Increased platelet and red cell counts, blood viscosity, and plasma cholesterol levels during heat stress, and mortality from coronary and cerebral thrombosis.
Recorded deaths from coronary and cerebral thrombosis rise markedly in heat waves. In a British heat wave with little or no distortion due to air-conditioning, outside temperatures of 34.6 degrees C (maximum) and 20.8 degrees C (minimum) were followed by peak mortalities from coronary and cerebral thrombosis one to two days later. Experimental exposure of volunteers to moving air at 41 degrees C for six hours caused core temperature to rise 0.84 degree C, weight to fall 1.83 kg with sweating despite access to water, heart rate to increase 32 beats per minute, and arterial pressure to fall, particularly on standing. The red blood cell count increased 9 percent, and blood viscosity increased 24 percent, mostly after the first hour. The platelet count rose 18 percent, and the platelet volume fell, mostly in the first hour. The plasma cholesterol level increased 14 percent without a change in distribution among lipoprotein fractions. The changes seem able to explain the increased mortality from arterial thrombosis in hot weather.
D000328:Adult; D001809:Blood Viscosity; D002784:Cholesterol / Q000097:blood*; D003327:Coronary Disease / Q000401:mortality*; D003328:Coronary Thrombosis / Q000401:mortality*; D004906:Erythrocyte Count; D005260:Female; D006358:Hot Temperature / Q000009:adverse effects*; D006801:Humans; D002542:Intracranial Embolism and Thrombosis / Q000401:mortality*; D008131:London; D008297:Male; D010976:Platelet Count; D013312:Stress, Physiological; D013546:Sweating
D002784:Cholesterol