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The present study attempted to ascertain whether hypothermia attenuated the heat stroke-induced dopamine overload and gliosis in rat brain. Urethane-anesthetized rats were exposed to water blanket temperature (T(blanket)) of 42 degrees C until mean arterial pressure (MAP) began to decrease from their peak levels, which was arbitrarily defined as the onset of heat stroke. Extracellular concentrations of dopamine in brain were assessed by microdialysis methods. Hypothermia was accomplished by decreasing T(blanket) from 42 to 16 degrees C. The animals exposed to T(blanket) of 26 degrees C served as the normothermic controls. The values of MAP in heat stroke rats without hypothermia were all significantly lower than those in normothermic controls. However, the extracellular levels of dopamine and the number of glial fibrillary acidic protein-reactive cells in brain were greater. Hypothermia immediately after the onset of heat stroke reduced the heat stroke-induced circulatory shock as well as dopamine overload and gliosis in brain. The data demonstrate that hypothermia attenuates both dopamine overload and gliosis in rat brain associated with heatstroke.

The quantitative autoradiographic 2-[(14)C]-deoxy-D-glucose methods were used to assess the local cerebral glucose utilization (LCGU) in 46 brain structures in rats suffering from heatstroke. Heatstroke was induced by exposing the animals to an ambient temperature of 42 degrees C. The time at which the local cerebral blood flow (CBF) and mean arterial pressure (MAP) decreased from their peak levels was taken as the onset of heatstroke. Control rats were exposed to a temperature of 24 degrees C. The values of local CBF, MAP and means of total LCGU after heatstroke onset were all significantly lower than those in control rats. However, the values of colonic temperature were greater. Thus, it appears that the decreased cerebral metabolism and perfusion can be due to secondary effect of hypertension after heatstroke onset.

We induced heat stress in urethane-anesthetized rats (the animals were exposed to an ambient temperature at 42 degrees C), and monitored their colon temperature, mean arterial pressure and local cerebral blood flow. Rats 0, 20, 40 or 80 min after heat stress were sacrificed for determination of c-fos mRNA and protein expression in the paraventricular nucleus (PVN), supraoptic nucleus (SON) and preoptic nucleus (PON). The heatstroke, which appears as profound decreases in both mean arterial pressure and local cerebral blood flow and increases in colon temperature, is produced 80 min after heat stress. We show the c-fos mRNA and protein is strongly induced in all these nuclei of rat hypothalamus after the onset of heatstroke. We conclude that c-fos expression in the hypothalamus during rat heatstroke is associated with hyperthermia, arterial hypotension and cerebral ischemia.

Rats 0, 16, or 48 h after heat shock (42 degrees C core temperature for 15 min) or chemical stress (5 mg/kg sodium arsenite, i.p.) were exposed to a high ambient temperature (43 degrees C) to induce heatstroke onset. The moment in which the mean arterial pressure and cerebral blood flow began to decrease from their peak values was taken as the onset of heatstroke. Prior heat shock or chemical stress conferred significant protection against heatstroke-induced arterial hypotension, cerebral ischemia, cerebral neuronal damage and death, and correlated with expression of HSP72 in brain, heart, liver and kidney at 16 h. However, at 48 h, when HSP72 expression returned to basal values, the above responses that occurred after the onset of heatstroke of two groups (0 h group VS 48 h group) were indistinguishable. The data suggest that HSP72 presence increases survival in rat heatstroke by attenuating arterial hypotension, cerebral ischemia and neuronal damage.

Anesthetized rats exposed to a high ambient temperature develop heatstroke with brain ischemia. Since nitric oxide (NO) plays an important role during normothermic ischemia, its cortical and cerebellar production were continuously assessed in pentobarbital anesthetized rats exposed to heat by using differential pulsed voltammetry. After 60 min at thermoneutrality, the rats were submitted to an ambient temperature of 40 degrees C until death. After 60 min in the heat, the rats were injected intraperitoneally with saline, MK801 (1 mg.kg(-1)), an antagonist of N-methyl-D-aspartate (NMDA) receptors, or L-arginine p-nitroanilide (L-ANA; 100 mg.kg(-1)), an inhibitor of NO synthase. Just before death, a 70% increase in NO production was observed in both the cerebellum and the cortex of saline-treated rats. The cortical increase in NO was not modified by MK801 while the NO signal was suppressed by L-ANA.