Cardiovascular origins of heatstroke pathophysiology: an anesthetized rat model.
Opinion is divided on issues concerning a cardiovascular origin of heatstroke pathophysiology as well as those concerning the mechanism of circulatory failure in heat. Such controversies seem to arise because of insufficient data covering the prodromal period of heatstroke. A reappraisal of the nature and sequence of early circulatory responses to heat stress was, consequently, undertaken by subjecting male albino rats to an environmental temperature of 45 degrees C at 15% relative humidity until overt circulatory failure occurred. Although the initial circulatory responses were normal for mild exertion, an inapparent circulatory crisis developed, probably a result of the abolishment of compensatory splanchnic vasoconstriction. The impending threat of functional hypovolemia was, temporarily at least, obscured by cardiac compensation and the extent of cardiovascular commitments may, therefore, have been underestimated. This also suggests that cardiovascular adjustments during the stress of heat may prove to be an essential feature of heatstroke pathophysiology.
D000818:Animals; D001794:Blood Pressure; D001831:Body Temperature; D001833:Body Temperature Regulation; D002319:Cardiovascular System / Q000503:physiopathology*; D004562:Electrocardiography; D006339:Heart Rate; D006347:Heart Sounds; D006359:Heat Exhaustion / Q000503:physiopathology*; D008297:Male; D008954:Models, Biological; D051381:Rats / Q000502:physiology*; D012881:Skin Temperature; D013997:Time Factors