CENTRAL AND PERIPHERAL MECHANISMS OF SWEATING CONTROL

人类和猕猴依靠汗液蒸发来调节身体 运动和热暴露时的温度。 下止汗 这些情况会导致体温过高和死亡。 热和非热 刺激参与出汗的控制，证据表明， 涉及中枢和外周机制。 非热的 输入，液体-电解质平衡的变化对 出汗的反应。 然而，中央和外围的重要性 急性体温调节反应，中暑， 热适应尚不清楚。 我们假设出汗反应 对热和离子渗透刺激有中枢和外周成分。 我们的具体目标是确定（a）如果渗透压，血液 体积和特定的阳离子作用于中心或外周， 出汗;（B）如果（a）中观察到的出汗变化是由 抗利尿激素（AVP）的中枢或外周作用;（c） 参与中枢控制的假定神经递质 出汗;（d）内源性肽对外周机制的作用， 汗腺功能;（e）如果热适应增加汗腺大小 和功能以及中央控制器的灵敏度;以及（f） 如果与中暑相关的无汗症是中枢介导的和/或 外围的 中央控制机制将使用 微量注射和脑室灌注技术 叠加在下丘脑加热上。 测量将包括中央 以及皮肤温度、心率、血压和血浆 [Na +]、[K +]、[Ca2 +]、AVP浓度和血浆容量， 渗透压 外周机制将通过检查影响进行研究 不同的解决方案，内源性肽，和温度本身， 离体外泌汗的胆碱能反应性 体外腺体。 热适应将通过在高温下运动来实现 并在35 ℃下饲养动物。 耐热性测试，汗腺结构 和功能，以及对先前确定的假定的 将评估参与出汗控制的递质。 的 这项研究的意义在于它有助于理解 控制出汗的基本生理机制。 它还将 提供深入了解为什么无汗症的发展在中暑，尽管 核心温度明显升高

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.