Influence of higher brain centres and vasopressin on the haemodynamic response to acute central hypovolaemia in rabbits.

We tested whether suprapontine brain centres contribute to the sudden failure of vasoconstriction that occurs in unanaesthetized rabbits during acute reduction in central blood volume. Haemorrhage was simulated by gradually inflating a cuff around the thoracic inferior vena cava so that cardiac output fell by about 8% per min. In intact rabbits, and in rabbits that had undergone craniectomy but not decerebration, the haemodynamic response to simulated haemorrhage was always biphasic. During the first, compensatory phase, systemic vascular conductance fell almost in proportion to the fall in cardiac output so that arterial pressure fell by only about 10 mmHg. When cardiac output had fallen by about 50%, a decompensatory phase supervened in which systemic vascular conductance rose abruptly, arterial pressure fell steeply to less than 40 mmHg, and the plasma arginine vasopressin (AVP) level rose. High mesencephalic decerebration did not affect the compensatory phase, but it abolished the decompensatory phase and there was no rise in the plasma AVP level. The decompensatory phase was not restored by intravenous administration of AVP. We came to two conclusions as a result of this study. Suprapontine brain centres do not influence the arterial baroreflex-mediated vasoconstriction that occurs during the first phase of acute central hypovolaemia. However, the sudden failure of vasoconstriction that occurs during the second phase of acute central hypovolaemia, attributable to a signal from the heart and mediated by a delta-opioid receptor mechanism in the brainstem, does depend on the integrity of suprapontine brain centres, though not on neurohypophysial AVP release.