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

We have studied arterial baroreceptor reflexes in the conscious rabbit 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 was no 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 approximately 50% at 40 minutes, 4 hours, and 24 hours after the lesions, compared to preoperative values and to values at corresponding times in sham operated animals, but was restored to control levels 2 weeks after the lesions. Ventrolateral medullary lesions therefore destroy neurons that normally act to facilitate the baroreceptor heart period reflex, though it is clear that other neurons not affected by the lesions also participate in the reflex. Bilateral ventrolateral medullary lesions also participate in the reflex. Bilateral ventrolateral medullary lesions produced a greater than 50% reduction in the gain of the mean arterial pressure distal aortic flow curves evident throughout the 2-week observation period, indicating a persistent severe attenuation in the sensitivity of the baroreceptor-vasoconstriction reflex, similar in magnitude to that obtained after peripheral α-adrenergic blockade. It is our 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.