Hubbard R W
Med Sci Sports. 1979 Spring;11(1):66-71.
This article reviews briefly the historical origins for both the cardiovascular and neural-anhidrotic concepts of heatstroke pathophysiology. It describes how deemphasis of the role of anhidrosis as the primary cause of heatstroke has resulted in: (a) an increased acceptance of animal models for heatstroke research; (b) further evidence that rigid reliance on the classic heatstroke symptoms (coma, anhidrosis, and a fever over 106 degrees F) can result in underdiagnosis; and (c) new research consistant with the hypothesis that exhaustive physical effort, by worsening circulatory collapse and metabolic acidosis predisposes tissue to hyperthermic injury and, as a result, substantially lowers the threshold for heatstroke injury and mortality. Thus, a new hypothesis combining the essential features of both direct thermal injury and cardiovascular origins of heatstroke pathophysiology may be necessary.
本文简要回顾了中暑病理生理学中心血管和神经无汗概念的历史起源。它描述了对无汗作为中暑主要原因这一作用的淡化是如何导致以下结果的：（a）对中暑研究动物模型的接受度增加；（b）进一步证明，严格依赖经典中暑症状（昏迷、无汗和体温超过106华氏度）可能导致诊断不足；（c）新的研究与以下假设一致，即竭尽全力的体力活动会通过加重循环衰竭和代谢性酸中毒使组织易受热损伤，从而显著降低中暑损伤和死亡率的阈值。因此，可能需要一个结合直接热损伤和中暑病理生理学心血管起源基本特征的新假设。
