ON THE TRAIL OF POTASSIUM IN HEAT INJURY

In both classical and exertional heatstroke and in various animal mode ls of human heat injury, clinical manifestations have included observa tions of normokalemia, hyperkalemia, and hypokalemia. This review atte mpts to address these observations as well as the role of potassium an d potassium depletion in heat injury with an emphasis on the integrati on of information from the level of transmembrane potassium transport mechanisms to systems physiology. Under moderate conditions of passive heat exposure or exercise in the heat, the adaptive capacity of the N a-K pump (Na+-K+ ATPase activity) and cotransport mechanisms can ordin arily accommodate the attendant increased efflux of intracellular K+ a nd influx of extracellular Na+ to maintain ionic equilibrium. Several factors affecting transmembrane K+ kinetics include protracted K+ defi ciency, extreme hyperthermia, dehydration, and excessive exertion. The se could elicit reduced membrane potentials and conductance, futile cy cling of the Na-K pump with concomitant energy depletion and greatly i ncreased metabolic heat production, reduced arteriolar vasodilation, a ltered neurotransmitter release, or cell swelling, each of which could contribute to the pathophysiology of heat injury. This review represe nts a preliminary attempt to link transmembrane K+ pathophysiology wit h clinical heat injury.