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本文旨在探讨热暴露是否可引起兔内毒素（ＬＰＳ）血症并观察其生理反应及病理生理学变化。在干球温度（４２±０．５）℃，湿球温度（３５±０．５）℃，相对湿度（６０±５）％条件下，测定了２４只热暴露兔的心率、平均动脉压、呼吸频率、肛温及血浆ＬＰＳ浓度等指标。结果：（１）在动物热暴露过程中，其血浆ＬＰＳ浓度明显增加，临近死亡时，Ⅰ、Ⅱ组分别由实验前的０．１３９、０．１３１ｎｇ／ｍｌ升高至０．２８５、０．２４９ｎｇ／ｍｌ（Ｐ＜０．０１）；（２）当Ｔｒ升至４３℃左右时，Ⅰ、Ⅱ组动物的ＨＲ、ＭＡＰ分别达到或接近峰值水平，而呼吸频率已开始下降，此时血浆ＬＰＳ浓度与实验前相比，已出现有意义的升高；（３）中暑ＬＰＳ血症的发生与高温时内脏血流的减少和热的直接损伤有关。上述结果提示，ＬＰＳ在中暑的病理生理学过程中是一个值得重视的因素
This article aims to investigate whether thermal exposure can cause rabbit endotoxin (LPS) hyperlipidemia and observe its physiological response and pathophysiological changes. The heart rate and mean arterial pressure of 24 rabbits exposed to heat were measured under the conditions of dry bulb temperature (42 ± 0.5) ℃, wet bulb temperature (35 ± 0.5) ℃ and relative humidity (60 ± 5) Respiratory rate, rectal temperature and plasma LPS concentrations and other indicators. Results: (1) During the process of animal heat exposure, the concentration of LPS in plasma increased significantly. At the time of death, the concentration of LPS in group Ⅰ and Ⅱ increased from 0.139,0.131ng / ml before the experiment to 0.285,0 respectively. 249ng / ml (P <0.01). (2) When Tr increased to about 43 ℃, the HR and MAP of group Ⅰ and Ⅱ reached or near the peak level respectively, while the respiratory rate started to decrease. At this time, the plasma LPS Compared with the pre-experiment, there was a significant increase of concentration. (3) The incidence of LPS in stroke is related to the reduction of visceral blood flow and the direct heat damage at high temperature. The above results suggest that LPS is a factor worthy of attention in the pathophysiology of heat stroke