重度热射病合并内毒素血症大鼠模型的建立

Establishment of a rat model of severe heatstroke complicated with endotoxemia

目的建立热射病合并内毒素血症大鼠的动物模型,为进一步探讨重度热射病的发病机制奠定基础。方法雄性 SPF级Wistar大鼠随机分为:常温生理盐水组(C组)、高温生理盐水组(H组)、常温细菌脂多糖组(L组)、高温细菌脂多糖组(HL组)。持续监测动物肛温、心率、平均动脉压、呼吸频率的动态变化,观察致伤0、40、80、120min的外周血白细胞计数、肺病理改变。结果(1)HL组动物肛温上升到(43．04±0．11)℃,心率加快到(660±42)次／min,呼吸频率加快到(150± 11)次／min,平均动脉压下降到(49．0±3．5)mmHg;其中动物肛温、心率、呼吸频率、平均动脉压与L组之间存在显著性差异,心率、平均动脉压与H组之间存在显著性差异;(2)L组、HL组白细胞计数显著下降而H组白细胞计数显著上升,L 组、HL组白细胞计数与H组之间存在显著性差异;(3)HL组动物肺组织出现急性微血管损伤改变。结论本研究较好地模拟了临床热射病合并感染发展为重度热射病的过程,是重度热射病多器官损伤肺启动机制研究较好的模型。

Objective To establish a rat model of heatstroke complicated by endotoxemia for studying the pathogenesis of severe heatstroke. Methods Male specific pathogen-free Wistar rats were randomly assigned into 4 groups, namely normothermic saline group （group C）, heat exposure saline group （group H）, normothermic LPS group （group L）, and heat exposure LPS group （group HL）. The rectal temperature （Tr）, heart rate （HR）, mean arterial pressure （MAP）, and respiratory rate （RR） of the rats receiving different treatments were continually monitored and their white blood cell count （WBC） and histology of the lungs were observed at 0, 40, 80 and 120 min after the treatments. Results The rats in HL-Group displayed significantly higher Tr （43.04±0.11℃）, HR （660＋42 beats/min）, and RR （150±11/min） but lower MAP （49.0±3.5 mmHg） as compared with the C Group. There were significant differences in the values of Tr, HR, RR and MAP between HL and group L and in HR and MAP between H groups HL and. The rats in group H displayed significantly higher WBC than group C. In contrast, the rats in L groups HL and had significantly lower WBC. LPS injection and heat stress induced pulmonary edema and features characteristic of acute microvascular lung injury in the rats. Conclusion The rat model established by LPS injection and heat stress can successfully mimic the development of severe heatstroke after LPS challenge and heat stress, and provides a suitable model for studying the primordial role of the lungs in the pathogenesis of severe heatstroke.