Post-ischemic hypothermia ameliorates ischemic brain damage but not post-ischemic audiogenic seizures in rats

The objective of this study was to describe a pattern of recovery and histological nerve cell loss in Sprague-Dawley rats exposed to severe brain ischemia and to compare it to that of Wistar rats.

Ether- and ketamine-anesthetized Sprague-Dawley rats were exposed to 3, 5, 6 and 10 min of normothermic severe brain ischemia (4 groups) induced by hypotension and neck compression. In group No. 5, the brain temperature was rapidly lowered, after 10 min of ischemia, to 30 degrees C during 45-50 min of recirculation. Wistar rats (group No. 6) served as controls (10-min normothermic ischemia).

In Sprague-Dawley (S-D) rats, post-ischemic audiogenic seizures (PAS) increased with the duration of ischemia and reached 86% (6/7 rats), after 10 min of ischemia. Mortality rate was high (50% = 7/14 rats). No seizure activity was observed after 10 min of ischemia in 6 Wistar (W) rats, and all survived. In the S-D rats, 10 min of ischemia produced histopathological damage in all brain regions examined, except in the thalamus. Damage was less severe in the W rats. Post-ischemic hypothermia ameliorated hippocampal and cortical nerve cell damage, but had no effect on the incidence of PAS activity and mortality. In W rats, hippocampal nerve cell loss was much less severe than in the S-D rats and cortical damage was not observed.

Sprague-Dawley rats develop post-ischemic audiogenic seizures more frequently than Wistar rats and mortality rate is high. The incidence of post-ischemic audiogenic seizures and mortality correlates well with the duration of ischemia. Post-ischemic moderate hypothermia (30 degrees C) significantly ameliorated the hippocampal and cortical nerve cell losses after 10 min of severe brain ischemia, but did not improve outcome. It appears that the high mortality rate of S-D rats following brain ischemia is related to frequent post-ischemic audiogenic seizures.