Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan 73657, Taiwan; Department of Dental Laboratory Technology, Min-Hwei College of Health Care Management, Tainan 73657, Taiwan.
Department of Pediatrics, Chi Mei Medical Center, Tainan 710, Taiwan; Center for General Education, Southern Taiwan University of Science and Technology, Tainan City 71005, Taiwan; Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; School of Medicine, Kaohsiung Medical University, Kaohsiung 81201, Taiwan.
Life Sci. 2023 Jun 15;323:121640. doi: 10.1016/j.lfs.2023.121640. Epub 2023 Mar 31.
Relatively little information is available about the effect of an acute exertional heat stroke (EHS) on myocardium structure and function. Herein, we used a survival male rat model of EHS to answer the question.
Adult male Wistar rats underwent forced treadmill running at a 36 °C room temperature and 50 % relative humidity until EHS onset, characterized by hyperthermia and collapse. All rats that were followed for 14 days survived. Injury severity scores of both gastrocnemius and myocardium were determined histologically. Following an EHS event, pathological echocardiography, skeletal muscle and myocardial damage scores and indicators, myocardial fibrosis, hypertrophy, and autophagy were elucidated.
Rats with EHS onset displayed skeletal muscle damage, elevated serum levels of skeletal muscle damage indicators (e.g., creatinine kinase, myoglobin, and potassium), and myocardial injury indicators (e.g., cardiac troponin I, creatinine kinase, and lactate dehydrogenase) returning to homeostasis within 3 days post-EHS. However, EHS-induced myocardial damage, pathological echocardiography, myocardial fibrosis, hypertrophy, and deposited misfolded proteins lasted up to 14 days post-EHS at least.
First, we provide evidence to confirm that despite the apparent return to homeostasis, underlying processes may still be ongoing after EHS onset. Second, we provide several key findings emphasizing the pathophysiology and risk factors of EHS, highlighting gaps in knowledge with the aim of stimulating future studies.
关于急性运动性热射病（EHS）对心肌结构和功能的影响，相关信息相对较少。在此，我们使用 EHS 的雄性大鼠存活模型来回答这个问题。
成年雄性 Wistar 大鼠在 36°C 的室温及 50%相对湿度的环境下进行强制跑步机跑步，直至出现 EHS，表现为体温过高和衰竭。所有随访 14 天的大鼠均存活。对腓肠肌和心肌的损伤严重程度进行组织学评分。在 EHS 发生后，阐明病理超声心动图、骨骼肌和心肌损伤评分和指标、心肌纤维化、肥大和自噬情况。
出现 EHS 的大鼠表现出骨骼肌损伤，血清中骨骼肌损伤指标（如肌酸激酶、肌红蛋白和钾）升高，心肌损伤指标（如肌钙蛋白 I、肌酸激酶和乳酸脱氢酶）在 EHS 后 3 天内恢复到正常水平。然而，EHS 引起的心肌损伤、病理超声心动图、心肌纤维化、肥大和沉积的错误折叠蛋白至少在 EHS 后 14 天内持续存在。
首先，我们提供了证据证实，尽管明显恢复到正常状态，但在 EHS 发生后，潜在过程可能仍在继续。其次，我们提供了一些关键发现，强调了 EHS 的病理生理学和危险因素，突出了知识空白，旨在激发未来的研究。
