BACKGROUND: Controversy exists over the efficacy of different methods for protecting the spinal cord against experimental ischemic injury. Therefore, the authors compared the protective effects of thiopental with those of hypothermia (35 degrees C and 32 degrees C) on hindlimb motor functions and histopathology after transient spinal cord ischemia. METHODS: Twenty-seven New Zealand white rabbits were assigned to one of the four groups: a thiopental-normothermia group (burst-suppression dose of thiopental; esophageal temperature = 38 degrees C; n = 7), a halothane-mild hypothermia group (halothane, 1%; esophageal temperature = 35 degrees C; n = 7), a halothane-moderate hypothermia group (halothane, 1%; esophageal temperature = 32 degrees C; n = 6), and a halothane-normothermia group (halothane, 1%; esophageal temperature = 38 degrees C; n = 7). The animals were then subjected to 20 min of spinal cord ischemia produced by occlusion of the aorta distal to the origin of left renal artery. Hindlimb motor function was observed for 48 h after reperfusion. Histopathology of the lumbar spinal cord also was examined. RESULTS: All animals in the halothane-mild hypothermia and halothane-moderate hypothermia groups were neurologically normal 48 h after ischemia. There was no statistical difference in the final neurologic status and histopathology between the thiopental-normothermia and halothane-normothermia groups. However, the final neurologic status and histopathology in both groups were worse than in the halothane-mild hypothermia or halothane-moderate hypothermia groups. There was a strong correlation between the final neurologic status and the numbers of normal neurons in the anterior spinal cord. CONCLUSIONS: These results suggest that mild and moderate hypothermia protects against ischemic spinal cord injury in rabbits, and a burst-suppression dose of thiopental does not offer any advantage over halothane.
BACKGROUND: Controversy exists over the efficacy of different methods for protecting the spinal cord against experimental ischemic injury. Therefore, the authors compared the protective effects of thiopental with those of hypothermia (35 degrees C and 32 degrees C) on hindlimb motor functions and histopathology after transient spinal cord ischemia. METHODS: Twenty-seven New Zealand white rabbits were assigned to one of the four groups: a thiopental-normothermia group (burst-suppression dose of thiopental; esophageal temperature = 38 degrees C; n = 7), a halothane-mild hypothermia group (halothane, 1%; esophageal temperature = 35 degrees C; n = 7), a halothane-moderate hypothermia group (halothane, 1%; esophageal temperature = 32 degrees C; n = 6), and a halothane-normothermia group (halothane, 1%; esophageal temperature = 38 degrees C; n = 7). The animals were then subjected to 20 min of spinal cord ischemia produced by occlusion of the aorta distal to the origin of left renal artery. Hindlimb motor function was observed for 48 h after reperfusion. Histopathology of the lumbar spinal cord also was examined. RESULTS: All animals in the halothane-mild hypothermia and halothane-moderate hypothermia groups were neurologically normal 48 h after ischemia. There was no statistical difference in the final neurologic status and histopathology between the thiopental-normothermia and halothane-normothermia groups. However, the final neurologic status and histopathology in both groups were worse than in the halothane-mild hypothermia or halothane-moderate hypothermia groups. There was a strong correlation between the final neurologic status and the numbers of normal neurons in the anterior spinal cord. CONCLUSIONS: These results suggest that mild and moderate hypothermia protects against ischemic spinal cord injury in rabbits, and a burst-suppression dose of thiopental does not offer any advantage over halothane.