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Male Wistar rats with unilateral carotid ligation were exposed to arterial hypoxia (PaO2 20-23 torr for 20 min) while body temperature was controlled at 37 degrees C, 36 degrees C, or 34 degrees C. Brain cortical concentrations of ATP, phosphocreatine (PCr) and lactate were measured microfluorometrically. Normothermic hypoxic rats had severe metabolic changes with low brain ATP and extremely high brain lactate. When rectal temperature was controlled at 36 degrees C during hypoxia, brain ATP was not different from that observed in normothermic, normoxic rats, and brain lactate was significantly lower than during normothermic hypoxia. At 34 degrees C, brain lactate was even less, but still three times higher than that observed in normothermic normoxic rats. PCr was significantly higher following hypoxia at 34 degrees C than at 37 degrees C. In part, this latter finding may reflect preservation of intracellular pH at 34 degrees C. A decrease of body temperature of 1-3 degrees C can minimize or prevent brain energy failure during hypoxia as well as decrease the magnitude of brain tissue acidosis. Thus, in experiments examining "cerebral protective effects" of therapies during brain hypoxia-ischemia, stringent control of body temperature is necessary. Furthermore, a possible clinical benefit resulting from modest reduction in body temperature in patients with marginal cerebral oxygenation is suggested.
Berntman et al. (Sun,) studied this question.