Mordecai Y.-T. Globus

TL;DR: Results demonstrate that rectal temperature unreliably reflects brain temperature during ischemia, and that despite severe depletion of brain energy metabolites at all temperatures, small increments of intraischemic brain temperature markedly accentuate histopathological changes following 3-day survival.

TL;DR: The results suggest that mild intraischemic hypothermia does not affect the ischemia-induced local cerebral blood flow reduction or free fatty acid accumulation.

TL;DR: Levels of 1CBF, energy metabolites, and energy metabolites were uniformly reduced in both the ipsi‐ and contralateral striata at the end of the ischemic period, a finding implying that the lesion did not affect the severity of theIschemic insult itself, and suggests that excessive release of DA is important for the development of isChemic cell damage in the striatum.

TL;DR: The present data indicate that TBI is followed by prompt increases in both glutamate release and hydroxyl radical production from cortical regions adjacent to the impact site, suggesting a mechanism by which hypothermia confers protection following TBI.

TL;DR: It is indicated that intraischemic, but not postischemi, brain hypothermia provides chronic protection to the hippocampus after transient brain ischemia.