Cerebrovascular responses to haemorrhagic hypotension in anaesthetized cats. Effects of α‐adrenoceptor antagonists

Abstract

Hemorrhagic hypotension induces the phenomenon of cerebrovascular autoregulation and, concomitantly, involves an activation of the sympathetic nervous system. As brain vessels in cats have an atypical adrenoceptor distribution the effects of an .alpha.-adrenoreceptor antagonist on the autoregulatory response to hemorrhage were studied. Cortical blood flow was studied by the H2 technique in chloralose-anesthetized cats subjected to a period of graded hemorrhage over 3 h. Three groups of cats were studied: control, i.e., those receiving saline (n = 10); yohimbine-treated (200 .mu.g/kg per h, n = 7); and prazosin-treated (50 .mu.g/kg per h, n = 6). In the control group, cortical blood flow remained relatively constant when mean arterial pressure was decreased from 102 .+-. 1 mmHg (mean .+-. SE) to .apprx. 50 .+-. 1 mmHg; thereafter, blood flow decreased with decreasing perfusion pressure. In the arterial pressure range 64-55 mm Hg, cortical blood flow was significantly higher in the yohimbine group (109 .+-. 12 ml/100 g per min) compared to the control group (69 .+-. 6 ml/100 g per min) and remained higher in the yohimbine-treated cats at more extreme levels of hypotension. Blood flow did not fall significantly in the yohimbine-treated cats until mean arterial pressures of 31 .+-. 1 mmHg were attained. In the prazosin-treated cats, flow began to decrease at arterial pressures even greater than those observed in the control group. There is a sympathetic vasoconstriction of brain arteries that is primarily mediated by .alpha.-adrenoceptors in the feline cerebrovascular bed.