Episodic hypertension due to autonomic dysreflexia in acute and chronic spinal cord-injured rats.

Spinal cord injury results in abnormal sympathetic control of the cardiovascular system, consisting of exaggerated reflexes with resulting hypertension and bradycardia that has been termed autonomic dysreflexia. We studied changes in arterial pressure and heart rate caused by colon or urinary bladder distension in unanesthetized acute (7 day) and chronic (30 day) spinal cord-injured rats to evaluate the time course of these responses in an animal model of spinal cord injury. In conscious control rats colon and bladder distension caused brief (2-10 s) pressor responses of 10 mmHg associated with tachycardia and escape reactions. Colon distension in spinal cord-injured rats increased arterial pressure by 41 +/- 2, 22 +/- 3; and 49 +/- 5 mmHg at 24 h and 7 and 30 days after cord transection, respectively. These responses lasted 30 s-5 min and were accompanied by bradycardia. Distension of the urinary bladder caused similar responses in spinal rats after 24 h and 30 days of cord transection. We propose that the initial responses may be related to loss of descending inhibition of spinal reflexes but that plastic changes in the spinal cord is one of the mechanisms for the autonomic dysreflexia occurring 1 mo after injury.