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.
Department of Medicine, Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond, VA.
J
J
Koh
T E
TE
Brown
L A
LA
Beightol
C Y
CY
Ha
D L
DL
Eckberg
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