heart rate (HR) and intraocular pressure (IOP). Gabapentin has been used effectively to attenuate the pressor response to laryngoscopy and tracheal intubation. We investigated whether the pre-treatment with gabapentin attenuates the IOP in addition to a haemodynamic response to tracheal intubation.
                Sixty ASA I-II patients were randomly allocated into two groups who received either gabapentin (800 mg) or placebo 2 h before surgery. IOP, mean arterial pressure (MAP) and HR were measured before and after the induction of anaesthesia as well as at 0, 1, 3, 5, 10 and 15 min following intubation.
                IOP and MAP increased from baseline immediately after intubation in the placebo group (P=0.001 and 0.002, respectively). When compared with the placebo group, IOP values of the gabapentin group were significantly lower for the first 15 min after tracheal intubation (P=0.002 at 0 min, P=0.006 at 1 min, P<0.001 at 3 min, P<0.001 at 5 min, P<0.001 at 10 min and P=0.003 at 15 min) while MAP was lower in the first 10 min (P=0.001 at 0 min, P=0.002 at 1 min, P<0.001 at 3 min, P<0.001 at 5 min and P=0.028 at 10 min). These results showed that gabapentin effectively suppresses the increase in IOP secondary to endotracheal intubation and attenuates the increases in MAP.
                It is suggested that gabapentin is a useful adjuvant in order to prevent an increase in the IOP in response to laryngoscopy and tracheal intubation. To compare the safety and efficacy of lidocaine, esmolol, and nitroglycerin in modifying the hemodynamic response to laryngoscopy and intubation.
                Randomized, placebo-controlled, double-blind study.
                University-affiliated VA medical center.
                40 ASA physical status I and II patients undergoing electric surgery with general endotracheal anesthesia.
                Anesthesia was induced with thiopental sodium 5 mg/kg, and intubation was facilitated with vecuronium 0.15 mg/kg. Isoflurane (0.5% to 1%) and 50% nitrous oxide in oxygen were used for maintenance of anesthesia. In addition, patients received one of the following four study drugs intravenously (i.v.) prior to laryngoscopy: Group 1 (control) = saline 5 ml; Group 2 = lidocaine 1.5 mg/kg; Group 3 = esmolol 1.4 mg/kg; Group 4 = nitroglycerin 2 micrograms/kg.
                Mean arterial pressure (MAP) and heart rate (HR) were recorded every minute for 20 minutes following induction of anesthesia. Following laryngoscopy and intubation, MAP increased significantly in all four treatment groups (control 49% +/- 19%, lidocaine 55% +/- 26%, esmolol 25% +/- 11%, nitroglycerin 45% +/- 21%) compared with preinduction baseline values. In the esmolol-pretreated patients, the increase in HR was significantly lower (20% +/- 3%) compared with the nitroglycerin (37% +/- 8%), lidocaine (52% +/- 8%), and control (29% +/- 4%) groups.
