MECHANISM OF CIRCULATORY INSUFFICIENCY IN HEAT STROKE

劳累导致的中暑是第二个最常见的原因 美国运动员头部和脊椎受伤致死。 此外，在美国，典型的中暑导致数百人死亡， 1987年热浪中的希腊。这种病的病理生理学 疾病仍不清楚，但心血管疾病的突出作用 系统得到了很好的认可。在最近一次关于热能的国际研讨会上 中风的动物模型被建议发展成 专门研究流向肝脏、肾脏的血流分布， 体温过高时皮肤和中枢神经系统的损伤。我们花了3年时间建立了这样的模式 根据我们目前的发现，我们假设体温过高 会导致心血管功能不全，在高温下的致命机制 中风涉及内脏血管控制的选择性丧失。这 提案继续侧重于血管控制的系统性机制 并开始探索其中涉及的组织机制。我们的具体目标 评估(A)高温症患者内脏血管收缩 大鼠在小肠产生粘膜损害，毛细血管增加 通透性，并导致内毒素血症导致低血压； 生存能力，(C)心肺压力反射的作用，氧气 自由基、内毒素和神经体液机制在介导 高温期间内脏血管阻力的变化；及(D) 训练和热习服对循环反应的影响 为了体温过高。我们还计划识别该区域的船只 对内脏血管有贡献的体内微循环 并建立一种隔离血管制剂，将 使我们能够确定(A)耐高温容器的温度 扩张，(B)血管内皮细胞在调节血管内皮功能中的作用 热应激动物内脏阻力的降低，以及(C) 如果受体对去甲肾上腺素的敏感性因高温而显著改变。 活体测量将包括肾脏、肠系膜上段和尾部。 动脉血流量、平均动脉压、心率、核心身体 温度和一阶、二阶和三阶的内部尺寸 肠血管系统内的小动脉。体外测量 隔离容器将包括压力和尺寸分析 血管内皮细胞和不内皮细胞都完好无损。具体而言 协议，我们还将测量交感神经活动，渗透压 反射系数和血浆内毒素水平。这个 这项研究的意义在于它对理解 中暑和休克综合征的基本机制 血容量减少。因此，这项研究产生的信息具有 应用于众多临床问题。

Exertion induced heat exhaustion is the second most common cause of death following head and spinal injuries among American athletes. Moreover, classical heat stroke killed hundreds of people in the USA and Greece during the heat waves of 1987. The pathophysiology of this disorder remains obscure, but the preeminent role of the cardiovascular system is well recognized. At a recent international workshop on heat stroke it was recommended that animal models be developed to specifically investigate blood flow distribution to the liver, kidney, skin, and CNS during hyperthermia. We established such a model 3 years ago and based on our current findings we hypothesize that hyperthermia causes cardiovascular insufficiency and that the fatal mechanism in heat stroke involves the selective loss of splanchnic vascular control. This proposal continues to focus on systemic mechanisms of vascular control and begins to explore the tissue mechanisms involved. Our specific aims are to evaluate (a) if splanchnic vasoconstriction in the hyperthermic rat produces mucosal lesions in the small intestine, increases capillary permeability, and causes endotoxemia leading to hypotension; (b) survivability, (c) the role of cardiopulmonary baroreflexes, oxygen radicals, endotoxins, and neurohumoral mechanisms in mediating the changes in splanchnic vascular resistance during hyperthermia; and (d) the effects of training and heat acclimation on the circulatory response to hyperthermia. We also plan to identify the vessels within the microcirculation, in vivo, that contribute to splanchnic vascular resistance and to establish an isolated vessel preparation that will enable us to determine (a) at what temperature resistance vessels dilate, (b) the role of the vascular endothelium in mediating the reduction in splanchnic resistance in the heat-stressed animal, and (c) if receptor sensitivity to NE is significantly altered by hyperthermia. In vivo measurements will include renal, superior mesenteric, and caudal artery blood flows, mean arterial pressure, heart rate, core body temperature, and internal dimensions of 1st, 2nd, and 3rd order arterioles within the intestinal vasculature. In vitro measurements on isolated vessels will include pressure and dimensional analysis on vessels with and without their endothelium intact. In specific protocols, we will also measure sympathetic nerve activity, the osmotic reflection coefficient, and endotoxins levels in the plasma. The significance of this research lies in its contribution to understanding basic mechanisms underlying heat stroke and shock syndromes produced by hypovolemia. Thus, the information generated by this research has application to numerous clinical problems.