With heat stress and exertion, homeostatic mechanisms become deranged and feedback mechanisms are activated (Fig 1). This scheme is based on the assumption that heat load associated with excessive sweating may lead to hypovolemia and subsequent heatstroke shock. Early signs of heat illness do not seem to be associated with hypovolemia. However, the interactions of pertinent vasoactive forces seem to be more complicated. The skin of heatstroke patients is usually hot and dry. When sweating no longer occurs, this may indicate an ineffective or defective sympathetic response. Experimentally, sympathectomy will increase blood supply through vasodilation. Renin, which stimulates the formation of the potent vasoconstrictor angiotensin, has been found in high concentrations in the plasma of heat exhaustion patients (Kashmeery199§.§). A well-established lag in rectal temperature (As..h.§L§l 1992) and frequent occurrence of acute renal failure strongly suggest dramatic splanchnic vasoconstriction, a function controlled by the sympathetic nervous system. In addition, individuals with prolonged exposure to elevated environmental temperatures and physical stress have been shown to have an increase in neutrophils, which secrete vasodilators such as bradykinin which may serve to redistribute blood flow to the periphery. Thus the possibility that vasodilatory mechanisms overcome elevated sympathetic nervous system response in heatstroke patients cannot be excluded.
Fig. 1 In progressive circulatory shock, homeostatic mechanisms become inadequate when positive feedback mechanisms are triggered and shock is deepened.
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