Central neural mechanisms of the cerebral ischemic response. Characterization, effect of brainstem and cranial nerve transections, and simulation by electrical stimulation of restricted regions of medulla oblongata in rabbit.

Abstract

Cerebral ischemia was elicited in anesthetized rabbits by briefly clamping both common carotid arteries after previously occluding the vertebral arteries. The primary cerebral ischemic response, elicited after elimination of baroreceptors, consisted of arterial hypertension, bradycardia, and apnea. The hypertension resulted from a stereotyped and differentiated pattern of vasoconstriction in renal, mesenteric and femoral arteries. Total peripheral conductance and cardiac output were decreased. Vagotomy usually changed the bradycardia to a tachycardia unaffected by adrenalectomy. With baroreceptors intact the magnitude of the bradycardia increased and its latency decreased. The ischemic response persisted after transection of brainstem at the pontomedullary junction and/or of lower cranial nerves (except for the bradycardia which was abolished by transection of vagal rootlets). Transection of the spinal cord at C1 abolished the reflex hypertension and apnea, but not the bradycardia. Hypertension and changes of regional blood flow, comparable qualitatively and quantitatively to those elicited by ischemia, were produced by electrical stimulation of areas of the medullary reticular formation encompassing portions of the gigantocellular and parvocellular reticular nuclei. The primary cerebral ischemic response is associated with a neurally mediated and differentiated pattern of vasoconstriction and with coactivation of the cardiac vagal and sympathetic nerves. The reflex cardiac, but not vasomotor, components are secondarily modified by baroreceptor reflexes. The ischemic response results from direct stimulation of neurons in the medulla oblongata. The parvocellular and gigantocellular nuclei mediate the vasomotor but not the cardiac and respiratory components of the response.