[Effect of different delayed cooling time on organ injuries in rat models of exertional heat stroke].

J Zhao, Y Jia, H Mao, S Wang, F Xu, X Li, Y Tao, L Xue, S Liu, Q Song, B Zhou
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Abstract

Methods: To investigate how the timing of cooling therapy affects organ injuries in rats with exertional heat stroke (EHS) and explore the possible mechanisms.

Methods: 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.

Results: 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 (r=0.996, P=0.004) while the cooling rate negatively correlated with the mortality rate (r=-0.961, P=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.

Conclusion: 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.

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[不同延迟冷却时间对大鼠劳累性中暑模型器官损伤的影响]
方法研究降温治疗的时机对劳累性中暑(EHS)大鼠器官损伤的影响,并探讨可能的机制:方法:将60只成年雄性EHS模型Wistar大鼠随机分为建模后不主动降温模型组、建模后立即冷水浴降温组、建模后5、15和30 min冷水浴延迟降温组,另12只无EHS的小鼠为正常对照组。记录小鼠核心体温的变化并计算降温率。观察 24 小时后,对小鼠实施安乐死,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,然后对重要器官进行病理检查。对 24 小时内死亡的大鼠立即进行解剖检查:结果:模型大鼠在 24 小时内死亡的数量随着降温时间的延迟而显著增加。降温延迟时间与死亡率呈正相关(r=0.996,P=0.004),而降温速度与死亡率呈负相关(r=-0.961,P=0.009)。冷却干预组的炎症细胞因子水平呈现出不同的变化规律。所有EHS模型大鼠的器官均有明显损伤,主要表现为上皮脱落、水肿、渗出和炎性细胞浸润,脑和肾损伤在EHS后24小时达到高峰:结论:EHS 会对大鼠的重要器官造成严重程度不同的非特异性病变,而且随着冷却时间的延迟,损伤会逐渐加重。在 EHS 后不同的降温干预时间,大鼠血清炎症细胞因子的变化具有明显的异质性。
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来源期刊
南方医科大学学报杂志
南方医科大学学报杂志 Medicine-Medicine (all)
CiteScore
1.50
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0.00%
发文量
208
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