On the trail of potassium in heat injury.
In both classical and exertional heatstroke and in various animal models of human heat injury, clinical manifestations have included observations of normokalemia, hyperkalemia, and hypokalemia. This review attempts to address these observations as well as the role of potassium and potassium depletion in heat injury with an emphasis on the integration 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 Na-K pump (Na+-K+ ATPase activity) and cotransport mechanisms can ordinarily accommodate the attendant increased efflux of intracellular K+ and influx of extracellular Na+ to maintain ionic equilibrium. Several factors affecting transmembrane K+ kinetics include protracted K+ deficiency, extreme hyperthermia, dehydration, and excessive exertion. These could elicit reduced membrane potentials and conductance, futile cycling of the Na-K pump with concomitant energy depletion and greatly increased metabolic heat production, reduced arteriolar vasodilation, altered neurotransmitter release, or cell swelling, each of which could contribute to the pathophysiology of heat injury. This review represents a preliminary attempt to link transmembrane K+ pathophysiology with clinical heat injury.
Francesconi
R P
RP
Military Nutrition and Biochemistry Division, US Army Research Institute of Environmental Medicine, Natick, MA 01760-5007, USA.
Willis
J S
JS
Gaffin
S L
SL
Hubbard
R W
RW
D001692:Biological Transport; D018883:Heat Stroke / Q000503:physiopathology*; D006801:Humans; D006947:Hyperkalemia / Q000503:physiopathology; D007008:Hypokalemia / Q000503:physiopathology; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism
D012964:Sodium; D011188:Potassium