                Lidocaine 1.5 mg/kg i.v. and nitroglycerin 2 micrograms/kg i.v. were ineffective in controlling the acute hemodynamic response following laryngoscopy and intubation. Esmolol 1.4 mg/kg i.v. was significantly more effective than either lidocaine or nitroglycerin in controlling the HR response to laryngoscopy and intubation (p < 0.05). Esmolol also was significantly more effective than lidocaine in minimizing the increase in MAP (25% vs. 55%). Arterial blood pressure and pulse rate changes following tracheal intubation were studied in 20 patients undergoing intracranial surgery who received a thiopentone/suxamethonium anaesthetic induction sequence. Ten of the patients were pretreated with 0.4 mg/kg of hydrallazine and 10 with saline to determine whether hydrallazine prevents intubation hypertension. The results show that the incidence of intubation hypertension can be reduced using this dose of hydrallazine. Hydrallazine pretreatment is therefore recommended in patients at risk from hypertension following tracheal intubation. Labetalol, a new adrenergic receptor antagonist, has both alpha- and beta-blocking properties. Intravenous labetalol (0.25 and 0.5 mg/kg), practolol (0.4 mg/kg) and saline (1 ml), injected prior to anaesthesia, were compared with respect to their effect on the haemodynamic consequences of direct laryngoscopy followed by the passage of an endotracheal tube. When compared with intravenous saline injection, both labetalol and practolol obtunded the tachycardia induced by endotracheal intubation. The higher dose of labetalol was more effective in reducing the hypertensive response than the lower dose of practolol. However, none of the regimens completely abolished the adverse haemodynamic consequences of laryngotracheal manipulations. The effects of sufentanil 0.5 or 1 microgram/kg, given intravenously after induction of anaesthesia, on the cardiovascular responses to tracheal intubation were examined in a controlled, randomised, double-blind investigation. The control group of patients exhibited significant rises in arterial blood pressure and heart rate for 4 minutes after tracheal intubation. Heart rate exceeded 100 beats/minute and systolic pressure increased by over 20% in every patient. All patients moved or breathed within 10 minutes of the administration of suxamethonium. Sufentanil 0.5 microgram/kg prevented increases in the mean values of heart rate and arterial blood pressure, although increases were observed in five patients. Significant falls in the mean values of heart rate and arterial pressure occurred from 4 minutes after intubation until observations ended 15 minutes after induction of anaesthesia. Two patients moved or breathed during this time, although movement in response to nerve stimulation occurred in all patients 10 minutes after administration of suxamethonium. Sufentanil 1 microgram/kg was effective in suppressing a rise in heart rate or arterial pressure in every patient. Significant falls in these variables occurred from 2 minutes after tracheal intubation onwards. No patient moved or breathed for 15 minutes after induction of anaesthesia, although neuromuscular transmission was present 10 minutes after giving suxamethonium in each case. Laryngoscopy and endotracheal intubation may produce adverse hemodynamic effects. Magnesium has direct vasodilating properties on coronary arteries and inhibits catecholamine release, thus attenuating the hemodynamic effects during endotracheal intubation. We studied 36 patients with coronary artery disease (CAD) scheduled for elective coronary artery bypass grafting to evaluate the hemodynamic effects of magnesium and its efficacy in attenuating the response to endotracheal intubation. Patients received either 0.1 mL/kg (50%) magnesium sulfate (50 mg/kg) (Group A, n = 19) or isotonic sodium chloride solution (Group B, n = 17) before the induction of anesthesia and 0.05 mL/kg of isotonic sodium chloride solution (Group A) or lidocaine 2% (1 mg/kg) (Group B) before intubation. The hemodynamic variables were recorded before induction, after the trial drug, after induction, and after endotracheal intubation. Automatic ST segment analysis was performed throughout the study period. Magnesium sulfate administration was associated with increased cardiac index (P < 0.01), a minimal increase in heart rate, and a significant decrease in mean arterial pressure (MAP) and systemic vascular resistance (SVR) (P < 0.001). None of the patients in the magnesium group had significant ST depression compared with three patients in the control group. The magnesium group patients had a significantly lesser increase in MAP (P < 0.05) and SVR (P < 0.01) compared with the control group patients who received lidocaine before endotracheal intubation. Thus, magnesium is an useful adjuvant to attenuate endotracheal intubation response in patients with CAD.
