重症中暑临床救治方法现状与研究进展

中暑是一种严重威胁健康的危重疾病，病情进展迅速，可出现全身炎症反应综合征（SIRS）和多脏器功能障碍综合征（MODS）而导致高病死率，即使存活者也有近30%存在神经等系统后遗症。传统上重症中暑的治疗以积极降温为核心，被称为中暑救治"第一关键点"。但近来研究发现，除了降温，积极治疗早期脏器损害，防止单一脏器损害向MODS发展，是改善重症中暑预后的关键，并由此提出"第二关键点假说"。基于以上认识，近十年来逐渐发展出了一系列新的治疗手段，但目前重症中暑整体临床治疗仍缺乏规范、统一的方案，其中某些治疗的疗效也尚未明确。本文主要从降温及全身脏器支持保护的角度，围绕"第一和第二关键点"救治理论，总结近年来临床上重症中暑救治措施的现状与研究进展，为规范临床救治和深入研究提供参考。     

热打击可通过调控内质网应激通路促进神经细胞凋亡

Objective To explore the role of endoplasmic reticulum stress in heat stress-induced apoptosis of human neuroblastoma SH-SY5Y cells. Methods SH-SY5Y cells were incubated at 43 ℃ for 2 h followed by further culture at 37 ℃ for 0, 3 h, or 6 h. With the cells cultured at 37 ℃ as the control, the cells exposed to heat stress were examined for morphological changes under optical microscope and changes in cell viability using CCK-8 assay. Flow cytometry was performed for detecting apoptosis of the cells following heat stress, and intracellular Ca2 + level in the cells was determined using flow cytometry and immunofluorescence confocal microscopy. The mRNA expression levels of caspase-12, BIP and XBP-1 in the cells were detected using qRT-PCR, and the protein expressions of caspase-12, BIP, P- JNK, JNK and XBP-1 were examined using Western blotting. The effect of pretreatment with 4-PBA on cell apoptosis following heat stress was analyzed with Western blotting. Results SH-SY5Y cells showed obvious cell shrinkage immediately after the exposure to heat stress, followed then by gradual cell stretching over time. The cell viability decreased significantly after heat stress (P=0.001), and the intracellular Ca2+ level increased significantly at 0 h and gradually recovered the normal level at 3 and 6 h. Heat stress induced significant increase in the protein expression of cleaved caspase-3 and time-dependent increase of caspase-12 (P=0.002) and BIP (P=0.008) expression at both the protein and mRNA levels. The expression of P-JNK/JNK protein increased significantly at 0 h (P=0.003) followed by gradual decrease; the expression levels of XBP-1 protein and mRNA gradually decreased after heat stress (P=0.005, P=0.002). Pretreatment with 4-PBA significantly reduced the expression level of cleaved caspase-3 in SH-SY5Y cells following heat stress. Conclusion Heat stress induces apoptosis of SH- SY5Y cells by triggering endoplasmic reticulum stress and the imbalance of intracellular calcium ion homeostasis.     

乌司他丁对重症中暑小鼠心功能损害的保护作用及机制研究

目的 研究乌司他丁对重症中暑所致小鼠心功能损害的保护作用,并进一步探讨其可能机制.方法 BALB/c小鼠20只按随机数字表法分为常温+生理盐水组(Sham+NS组)、常温+乌司他丁组(Sham+UTI组)、热打击+生理盐水组(HS+NS组)、热打击+乌司他丁组(HS+UTI组)4组,每组5只.在热打击开始前腹腔注射乌司他丁105U/kg进行预处理.常温两组置于环境温度23.0±0.5℃条件下,热打击两组置于高温气候动物培养箱(温度36.5±0.5℃,湿度65.0％±2.0％)内,以直肠温度(Tr)达42℃作为重症中暑标准.达中暑标准后,移至常温(23.0±0.5℃)进行自然降温处理,降温6h后进行心脏超声检测,分离心肌组织,进行病理学观察,Western blotting检测总p38及磷酸化p38(p-p38)含量.结果 在中暑热打击组中,HS+UTI组小鼠体温达42℃的时间较HS+NS组明显延长(P=0.044).与Sham+NS组相比,HS+UTI组与HS+NS组动物心输出量(CO)均明显下降(P=0.017),炎症损伤评分明显升高(P＜0.001),p-p38/p38比值升高(P＜0.001),而HS+UTI组CO下降程度明显低于HS+NS组(P=0.030),对应的炎症损伤评分(p＜0.001)及p-p38/p38比值(P=0.001)也均明显低于HS+NS组.结论 重症中暑热打击可导致小鼠心肌炎性损伤和心功能障碍,而乌司他丁对重症中暑小鼠心功能具有保护作用,可能与其下调p-p38水平,减轻心肌组织炎症损伤有关.     

分析综合保温护理在老年全身麻醉手术患者预防术中低体温的效果

目的 探讨在预防老年全身麻醉手术患者低体温中运用综合保温护理的效果。方法 我院在 2021 年 12 月至 2022 年 12 月 实施全身麻醉手术治疗的 80 例老年患者，按随机数字表法分为对照组和实验组，每组各 40 例。对照组护理方案为常规保温护 理，实验组护理方案为综合保温护理。比较两组的心体温、生命体征、凝血功能、并发症。结果 实验组核心体温高于对照组 （P<0.05）。实验组 PT、APTT、TT 水平高于对照组，FIB 水平低于对照组（P<0.05）。实验组 SBP、DBP、HR 水平高于对 照组（P<0.05）。实验组并发症率低于对照组（P<0.05）。结论 老年全身麻醉手术患者实施综合保温护理，可较好维持患者体 温，稳定生命体征、改善凝血功能，减少并发症。