Abstract
The importance of small variations in brain temperature on ischemic outcome was first investigated in models of transient forebrain global ischemia [2]. These controlled studies followed preliminary observations in experiments in which only core (rectal) temperature was monitored and maintained (36.5°C) indicating that 1) ischemic CA1 hippocampal pathology commonly varied from one study to the next, 2) that rectal (core) and intraischemic brain temperature differed significantly, and 3) that in anesthetized rats, intraischemic brain temperature was commonly hypothermic. Thus, selectively decreasing intraischemic brain temperature to 30°–34°C protected the CA1 hippocampus and dorsolateral striatum [2,4]. In gerbils, a 2°C drop in body temperature provided 100% protection in the CA1 hippocampus [6]. Brain cooling during prolonged (30min) global ischemia also protected the cerebral cortex from histopathological damage [12]. In models of cardiac arrest and cardiopulmonary bypass (CPB), hypothermic protection has also been reported [9,13–15,22].
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Hayashi, N., Dietrich, D.W. (2004). Global and Focal Cerebral Ischemia. In: Brain Hypothermia Treatment. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53953-7_2
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DOI: https://doi.org/10.1007/978-4-431-53953-7_2
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