Cardiovascular effects of whole-body heating in spontaneously hypertensive rats.
The cardiovascular response to severe whole-body heating was examined in anesthetized spontaneously hypertensive (SH) (mean BP = 140 Torr) and normotensive (N) rats (mean BP = 96 Torr). Elevation of colonic temperature to 44 degrees C resulted in an initial increase in arterial pressure (mean BP: SH = 199 Torr, N = 124 Torr) with a subsequent severe hypotension. There was little evidence to suggest that this collapse in systemic pressure was related to a direct heat impairment of cardiac function. It was more likely the result of a progressive venodilation which produced venous pooling and decreased venous return. The arterial blood pressure response to exogenous catecholamine challenge decreased at elevated temperatures. This suggests that there was a deterioration of the vasoconstrictor response and indicated a possible effect of heat at the receptor or effector level. There were significant differences between the responses of normotensive and hypertensive rats to whole-body heating suggesting an enhanced cardiovascular sensitivity in hypertensive rats that may partially explain earlier reports of inferior thermoregulation and heat intolerance in these animals.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001833:Body Temperature Regulation; D004837:Epinephrine / Q000494:pharmacology; D006358:Hot Temperature; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D008168:Lung / Q000502:physiology; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D013990:Tidal Volume
D009638:Norepinephrine; D004837:Epinephrine