Experimental study on the pathogenesis of heat stroke.

A heat-balance study was carried out on conscious rabbits exposed to ambient temperatures (Ta) from 8 degrees to 40 degrees C. At Ta = 40 degrees C, heat gain exceeded heat loss and led to hyperthermia and heat stroke, and the latency for the onset of heat stroke was found to be around 87 minutes. At the onset of heat stroke, the comatose animals showed higher levels of rectal temperature, ear skin blood flow, respiratory evaporative heat loss, metabolic rate, intracranial pressure (ICP), and cerebral water content as compared to those of control animals (kept at an ambient temperature of 24 degrees C). Before the start of heat stress, the animals had an average mean arterial blood pressure (MABP) of 94 mm Hg and cerebral perfusion pressure (CPP) of 80 mm Hg. However, at the onset of heat stroke, the average MABP and CPP decreased to 67 and 19 mm Hg, respectively. The reduction in CPP at the onset of heat stroke was due to both a decrease in MABP and an increase in ICP. In addition, the comatose animals which received an intravenous infusion of 10% glycerol (3 ml/min) had a survival time (interval between onset of heat stroke and death) longer than that of the comatose animals which received the control-vehicle solution. The prolongation of survival time in the glycerol-treated animals may be due to lower rectal temperature, lower cerebral water content, or lower ICP during the development of heat stroke. The present data indicate that not only hyperthermia but also cerebral edema, intracranial hypertension, decreased MABP, and decreased CPP are the main causes of heat stroke. The therapeutic values of glycerol on heat stroke may be related to the depressant action on cerebral edema, intracranial hypertension, and body temperature.