Arterial baroreceptor reflex function in the conscious rabbit after brainstem lesions coinciding with the A1 group of catecholamine neurons.

Abstract

Arterial baroreceptor reflexes in the conscious rabbit were studied after bilateral electrolytic lesions of the ventrolateral medulla, coinciding with the A1 group of catecholamine cells. Baroreflex function was determined from the changes induced in heart period and distal aortic blood flow in response to graded alterations in mean arterial pressure produced by inflation of balloon occluders around the thoracic inferior vena cava and the upper abdominal aorta. Distal aortic blood flow was determined using a Doppler ultrasonic flowmeter placed around the lower abdominal aorta. There were not significant changes in baroreflex function in sham-operated animals in which electrodes were inserted without the passage of current. The gain of the baroreceptor-heart period curves was reduced by .apprx. 50% at 40 min, 4 h and 24 h after the lesions, compared to preoperative values and to values at corresponding times in sham-operated animals, but was restored to control levels 2 wk after the lesions. Ventrolateral medullary lesions destroy neurons that normally act to facilitate the baroreceptor-heart period reflex though other neurons unaffected by the lesions also participate in the reflex. Bilateral ventrolateral medullary lesions produced > 50% reduction in the gain of the mean arterial pressure-distal aortic flow curves evident throughout the 2-wk observation period, indicating a persistent severe attenuation in the sensitivity of the baroreceptor-vasoconstriction reflex, similar in magnitude to that obtained after peripheral .alpha.-adrenergic blockade. It is a hypothesis that the persistent loss of the baroreceptor-vasoconstriction reflex results from destruction of A1 noradrenergic nerves that normally act in concert with the afferent connections of arterial baroreceptor reflexes to inhibit sympathetic vasoconstrictor tone and that the temporary loss in sensitivity of the baroreceptor-heart period reflex is caused by destruction of A1 neurons that participate in the control of heart rate.