Pathogenesis of an experimental heatstroke model.

1. Heatstroke was induced by exposure under general anaesthesia to a high ambient temperature. The moment in which the mean arterial pressure (MAP) began to decrease from its peak level was taken as the onset of heatstroke. 2. Compared with normothermic controls, rats with heatstroke had higher values for colon temperature, neuronal damage score and heart rate, but lower MAP and cerebral blood flow. 3. Induction of heat shock protein, antagonism of interleukin-1 or N-methyl-D-aspartate receptors or depletion of brain monoamines protects against the heatstroke-induced arterial hypotension and cerebral ischaemic injury. 4. Thus, it appears that arterial hypotension and cerebral ischaemic damage is the main reason for development of heatstroke syndromes.