Graded caval occlusion in conscious rabbits caused a biphasic response. Phase I was characterized by a fall in conductance so that arterial pressure was maintained. When cardiac output had fallen to 71 +/- 4% of its baseline level, phase II supervened. During phase II, conductance rose abruptly and arterial pressure fell to a life threatening level (< 40 mm Hg). When administered into the fourth ventricle, the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester prevented the onset of phase II. The mean threshold dose for this effect was 4 mumol (range: 0.4-11). When administered intravenously, a dose of 275 mumol N-nitro-L-arginine methyl ester prevented the onset of phase II in only one out of six rabbits. It is concluded that a central brainstem nitrergic mechanism is involved in the onset of the decompensatory phase II of the haemodynamic response to hypovolaemia.
Analysis of Variance Animals