• D N Maiorov, M G Fehlings, and A V Krassioukov.
• The John P. Robarts Research Institute and The Department of Physiology, University of Western Ontario, London, Canada.
• J. Neurotrauma. 1998 May 1; 15 (5): 365-74.

AbstractAbnormal sympathetic tone after spinal cord injury (SCI) initially results in hypotension and is subsequently associated with autonomic dysreflexia characterized by paroxysmal hypertension and bradycardia in response to noxious or visceral stimuli. To evaluate the effect of a clinically relevant compression model of SCI on cardiovascular control in the early postinjury period, we monitored arterial pressure (AP) and heart rate under control resting conditions and after visceral stimulation (colon distension) in conscious rats for 1 week after clip compression injury of the cord at T5. Rats were randomly allocated into 4 groups (n = 8 each): sham-operated, 20, 35, and 50 g injuries. Only the 50 g injury was associated with significant hypotension (73 +/- 4 mmHg) at 1 day post-SCI when compared to sham-injured rats (91 +/- 3 mmHg). In control rats, colon distention caused a transient pressor response of 16 +/- 3 mmHg and tachycardia. In rats with 20 g 35 g, and 50 g injuries, colon distension 1 day after SCI increased AP by 8 +/- 2, 15 +/- 3, and 21 +/- 1 mmHg, respectively. The hypertensive response correlated with injury severity (r = 0.75; p < 0.0001) and was associated with bradycardia. By 7 days after SCI, only rats with 50 g cord injuries experienced hypertension with reflex bradycardia with visceral stimulation. These data show that dysfunctional cardiovascular control after SCI is correlated with the severity of injury. Mild and moderate compressive SCI result in transient cardiovascular abnormalities which normalize by 1 week. In contrast, more severe injuries are associated with neurogenic hypotension and autonomic dysreflexia.

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