Centrally evoked sympathetic discharge: a functional study of medullary vasomotor areas

Abstract
The medulla oblongata was stimulated electrically in decerebrate cats following bilateral vagotomy. Changes in splanchnic nerve discharge evoked by stimulation of pressor and depressor areas in the medulla were correlated with changes in arterial pressure. An interaction of baroreceptor afferents with the efferent sympathetic system at the level of the medulla and/or spinal cord was demonstrated. It may be possible to alter activity selectively in a given division (splanchnic) of the sympathetic outflow. Evoked responses were categorized. Sustained splanchnic activation; an immediate increase in total splanchnic activity, occurred with only a small, gradual decline in activity during the stimulation period. Mild stimulation (150-200 [mu]A) raised systolic pressure by 60-80 mm Hg and stronger stimulation (300-400 [mu]A) increased pressure by 100-150 mmHg. When comparable pressor responses were elicited from points on either side of the mid line, splanchnic excitation was greater with homolateral stimulation (left side). Unsustained splanchnic activation; an immediate increase in activity occurred which declined sharply as systolic pressure rose by 60-100 mm Hg during stimulation. Such a decline was attributed to the influence of baroreceptor afferents. Thus, if previous carotid occlusion was maintained during stimulation, the decline in activity was minimized although the pressor response increased. The structures yielding unsustained responses apparently differ from chose yielding sustained responses in their functional relation with the baroreceptor afferents. Reduced splanchnic discharge during direct medullary stimulation; a partial or complete inhibition of splanchnic activity was obtained, sometimes accompanied by a 20-40 mm Hg reduction in systolic pressure. However, the direction and magnitude of the systemic pressure change were not as consistently related to the splanchnic response as they were during activation. Even if splanchnic efferent activity were elevated by carotid occlusion, stimulation still reduced discharge.

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