Coronary vascular response to the cerebral ischemia reflex.

Most centrally mediated sympathoexcitatory reflexes produce increases in arterial pressure, heart rate, and peripheral vascular resistance, including coronary vasoconstriction. Cerebral ischemia also causes large increases in arterial pressure and peripheral vasoconstriction but with modest or variable changes in heart rate. To examine the effect of cerebral ischemia on coronary vascular resistance, we produced cerebral ischemia in 14 cats by occluding the right brachiocephalic and left subclavian arteries for 30 seconds. After vagotomy and beta-blockade, a marked increase in arterial pressure (89 +/- 14%) and coronary vascular resistance (52 +/- 7%) was seen. After inhibition of the carotid baroreceptor reflex by surgical denervation and application of topical lidocaine, the increase in arterial pressure to cerebral ischemia was not affected, but the increase in coronary vascular resistance was attenuated (33 +/- 6%; p < 0.05 versus before denervation) to a level expected with autoregulation. To evaluate the possible contribution of the chemoreflex on coronary blood flow during cerebral ischemia, we conducted separate experiments in which nicotine was injected into both carotid arteries. Coronary constriction was not observed. Adrenalectomy and upper extremity ischemia likewise did not alter coronary vascular resistance. We conclude that cerebral ischemia elicits neurally mediated coronary vasoconstriction as a result of baroreceptor hypotension rather than directly. The relative absence of neurogenic coronary constriction and changes in heart rate suggest that sympathoexcitation during cerebral ischemia is directed more toward the peripheral vasculature than the heart.