Department of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Hongo Bunkyo-ku, Tokyo, 113-8421, Japan.
Medical Intensive Care Unit-NHC, Strasbourg University (UNISTRA) Strasbourg University Hospital INSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine (RNM), FMTS, Strasbourg, France.
Inflamm Res. 2023 Mar;72(3):463-473. doi: 10.1007/s00011-022-01687-8. Epub 2023 Jan 7.
The number of heatstroke victims hit record numbers in 2022 as global warming continues. In heat-induced injuries, circulatory shock is the most severe and deadly complication. This review aims to examine the mechanisms and potential approaches to heat-induced shock and the life-threatening complications of heatstroke.
A computer-based online search was performed using the PubMed database and Web of Science database for published articles concerning heatstroke, shock, inflammation, coagulopathy, endothelial cell, cell death, and heat shock proteins.
Dehydration and heat-induced cardiomyopathy were reported as the major causes of heat-induced shock, although other heat-induced injuries are also involved in the pathogenesis of circulatory shock. In addition to dehydration, the blood volume decreases considerably due to the increased vascular permeability as a consequence of endothelial damage. Systemic inflammation is induced by factors that include elevated cytokine and chemokine levels, dysregulated coagulation/fibrinolytic responses, and the release of damage-associated molecular patterns (DAMPs) from necrotic cell death that cause distributive shock. The cytoprotective heat shock proteins can also facilitate circulatory disturbance under excess heat stress.
Multiple mechanisms are involved in the pathogenesis of heat-induced shock. In addition to dehydration, heat stress-induced cardiomyopathy due to the thermal damage of mitochondria, upregulated inflammation via damage-associated molecular patterns released from oncotic cells, unbalanced coagulation/fibrinolysis, and endothelial damage are the major factors that are related to circulatory shock.
随着全球变暖的持续，2022 年中暑患者人数创下历史新高。在热诱导损伤中，循环休克是最严重和致命的并发症。本综述旨在探讨热诱导休克的机制和潜在方法以及中暑的危及生命的并发症。
使用 PubMed 数据库和 Web of Science 数据库，基于计算机的在线搜索检索了有关中暑、休克、炎症、凝血障碍、内皮细胞、细胞死亡和热休克蛋白的已发表文章。
脱水和热诱导性心肌病被报道为热诱导性休克的主要原因，尽管其他热诱导性损伤也参与了循环性休克的发病机制。除脱水外，由于内皮损伤导致的血管通透性增加，血容量也会大大减少。全身性炎症是由细胞因子和趋化因子水平升高、凝血/纤溶反应失调以及来自坏死细胞死亡的损伤相关分子模式 (DAMPs) 的释放等因素引起的，导致分布性休克。细胞保护性热休克蛋白也可以在过热应激下促进循环障碍。
多种机制参与了热诱导性休克的发病机制。除脱水外，热应激诱导的心肌病是由于线粒体的热损伤、来自膨胀细胞的损伤相关分子模式上调炎症、失衡的凝血/纤溶以及内皮损伤是与循环性休克相关的主要因素。
