Abstract

The paradoxical phenomena of hyperthermia-induced vasoconstriction, hyperthermia-induced hypothermia, and hyperthermia induced arterial vasoconstriction have been observed in animal heatstroke clinical case studies. We attempt to explain the basic mechanism behind such findings in terms of the principle of body heat conservation and natural countermeasure against heat exposure through reduction in the extent of vascular surface area exposed. Hyperthermia-induced vasoconstriction is a paradoxical physiological phenomenon that has limited explanation and exploration in research, despite being observed in clinical case studies. The bodily response of vasoconstriction and vasodilation to increased heat loss and gain work on the principle that heat transfer through the amount of vascular surface area exposed can be moderated in order to be minimised or maximised. Hyperthermia-induced vasoconstriction likely transitions from the break point of maximal limit of vasodilation to counter further rapid heat loss beyond this point. We also propose an explanation of this physiological counter mechanism from the perspective of body core-peripheral steep temperature gradient reduction during hyperthermia or extreme temperature conditions and a spontaneous tendency to avoid unstable blood pressure perturbation. One study which examined the outcome of heating a rabbit's carotid artery produced graded vasoconstriction which is proportional to temperature increase (Mustafa, Thulesius, & Ismael, 2004). These interesting results point out a spontaneous physiological counteractive measure to minimise organ and/or arterial surface area heat exposure through extreme vasodilation by inducing vasoconstriction to counter against persistent excessive heat loss from rapidly increasing temperature of internal organ(s) to the ambient environment, as well as to restore and re-elevate the simultaneous significant arterial blood pressure reduction due to extreme heat gain.