大鼠肝缺血再灌注损伤时血清内毒素的变化及对心功能的影响

The alteration of serum endotoxin and the influence on cardiac function during liver ischemia reperfusion injury in rats

目的：探讨肝缺血再灌注损伤时内毒素变化对心功能的影响及其可能的发生机制. 方法：健康雄性Wistar大鼠48只随机分为对照组、缺血30 min组（Ⅰ组）及缺血30 min再灌注即刻、2 h、4 h和6 h组（I/R及I/R2、4、6 h 组）,每组8只,采用BL-420生物信号采集系统测定各组心功能[包括心率（HR）、左室收缩压（LVSP）、左室舒张末期压力（LVEDP）、左室内压最大上升/下降速率（±dp/dtmax）],采用偶氮显色法测定血清中的内毒素水平. 结果：在肝缺血再灌注损伤过程中,Ⅰ组、I/R组HR明显低于对照组（P＜0.05）,随着再灌注时间的延长呈上升趋势,但与对照组比较差异无统计学意义（P＞0.05）;I/R6 h组LVSP 、±dp/dtmax明显低于对照组（P＜0.05～0.01）,LVEDP明显高于对照组（P＜0.01）;Ⅰ组和I/R组内毒素水平达到高峰,随着再灌注时间的延长逐渐下降,但仍高于对照组（P＜0.05）. 结论：肝缺血再灌注损伤过程中,肠源性内毒素吸收入血及肝脏解毒功能的降低所致的内毒素血症是引起心功能改变的始动环节之一.

Objective： To investigate the effect and mechanism of serum endotoxin on cardiac function during liver I/R injury. Methods： Forty eight healthy Wistar male rats were randomly divided into 6 groups as following （n =8） ： the control group （CTL）, simply ischemia 30min without reperfusion （Ⅰ group）, reperfusion following ischemia 30 rain （I/R group）, 2 hours reperfusion following ischemia 30 rain （I/R2h group）, 4 hours reperfusion following ischemia 30 min （I/R4h group） and 6 hours reperfusion following ischemia 30min （I/R6h group）. The cardiac functions were measured by BL-420 E^＋ data acquisition and analysis system, including HR, LVSP, LVEDP,±dp/dtmax. The level of serum endotoxin was measured by kit. Results： During liver I/R injury, HR decreased obviously in the Ⅰ group and the I/R group （P 〈 0.05）, but the amount increased gradually with the prolongation of reperfusion, there was no statistic significance compared with CTL （P 〉0.05）. The levels of LVSP, LVEDP, ±dp/dtmax were statistic significantly in I/R6h group compared with that of CTL （P 〈0.05）. The level of endotoxin reached to peak in Ⅰ group and I/R group, the amount decreased gradually with the prolongation of reperfusion, but still higher than CTL （P 〈0.05）. Conclusion： During the process of liver I/R injury, endotoxin was absorbed from intestine and reducement of hepatic deintoxication led to endotoxemia which plays one of the initial roles in the changes of the cardiac function.