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The effects of hypothermia on blood flow and neural activity were investigated in rabbit spinal cord during the acute phase of ischemia/reperfusion. Rabbits were exposed to ischemia for 10 or 40 min by occluding the abdominal aorta, using a balloon catheter. The body temperature was maintained either at 38 degrees C (normothermia) or 34 degrees C (hypothermia). Hyperperfusion was observed within 10 min after the cessation of ischemia in all rabbits exposed to ischemia. The magnitude of hyperperfusion in spinal cord blood flow (SCBF) was not significantly different between the 10 and 40 min ischemia rabbits, but the time for 50% recovery from the hyperperfusion was longer in the 40 min ischemia group (26.1 +/- 2.5 min) than in the 10 min group (15.1 +/- 2.1 min). The amplitude of evoked spinal cord potential decreased during ischemia and recovered to the baseline level during 8 h of reperfusion in the 10 min ischemia group. However, in the 40 min ischemia group, the amplitude was 40 +/- 8% of the baseline value after 8 h of reperfusion. Hypothermia prevented the delay of recovery from hyperperfusion and the reduction of evoked spinal cord potential. These results suggest that hypothermia plays a beneficial role in protecting tissue injury in the acute phase of ischemia/reperfusion in the spinal cord by shortening the time for recovery from postischemic hyperperfusion.

Effects of Hypothermia on Blood Flow and Neural Activity in Rabbit Spinal Cord during Postischemic Reperfusion.