Protection against experimental ischemic spinal cord injury.
The authors have studied the protection against ischemic damage to rabbit spinal cord by pretreatment with agents that block neuronal activity and directly or indirectly reduce tissue metabolism. Hypothermia, thiopental, magnesium, lidocaine, and naloxone were used to pretreat the spinal cord prior to ischemia. Hypothermia and thiopental provided comparable protection: they each increased the duration of ischemia required to produce neurological deficits in 50% of the animals from 26 to 41 minutes. They also increased from 10 to 30 minutes the time that the postsynaptic waves of the spinal somatosensory evoked potential (SSEP) could be absent and the animal still have neurological recovery. Hypothermia and thiopental, when used together, increased the duration of ischemia required to produce neurological deficits to 57 minutes in 50% of the animals. Naloxone increased the duration of ischemia required to produce neurological deficits to 36 minutes in 50% of the animals, and increased to 20 minutes the time that the postsynaptic waves of the SSEP could be absent and the animal still have neurological recovery. Magnesium pretreatment improved neurological outcome, possibly by improving collateral circulation as the SSEP did not fail completely during aortic occlusion in all animals. Lidocaine was not beneficial, perhaps because of the prolonged hypotension that resulted.
D000818:Animals; D001012:Aorta, Abdominal; D005073:Evoked Potentials, Somatosensory / Q000187:drug effects; D007036:Hypothermia, Induced; D007511:Ischemia / Q000188:drug therapy* / Q000628:therapy; D008012:Lidocaine / Q000627:therapeutic use; D008278:Magnesium Sulfate / Q000627:therapeutic use; D009270:Naloxone / Q000627:therapeutic use; D011817:Rabbits; D013116:Spinal Cord / Q000098:blood supply* / Q000502:physiology; D013874:Thiopental / Q000627:therapeutic use
D009270:Naloxone; D008278:Magnesium Sulfate; D008012:Lidocaine; D013874:Thiopental