CENTRAL AND PERIPHERAL MECHANISMS OF SWEATING CONTROL

点击翻译按钮获取中文摘要

Humans and patas monkeys depend on sweat evaporation to regulate body temperature during exercies and heat exposure. Cessation of sweating under these conditions can cause hyperthermia and death. Thermal and non-thermal stimuli participate in the control of sweating and evidence indicates that both central and peripheral mechanisms are involved. Of the non-thermal inputs, changes in fluid-electrolyte balance have a profound influence on the sweating response. However, the importance of central and peripheral adjustments in acute thermoregulatory responses, in heat stroke, and in heat acclimation remain unclear. We hypothesize that the sweating response to thermal and ion-osmotic stimuli has a central and peripheral component. Our specific aims are to determine (a) if changes in osmolarity, blood volume, and specific cations act centrally or peripherally to alter sweating; (b) if the changes in sweating observed in (a) are mediated by a central or peripheral action of antidiuretic hormone (AVP); (c) the putative neurotransmitter(s) that participate in the central control of sweating; (d) the role of endogenous peptides on peripheral mechanisms of sweat gland function; (e) if heat acclimation increases sweat gland size and function as well as the sensitivity of the central controller; and (f) if anhidrosis associated with heat stroke is mediated centrally and/or peripherally. Central control mechanisms will be studied using the techniques of micro injection and intracerebroventricular infusion superimposed on hypothalamic heating. Measurements will include central and skin temperatures, heart rate, blood pressure, and plasma concentrations of [Na+], [K+], [Ca2+], AVP, and plasma volume and osmolarity. Peripheral mechanisms will be studied by examining the effects of different solutions, endogenous peptides, and temperatures per se on cholinergic (MCH) responsiveness of isolated cannulated eccrine sweat glands in-vitro. Heat acclimation will be achieved by exercise in the heat and housing animals at 35C. Heat tolerance tests, sweat gland structure and function, and central sensitivity to previously determined putative transmitters that participate in sweating control will be assessed. The significance of this research lies in its contribution to understanding basic physiological mechanisms underlying sweating control. It will also provide insight into why anhidrosis develops during heat stroke despite markedly elevated core temperature.