Sympathetic outflow in man after anaesthesia of the glossopharyngeal and vagus nerves.

Bilateral lidocaine blocks of glossopharyngeal and vagus nerves in the neck were made in two healthy subjects to achieve deafferentation of arterial and cardiopulmonary baroreceptors. Microelectrode recordings of muscle nerve sympathetic activity (MSA) were made in one peroneal nerve; in one subject skin sympathetic activity (SSA) was recorded simultaneously in the other peroneal nerve. Following the nerve block in the neck there was a strong increase of MSA accompanied by temporary hypertension and tachycardia. The normal cardiac rhythmicity of MSA disappeared and the outflow appeared as bursts of impulses of variable duration occurring in a slow, irregular rhythm. Thus MSA became similar to SSA, but the activities never became synchronous. During the nerve block arousal stimuli evoked single bursts of MSA, a reflex response which normally occurs in SSA but not in MSA. It is concluded that (1) cardiac rhythmicity of MSA is due to baroreceptor influence; (2) a low level of MSA at rest depends on strong baroreceptor inhibition and not on a weak central drive; (3) central sympathetic outflows to skin and muscle are similar though not identical and the different characteristics normally observed are due to a large extent to different modulatory influences from afferent activity (presumably of baroreceptor origin) in glossopharyngeal and vagus nerves; and (4) baroreceptor deafferentation resulting in resting tachycardia and hypertension may explain sympathetic hyperactivity in the Guillain-Barré syndrome.