N-nitro-L-arginine methyl ester blocks the decompensatory phase of acute hypovolaemia in conscious rabbits by a brainstem mechanism.
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.
D000704:Analysis of Variance; D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D001810:Blood Volume / Q000187:drug effects*; D001933:Brain Stem / Q000187:drug effects* / Q000378:metabolism; D002302:Cardiac Output / Q000187:drug effects; D002405:Catheterization, Central Venous; D002406:Catheterization, Peripheral; D006329:Heart Conduction System / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D066298:In Vitro Techniques; D007275:Injections, Intravenous; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000037:antagonists & inhibitors* / Q000378:metabolism; D011817:Rabbits; D012769:Shock / Q000188:drug therapy*; D014684:Venae Cavae / Q000187:drug effects
D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester