• R G Evans, J Ludbrook, and S Ventura.
• Baker Medical Research Institute, Prahran, Victoria, Australia.
• J. Auton. Nerv. Syst. 1994 Mar 1;46(3):251-60.

AbstractIn unanaesthetized mammals, including rabbits, the response to acute central hypovolaemia is biphasic. An initial phase of baroreflex-mediated systemic vasoconstriction is succeeded by an abrupt failure of sympathetic vasoconstrictor drive and haemodynamic decompensation. We have tested whether a signal travelling in the cervical vagus nerves is responsible for the second phase. An inflatable vena caval cuff, an ascending aortic flow probe, and diaphragmatic electrodes were chronically implanted into 7 rabbits. Haemorrhage was simulated by gradual caval constriction so cardiac index (CI) fell linearly at 9% per minute. In Study 1, caval constriction was performed under control conditions, after muscarinic cholinoceptor blockade (MCB), and was repeated twice under MCB after a sham operation. In Study 2, the steps were identical but bilateral cervical vagotomy plus tracheostomy was substituted for sham operation. With or without MCB, caval constriction caused a progressive fall of systemic vascular conductance index (SVCI), and a small decline in mean arterial pressure (MAP) (Phase I). When CI had fallen by approximately 40%, there was an abrupt rise of SVCI and fall of MAP (Phase II). Sham operation had no effect on either phase. Vagotomy had no effect on Phase I, but the onset of Phase II was delayed until CI had fallen by approximately 53% in 6 rabbits. In 1 rabbit, Phase II did not occur, even though CI had fallen by 67%. We conclude that an afferent vagal signal does not contribute to the compensatory Phase I, and is not essential for the occurrence of the decompensatory Phase II, of acute central hypovolaemia in unanaesthetized rabbits.

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