Résumé
Moderate hypothermia induced prior to recirculation of ischemic brain would conceivably inhibit the enzyme mediators of reperfusion injury. To challenge that hypothesis, groups of Wistar rats underwent 60 min or longer normothermic ischemia (37 degrees Celsius) induced by 4-vessel occlusion (4-VO). In group A, ischemia was prolonged for 30 min required for cooling and temperature stabilization at 33.O degrees Celsius, whilst in group B, the animals were reperfused at 60 min ischemia, maintained normothermic for 30 min, and then cooled down to 33 degrees Celsius. Hypothermia was sustained up to perfusion-fixation at 7 h and 7.5 h after recirculation in groups A and B respectively. Histological evaluation demonstrated partial neuronal loss in the hippocampus and cortex, without significant differences between the 2 groups (Mann-Whitney U-test). In constrast, untreated animals subjected to 60 min of normothermic ischemia (group C) consistently died prior to 7 h recovery, showing massive necrosis upon macroscopic examination of fresh brains. The animals of an additional group (D) initially treated as group A and rewarmed at 7 h recovery regained consciousness after rewarming, and showed no progression of neuronal loss at 24 h survival. These results indicate that the possible benefit of reperfusion under moderate hypothermia following 60 min normothermic ischemia does not surpass the consequences of a 50 per cent prolongation of carotid clamping.