Abstract
The influence of 5-min global cerebral ischemia on the facilitatory modulation of the vagal baroreflex through central α2-adrenoceptors or by the electrical stimulation of the septum was investigated in anesthetized dogs. Reflex bradycardia was produced by a bolus injection of phenylephrine at a dose which produces about a 25-mmHg increase in mean blood pressure. The ischemia was produced by the occlusion of the brachiocephalic and the left subclavian arteries with preceding ligation of the intercostal arteries. Clonidine at 10 μg, administered intracisternally, decreased the blood pressure and heart rate and facilitated the vagal reflex bradycardia. During the reperfusion period following ischemia, however, clonidine failed to affect the reflex bradycardia. Electrical stimulation of the septal region facilitated the reflex bradycardia without marked influences on the basal blood pressure and heart rate. The facilitatory effect was dependent on the frequency (10 to 75 Hz) and amplitude (3 to 15 V) of stimulation and was not observed after vagotomy or ischemic insult. These results suggest that 5-min global cerebral ischemia may produce the dysfunction of the neurons which are closely related to the baroreflex loop and receive the facilitatory modulation through α2-adrenoceptors and/or from the forebrain structures, leading to the dysfunction of the vagal baroreflex.
