Abstract

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 respectively 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 extreme heat loss beyond this point and to mitigate the potential detrimental effect in arterial pressure disturbance by extreme temperature condition. We also propose an additional explanation of this physiological counter mechanism based on the perspective of body core-peripheral steep temperature gradient reduction during hyperthermia or significant temperature increase, and a spontaneous tendency to avoid unstable blood pressure perturbation.