Although it is well established that patients with cervical spinal cord injury are prone to acute, marked, hypertensive episodes, i.e., autonomic hyperreflexia, the specific mechanisms mediating this sometimes-fatal phenomenon are not completely understood. In this report, we describe the preparation and characterization of a rat model of chronic cervical spinal cord injury and autonomic hyperreflexia. Adult male Sprague-Dawley rats were chronically instrumented with arterial, venous, and gastric catheters. Beginning the first day after a complete cervical spinal transection (CST) and continuing for 1 wk, acute hypertensive responses to a modest increase of urinary bladder pressure (0-20 mmHg) were studied. Mean arterial pressure increased 25.9 +/- 4.8 mmHg during bladder distension the first day after CST. This response was not significantly different 3, 5, and 7 days after CST (overall average = 18.0 +/- 2.3 mmHg). The pressor response to bladder distension was completely abolished by intravesical lidocaine and autonomic ganglionic blockade (atropine + hexamethonium). Responses to bladder distension were not observed after the administration of chloralose anesthesia. We conclude that after cervical spinal transection the rat exhibits autonomic hyperreflexia similar to that seen in humans with spinal injury. Furthermore, autonomic hyperreflexia is completely established within 24 h after CST in the rat. Finally, some spinal autonomic reflexes are suppressed by chloralose anesthesia in the rat.
Autonomic Hyperreflexia after Spinal Cord Injury