                Endotracheal intubation produces adverse hemodynamic effects, which may be more detrimental in patients with coronary artery disease than in healthy patients. The present study shows that magnesium administered before endotracheal intubation can attenuate this response better than lidocaine. Alfentanil 75 micrograms kg-1 or saline (control group) was given 1 min before induction of anaesthesia in 20 healthy patients premedicated with diazepam 0.14 mg kg-1 and pethidine 1 mg kg-1. Anaesthesia was induced with a sleep dose of thiopentone preceded by glycopyrrolate. Suxamethonium 1 mg kg-1 was used to facilitate laryngoscopy (which lasted 10 s) and tracheal intubation. Arterial pressure, heart rate and noradrenaline concentration in mixed venous plasma increased significantly after suxamethonium, and increased further after laryngoscopy and intubation in the control group (n = 10). The QT interval of the ECG was prolonged after the administration of suxamethonium, and was prolonged further after laryngoscopy and intubation. All these changes were attenuated in patients pretreated with alfentanil (n = 10), but four patients had chest wall rigidity. Changes in the QT interval correlated directly with the changes in plasma noradrenaline concentration (r = 0.67). Plasma adrenaline concentrations decreased during induction of anaesthesia in both groups. The effect of intravenous (IV) nitroglycerin (NTG) on perioperative myocardial ischemia as detected by single pass radionuclide angiocardiography was studied in 20 patients scheduled for elective coronary artery bypass grafting (CABG). Ten patients, selected at random, received IV NTG 1 microgram.kg-1.min-1 (NTG group) and 10 others, IV saline (control group). Anesthetic induction consisted of midazolam 0.2 mg.kg-1, vecuronium 0.1 mg.kg-1, and 50% N2O in O2. ECG leads I, II, and V5 were monitored for ST segment changes. Single pass radionuclide angiocardiography (RNA) was performed at 5 times: prior to induction, prior to tracheal intubation, and at 1, 3.5, and 6 min following intubation. The presence of new regional wall motion abnormalities (RWMA) was determined from each RNA study as compared with the preinduction measurement. Apart from one patient in the control group who developed a new "v" wave after intubation, there was no evidence of ischemia by pulmonary capillary wedge pressure. No ECG evidence of ischemia was detected in any patient. Despite this, new regional wall motion abnormalities were observed in 3 patients in the control group and 1 patient in the NTG group. Blood pressure and heart rate responses of patients with new RWMA were not significantly different from other patients. The low incidence of ischemia in this population precludes a definitive statement regarding the efficacy of IV NTG, but the lower incidence of RWMA in the NTG group suggests a protective effect. The effects of alfentanil and fentanyl on controlling the haemodynamic responses to laryngoscopy and intubation have been compared. Five groups of ten patients were studied. Induction was with thiopentone 4 mg/kg. Thirty seconds later group 1 received 1 ml/20 kg saline, group 2 received 15 micrograms/kg alfentanil, group 3 received 30 micrograms/kg alfentanil and group 4 received 5 micrograms/kg fentanyl one minute before induction. Suxamethonium was given 60 seconds after induction and intubation of the trachea was performed 150 seconds after the start of induction. Heart rate and mean arterial pressure were recorded every minute throughout and compared with pre-induction control values. Control patients (group 1) showed significant increases associated with tracheal intubation in all haemodynamic variables. No increases were noted in groups receiving 30 micrograms/kg alfentanil or 5 micrograms/kg fentanyl. The heart rate, but not blood pressure, increased with intubation after 15 micrograms/kg alfentanil. The mean time to movement in 50% of the control patients was 7 minutes. In those given 15 and 30 micrograms/kg alfentanil it was 11 and 12 minutes respectively. In those given 5 micrograms/kg fentanyl it was greater than 15 minutes. Alfentanil is shown to reduce the cardiovascular responses to laryngoscopy and intubation and the effect appears to have a shorter duration than that of fentanyl. The effectiveness of esmolol, an ultra short-acting cardioselective beta blocker, in the prevention and treatment of post-intubation haemodynamic perturbations, was investigated. Forty-eight ASA physical status I and II patients undergoing hysterectomy were randomly assigned to receive a single intravenous bolus of placebo, esmolol 100 mg, or esmolol 200 mg in a double-blind fashion. This was administered over 15 sec, and immediately followed by thiopentone 3-5 mg.kg-1, succinylcholine 1.5 mg.kg-1, and tracheal intubation 90 sec later. The heart rate following induction of anaesthesia was lower in the esmolol 200 mg group (P less than 0.01); following intubation, the increase in heart rate in the placebo group was greater than in the esmolol groups (P less than 0.05). The systolic blood pressure post-induction was lower in the esmolol 200 mg group (P less than 0.05); following intubation, however, no significant differences were seen among groups in systolic, diastolic, or mean blood pressures. Following tracheal intubation, the incidence of ventricular arrhythmias was lower in the esmolol groups (P less than 0.05). In summary, esmolol in 100 mg and 200 mg doses was effective in mitigating the haemodynamic response following tracheal intubation. We have compared the effects of gabapentin on arterial pressure and heart rate at induction of anaesthesia and tracheal intubation in a randomized double-blind study.
