MECHANISM OF CIRCULATORY INSUFFICIENCY IN HEAT STROKE

中暑是一种医疗紧急情况，已经变得更加严重 近几年流行的原因是“Fun”越来越受欢迎 这种疾病的病理生理学机制仍然不清楚，但是 心血管系统的主要作用当然是 被认可了。在最近一次关于这一主题的国际研讨会上 有人建议将动物模型开发成专门的 研究血流流向肝脏、肾脏、皮肤和 体温过高时中枢神经系统。本提案满足了这一需求 直接去吧。用氯醛糖麻醉大鼠作为动物 模型，我们有初步证据表明 内脏血管控制的丧失可能是致命性机制 在体温过高时会导致循环衰竭。我们假设 事实的确如此，损害是通过调解 部分是通过释放内源性阿片类药物与 持续的自主活动。我们建议(A)厘定 心脏和外周血管的顺序和性质 对中暑前驱期的反应；(B)与 血液化学变化与心血管事件和 组织学损害；(C)确定肾上腺切除术的效果 外周血管内脏交感神经切除术 对高温的反应；(D)监测内脏交感神经 神经活动以应对热应激；(E)确定大脑是否升高 体温加重心血管功能不全；(F) 测定纳洛酮对生存和循环的影响 稳定性；和(G)确定在高温下存活的动物 如果是的话，这些动物有没有表现出 体温调节功能受损。衡量标准将包括 肾脏、肠系膜上动脉和心脏尾部血流 输出量、平均动脉压、下丘脑、核心和平均 皮肤温度。在具体的协议中，我们还将测量 交感神经活动和血儿茶酚胺(NE、DA、E)， PH、Na、K、乳酸和内毒素。这件事的意义 研究在于它对理解基础知识的贡献 中暑和其他休克的生理机制 综合症。它还可以提供证据来支持替代方案 治疗中暑患者的方法。

Heat stroke is a medical emergency that has become more prevalent in recent years due to the increased popularity of "fun runs." The pathophysiology of this disorder remains obscure, but the preeminent role of the cardiovascular system is certainly recognized. At a recent international workshop on the subject it was recommended that animal models be developed to specifically investigate blood flow distribution to the liver, kidney, skin, and CNS during hyperthermia. This proposal addresses that need directly. Using the chloralose anesthetized rat as an animal model, we have preliminary evidence indicating that a selective loss of splanchnic vascular control may be the fatal mechanism leading to circulatory failure in hyperthermia. We hypothesize that this is indeed the case and that the impairment is mediated in part by the release of endogenous opioids that interact with ongoing autonomic activity. We propose to (a) determine the sequence and nature of the cardiac and peripheral vascular responses to the prodromal period of heat stroke; (b) correlate the changes in blood chemistry with cardiovascular events and histological damage; (c) determine the effects of adrenalectomy and splanchnic sympathectomy on the peripheral vascular response to hyperthermia; (d) monitor splanchnic sympathetic nerve activity to heat stress; (e) determine if an elevated brain temperature potentiates cardiovascular insufficiency; (f) determine the effects of naloxone on survival and circulatory stability; and (g) determine if animals that survive a hyperthermic episode sustain brain lesions, and if so, do these animals manifest impaired thermoregulatory function. Measurements will include renal, superior mesenteric, and caudal blood flows, cardiac output, mean arterial pressure, and hypothalamic, core, and mean skin temperatures. In specific protocols, we will also measure sympathetic nerve activity and blood catecholamines (NE,DA,E), pH, Na+, K+, lactate, and endotoxin. The significance of this research lies in its contribution to understanding basic physiological mechanisms underlying heat stroke and other shock syndromes. It may also provide evidence to support alternative means of treating heat stroke victims.