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...

Full description

Saved in:
Bibliographic Details
Published in:Brain (London, England : 1878) England : 1878), 1985-06, Vol.108 (2), p.423-438
Main Authors: FAGIUS, JAN, WALLIN, B. GUNNAR, SUNDLÖF, GÖRAN, NERHED, CHRISTER, ENGLESSON, SÖREN
Format: Article
Language:English
Subjects:
Adult
Animals
Arousal - physiology
Biological and medical sciences
Cats
Glossopharyngeal Nerve - physiology
Hemodynamics
Humans
Hypertension - etiology
Hypertension - physiopathology
Male
Medical sciences
Microelectrodes
Muscles - innervation
Muscles - physiology
Nerve Block
Nervous system involvement in other diseases. Miscellaneous
Neurology
Peroneal Nerve - physiology
Polyradiculoneuropathy - physiopathology
Pressoreceptors - physiology
Skin - innervation
Sympathetic Nervous System - physiology
Tachycardia - etiology
Tachycardia - physiopathology
Vagus Nerve - physiology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0006-8950
1460-2156
DOI:10.1093/brain/108.2.423