Zhao J, Jia Y, Mao H, Wang S, Xu F, Li X, Tao Y, Xue L, Liu S, Song Q, Zhou B
Department of Emergency Medicine, Sixth Medical Center of Chinese PLA General Hospital, Beijing 100048, China.
Graduate School of Medical School of Chinese PLA, Beijing 100853, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2024 Oct 20;44(10):1858-1865. doi: 10.12122/j.issn.1673-4254.2024.10.03.
To investigate how the timing of cooling therapy affects organ injuries in rats with exertional heat stroke (EHS) and explore the possible mechanisms.
A total of 60 adult male Wistar rat models of EHS were randomized into model group without active cooling after modeling, immediate cooling group with cold water bath immediately after modeling, delayed cooling groups with cold water bath at 5, 15 and 30 min after modeling, with another 12 mice without EHS as the normal control group. The changes in core body temperature of the mice were recorded and the cooling rate was calculated. After observation for 24 h, the mice were euthanized and blood samples were collected for detection of interleukin-1β (IL-1β), IL-2, IL-4, IL-6, IL-10, and interferon-γ, followed by pathological examination of the vital organs. The rats that died within 24 h were immediately dissected for examination.
The number of deaths of the model rats within 24 h increased significantly with the time of delay of cooling treatment. The delay of cooling was positively correlated (=0.996, =0.004) while the cooling rate negatively correlated with the mortality rate (=-0.961, =0.009). The inflammatory cytokine levels presented with different patterns of variations among the cooling intervention groups. All the rat models of EHS had significant organ damages characterized mainly by epithelial shedding, edema, effusion, and inflammatory cell infiltration, and brain and renal injuries reached the peak level at 24 h after EHS.
EHS causes significant nonspecific pathologies of varying severities in the vital organs of rats, and the injuries worsen progressively with the delay of cooling. There is a significant heterogeneity in changes of serum inflammatory cytokines in rats with different timing of cooling intervention following EHS.
研究降温治疗时机对劳力性热射病(EHS)大鼠器官损伤的影响,并探讨其可能机制。
将60只成年雄性Wistar大鼠EHS模型随机分为建模后未进行主动降温的模型组、建模后立即进行冷水浴的即刻降温组、建模后5、15和30分钟进行冷水浴的延迟降温组,另取12只未患EHS的小鼠作为正常对照组。记录小鼠体温变化并计算降温速率。观察24小时后,对小鼠实施安乐死并采集血样检测白细胞介素-1β(IL-1β)、IL-2、IL-4、IL-6、IL-10和干扰素-γ,随后对重要脏器进行病理检查。对24小时内死亡的大鼠立即进行解剖检查。
模型大鼠24小时内的死亡数随降温治疗延迟时间的延长而显著增加。降温延迟与死亡率呈正相关(r = 0.996,P = 0.004),而降温速率与死亡率呈负相关(r = -0.961,P = 0.009)。各降温干预组炎症细胞因子水平呈现不同变化模式。所有EHS大鼠模型均有明显的器官损伤,主要表现为上皮脱落、水肿、积液和炎症细胞浸润,脑和肾损伤在EHS后24小时达到峰值水平。
EHS可导致大鼠重要脏器出现不同程度的显著非特异性病变,且损伤随降温延迟而逐渐加重。EHS后不同降温干预时机的大鼠血清炎症细胞因子变化存在显著异质性。