Human autonomic rhythms: vagal cardiac mechanisms in tetraplegic subjects.
1. We studied eight young men (age range: 20-37 years) with chronic, clinically complete high cervical spinal cord injuries and ten age-matched healthy men to determine how interruption of connections between the central nervous system and spinal sympathetic motoneurones affects autonomic cardiovascular control. 2. Baseline diastolic pressures and R-R intervals (heart periods) were similar in the two groups. Slopes of R-R interval responses to brief neck pressure changes were significantly lower in tetraplegic than in healthy subjects, but slopes of R-R interval responses to steady-state arterial pressure reductions and increases were comparable. Plasma noradrenaline levels did not change significantly during steady-state arterial pressure reductions in tetraplegic patients, but rose sharply in healthy subjects. The range of arterial pressure and R-R interval responses to vasoactive drugs (nitroprusside and phenylephrine) was significantly greater in tetraplegic than healthy subjects. 3. Resting R-R interval spectral power at respiratory and low frequencies was similar in the two groups. During infusions of vasoactive drugs, low-frequency R-R interval spectral power was directly proportional to arterial pressure in tetraplegic patients, but was unrelated to arterial pressure in healthy subjects. Vagolytic doses of atropine nearly abolished both low- and respiratory-frequency R-R interval spectral power in both groups. 4. Our conclusions are as follows. First, since tetraplegic patients have significant levels of low-frequency arterial pressure and R-R interval spectral power, human Mayer arterial pressure waves may result from mechanisms that do not involve stimulation of spinal sympathetic motoneurones by brainstem neurones. Second, since in tetraplegic patients, low-frequency R-R interval spectral power is proportional to arterial pressure, it is likely to be mediated by a baroreflex mechanism. Third, since low-frequency R-R interval rhythms were nearly abolished by atropine in both tetraplegic and healthy subjects, these rhythms reflect in an important way rhythmic firing of vagal cardiac motoneurones.
Koh
J
J
Department of Medicine, Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond, VA.
Brown
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Beightol
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Ha
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Eckberg
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D000328:Adult; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure; D002339:Carotid Arteries / Q000294:innervation / Q000502:physiology; D002395:Catecholamines / Q000097:blood; D006321:Heart / Q000187:drug effects / Q000294:innervation / Q000502:physiology* / Q000503:physiopathology; D006801:Humans; D008297:Male; D009046:Motor Neurons / Q000502:physiology; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology; D011782:Quadriplegia / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000503:physiopathology; D014630:Vagus Nerve / Q000502:physiology
D002395:Catecholamines; D009599:Nitroprusside; D010656:Phenylephrine; D001285:Atropine