Background

This study aimed to establish a traumatic hemorrhagic shock (THS) model in swine and examine pathophysiological characteristics in a dry-heat environment.

Methods

Forty domestic Landrace piglets were randomly assigned to four study groups: normal temperature non-shock (NS), normal temperature THS (NTHS), desert dry-heat non-shock (DS), and desert dry-hot THS (DTHS) groups. The groups were exposed to either normal temperature (25°C) or dry heat (40.5°C) for 3 h. To induce THS, anesthetized piglets in the NTHS and DTHS groups were subjected to liver trauma and hypovolemic shock until death, and piglets in the NS and DS groups were euthanized at 11 h and 4 h, respectively. Body temperature, blood gas, cytokine production, and organ function were assessed before and after environmental exposure at 0 h and at every 30 min after shock to death. Hemodynamics was measured post exposure and post-shock at 0 h and at every 30 min after shock to death.

Results

Survival, body temperature, oxygen delivery, oxygen consumption, and cardiac output were significantly different for traumatic hemorrhagic shock in the dry-heat groups compared to those in the normal temperature groups. Lactic acid and IL-6 had a marked increase at 0.5 h, followed by a progressive and rapid increase in the DTHS group.

Conclusions

Our findings suggest that the combined action of a dry-heat environment and THS leads to higher oxygen metabolism, poorer hemodynamic stability, and earlier and more severe inflammatory response with higher mortality.

中文翻译：

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沙漠干热环境下猪失血性休克模型及病理生理变化

背景

本研究旨在建立猪创伤性失血性休克（THS）模型并研究干热环境下的病理生理特征。

方法

40头家养长白仔猪随机分为4个研究组：常温非休克组（NS）、常温THS组（NTHS）、沙漠干热非休克组（DS）和沙漠干热THS组（DTHS）。将各组暴露于常温（25°C）或干热（40.5°C）3小时。为了诱导THS，NTHS和DTHS组的麻醉仔猪受到肝损伤和低血容量休克直至死亡，NS和DS组的仔猪分别在11小时和4小时处死。在环境暴露前后0小时和休克致死后每30分钟评估体温、血气、细胞因子产生和器官功能。在暴露后和电击后 0 小时以及电击致死后每 30 分钟测量一次血流动力学。

结果

干热组创伤性失血性休克患者的生存率、体温、供氧量、耗氧量和心输出量与常温组有显着差异。乳酸和IL-6在0.5 h时显着增加，随后DTHS组进行性快速增加。

结论

我们的研究结果表明，干热环境和 THS 的共同作用会导致更高的氧代谢、更差的血流动力学稳定性、更早、更严重的炎症反应以及更高的死亡率。