动物受热致死过程内毒素血症的研究

A Study on Endotoxemia in HeatstrokeCausing Death in Animals

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。

This paper aimed to study whether heat exposure could cause endotoxemia and its main physiological response and pathophysiological changes.Heart rate,arterial blood pressure,respiratory rate,rectal temperature and plasma level of lipopolysaccharide (LPS) were measured in 24 rabbits exposed to heat at an average dry bulb temperature of (42±0.5)℃ wet bulb temperature of (35±0.5)℃ and relative humidity of (60±5)%.Results showed that (1) plasma LPS level in rabbits increased obviously during their heat exposure and reached 0.285 and 0.249 ng/ml before death from 0.139 and 0.131 ng/ml before exposure for Groups Ⅰ and Ⅱ,respectively (P<0.01);(2)as temperature rising to about 43℃,rabbits’heart rate and mean arterial blood pressure reached or approached to the peak,respiratory rate lowered,and plasma LPS concentration rose to a significant level,as compared with that before exposure both in Groups Ⅰ and Ⅱ;(3)occurrence of endotoxemia in heatstroke was due to decrease in animal's splanchnic blood flow and direct thermal damage.It suggested that LPS played an important role in pathophysiological process of heatstroke. 