Circulatory changes associated with heat stroke: observations in an experimental animal model

1. Although heat stroke is a frequent cause of death in both humans and animals as a result of climatic or exercise-imposed stress, underlying mechanisms are understood poorly. In order to develop more effective strategies for prevention and treatment of this cause of death and suffering, controlled experiments were conducted on a small number of sheep to examine cardiovascular involvement in the thermoregulatory failure of heat stroke. 2. Sheep were studied in a hot environment at rest and then during exercise until collapse. 3. With exercise, mean arterial pressure (MAP) increased slightly, cardiac output (CO) increased markedly and total peripheral resistance (TPR) decreased slightly. As collapse was imminent, MAP increased but CO and TPR did not change significantly. On collapse, MAP and TPR increased markedly and CO decreased markedly. 4. Radioactive microsphere measurements demonstrated during exercise a redistribution of blood flow (BF) away from abdominal viscera and torso skin, to muscles involved in exercise, respiratory muscles, myocardium, fat, limb skin and nasobuccal tissues. With progressively increasing heat stress and exercise, BF increased in exercise muscles and decreased in limb skin and fat. As collapse was imminent, there were sharp increases in BF in exercise muscles, brain and spinal cord. On collapse, BF decreased markedly in exercise and respiratory muscles and fat. 5. It is concluded that collapse and ultimately heat stroke are not due primarily to cardiovascular 'failure' but, rather, to consequences of high body temperatures resulting from thermoregulatory failure attributable to demands for blood pressure regulation dominating requirements for body temperature regulation.