                Ninety normotensive patients (ASA I) undergoing elective surgery were divided into three groups of 30 patients each. Patients received oral placebo (Group I), 400 mg of gabapentin (Group II) or 800 mg of gabapentin (Group III) 1 h prior to surgery in the operating theatre. After induction of anaesthesia heart rate and mean arterial pressure were recorded at baseline 1, 3, 5, 10 and 15 min after intubation.
                Patients receiving placebo and 400 mg gabapentin showed a significant increase in blood pressure and heart rate associated with tracheal intubation compared to baseline levels and Group III. There was significant decrease in heart rate and arterial pressure in Group III after intubation 1, 3, 5 and 10 min (P < 0.001, P < 0.001, P < 0.05 and P < 0.05, respectively) compared to Groups I and II.
                Given 1 h before operation gabapentin 800 mg blunted the arterial pressure and heart rate increase in first 10 min due to endotracheal intubation. Oral administration of gabapentin 800 mg before induction of anaesthesia is a simple and practical method for attenuating pressor response to laryngoscopy and tracheal intubation after standard elective induction. Eighty patients undergoing coronary artery surgery were randomly allocated to receive either 0, 2, 5, 10 or 15 micrograms/kg of fentanyl with induction of anaesthesia. Heart rate and blood pressure were measured before induction, after induction, and after intubation. The effects of fentanyl dose on both heart rate and mean arterial pressure (MAP) were evaluated in terms of both the mean and group responses. At all doses of fentanyl, mean heart rate increased after induction and rose further on intubation. The mean increase after induction was minimal at doses of 5 micrograms/kg and greater. The increase in heart rate after intubation was more difficult to block but with a fentanyl dose of 15 micrograms/kg, 87% of patients had heart rates below 100 bpm. As a group, the percentage of patients in whom the postintubation heart rate remained below 100 bpm increased progressively with the fentanyl dose. In contrast, mean MAP fell at all dose levels after induction, the mean fall being about 30 mmHg at 5 micrograms/kg and greater. Mean MAP exceeded pre-induction values after intubation with 0 and 2 micrograms/kg, and progressive attenuation of the MAP rise was found as the dose of fentanyl increased. The percentage of patients who did not exceed their preinduction MAP rose progressively with increasing dose of fentanyl with an ED50 of 3.7 micrograms/kg. If a minimal fall in mean MAP after induction with no rise above preinduction MAP is the sole criterion, a fentanyl dose of about 3 micrograms/kg is recommended. If heart rate is to be kept below 100 bpm, a dose of at least 10 micrograms/kg should be used.2+ dose or greater will cause the MAP to fall in some patients to less
The risk of arrhythmias associated with tracheal intubation was significantly reduced with pre-induction administration of local anaesthetics, calcium channel blockers, beta blockers and narcotics compared to placebo. Pharmacological intervention also reduced the risk of ECG evidence of myocardial ischaemia in the pooled data. Lignocaine pretreatment showed a significant effect but evidence came from one study only. The data suggested that there may be a reduction in ECG evidence of myocardial ischaemia with beta blocker pretreatment but this difference was not statistically significant. There is a need to focus on outcomes rather than haemodynamic measurements alone when studying this response in future trials.