title: Acute spinal cord ischemia: prevention of paraplegia with verapamil.
abstract: Although irreversible damage to the central nervous system has been considered inevitable after 6 min of circulatory deprivation, there has been evidence for almost 20 years that this may be the consequence of postischemic events. Recent investigations have implicated calcium-mediated phenomena as responsible for damage to neuronal cells in the reperfusion period. We studied the effect of verapamil on the neurologic sequelae of spinal cord ischemia using somatosensory evoked potential monitoring in a canine preparation of spinal cord ischemia. Ten mongrel dogs weighing between 20 and 30 kg each were divided into two groups. The experimental group was pretreated with 0.4 mg/kg verapamil and the control group received no treatment. The thoracic aorta was then occluded. Flow was restored 17 min after there was complete loss of somatosensory evoked potentials. Experimental dogs received additional doses of verapamil upon reperfusion and at 1, 2, 3, 4, 5, 6, and 10 hr after reperfusion. Four of five verapamil-treated dogs were able to walk postoperatively, whereas all of the control dogs suffered dense paraplegias (p = .02). We conclude that verapamil can ameliorate the sequelae of spinal cord ischemia and that this preparation is suitable for the study of the mechanisms of ischemic neuronal damage in an area outside the brain.
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology; D004285:Dogs; D005073:Evoked Potentials, Somatosensory; D007473:Ion Channels / Q000502:physiology; D007511:Ischemia / Q000150:complications*; D010264:Paraplegia / Q000209:etiology / Q000517:prevention & control*; D013116:Spinal Cord / Q000098:blood supply*; D014700:Verapamil / Q000627:therapeutic use*
chemical_list: D007473:Ion Channels; D014700:Verapamil; D002118:Calcium