Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Abstract: We used the model of bilateral cervical vagotomy of adult rabbits to cause respiratory failure characterized by pulmonary edema, decreased lung compliance, and atelectasis. We documented an 18-fold increase in radiolabeled albumin leak from the vascular space into alveolar washes of vagotomy vs. sham-operated rabbits (P less than 0.01). Despite a twofold increase in percent of prelabeled saturated phosphatidylcholine secreted (P less than 0.01), the alveolar wash saturated phosphatidylcholine pool sizes were not different. The minimum surface tensions were 19.6 +/- 2.5 vs. 9.4 +/- 2.2 dyn/cm for alveolar washes from vagotomy and control rabbits, respectively (P less than 0.01). The soluble proteins from alveolar washes inhibited the surface tension lowering properties of natural surfactant, whereas those from the control rabbits did not (P less than 0.01). When vagotomy rabbits in respiratory failure were treated with 50 mg natural surfactant lipid per kilogram arterial blood gas values and compliances improved relative to control rabbits. Vagotomy results in alveolar pulmonary edema, and surfactant dysfunction despite normal surfactant pool sizes and respiratory failure. A surfactant treatment can improve the respiratory failure.
Respiratory distress and surfactant inhibition following vagotomy in rabbits.

Abstract: We compared the MCR, volume of distribution, and rapid phase (rt1/2) and slow phase half-lives of purified pituitary rat (r) TSH, TSH from crude pituitary extracts of normal and hypothyroid rats, TSH from hypothyroid rat sera, and TSH secreted from hypothyroid rat pituitaries incubated in vitro. For 3 h after iv bolus injection into euthyroid rats, 125I-labeled rTSH was determined by acid precipitation in serum and various organs, and unlabeled TSH was measured by RIA. The MCR of TSH from normal pituitary extracts (0.53 +/- 0.02 ml/min) was similar to that of unlabeled purified rTSH (0.52 +/- 0.03), while those from hypothyroid pituitary extracts (0.32 +/- 0.03) and hypothyroid sera (0.33 +/- 0.01) were decreased. The reduced MCR of TSH from hypothyroid pituitaries was due to a decreased distribution volume (8.4 +/- 0.6 ml) compared to that from normal pituitaries (11.4 +/- 0.7) and hypothyroid sera (10.9 +/- 0.8). The decreased MCR of circulating TSH from hypothyroid sera reflected an increase in its rt1/2 (12.6 +/- 0.5 min) vs. that from both normal (5.1 +/- 0.5) and hypothyroid (5.7 +/- 0.4) pituitaries. The rt1/2 of secreted TSH from incubated hypothyroid rat pituitaries (8.5 +/- 0.9) was intermediate between those of circulating and pituitary forms of hypothyroid rTSH. The clearances of intact bovine TSH (bTSH) and deglycosylated bTSH (dg-bTSH) were compared. The dg-bTSH MCR was found to be increased (0.71 +/- 0.02 ml/min) compared to that of bTSH (0.59 +/- 0.02), primarily due to a decreased rt1/2 for dg-bTSH (3.8 +/- 0.1 min) vs. bTSH (4.7 +/- 0.2). Uptake of purified [125I]rTSH was highest in the kidney at all times, varying from 43% of the injected dose at 5 min to 54% at 180 min. We conclude that in the euthyroid rat, 1) the metabolic clearance of TSH differs between pituitary and serum forms and appears to depend on specific molecular features that vary with the physiological state of the animal from which the TSH is derived; 2) since chemical deglycosylation increased the clearance of TSH, we speculate that the chemical basis for changes in TSH clearance may be related to alterations in its carbohydrate structure; and 3) for normal pituitary TSH, the kidney is the major organ of clearance.
Differences in the metabolic clearance of pituitary and serum thyrotropin (TSH) derived from euthyroid and hypothyroid rats: effects of chemical deglycosylation of pituitary TSH.

Abstract: The influence of serotonin (5-hydroxytryptamine) on human detrusor and on pig detrusor, trigone, bladder neck and urethral smooth muscle was explored in a series of in vitro experiments. Serotonin evoked a dose-dependent and reversible contraction of the detrusor. The reverse response was triggered in trigone, bladder neck and urethral smooth muscle--a dose-dependent and reversible relaxation. The maximum amplitude of this relaxation was 85 +/- 15% of the relaxation produced by electrical nerve stimulation. The effect of serotonin was unaltered by blockade of ganglia, alpha- and beta-adrenergic receptors, cholinergic receptors and prostaglandin synthesis. The serotonin antagonists ketanserin, methysergide and cyproheptadine partly inhibited the effect of serotonin. The antagonism differed in potency on strips of different origin. The antagonists were ineffective or minimally effective in blocking responses to nerve stimulation. The effect of serotonin was probably mediated by specific serotonin receptors different from the serotonin-S2-receptors predominating in vascular smooth muscle. Serotonin is a potential neurotransmitter in lower urinary tract smooth muscle, but its importance in micturition physiology and pathophysiology is unknown.

Influence of serotonin on lower urinary tract smooth muscle in vitro.

