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目的探讨肠缺血再灌注损伤(I/R)对内毒素的增敏作用及其机制。方法大鼠肠系膜上动脉阻断45min 后松夹进行再灌注,静脉注射低剂量内毒素(LPS,1.5 mg/kg)。观察动物多脏器功能指标及体外诱生肿瘤坏死因子(TNF)的改变。结果 I/R+LPS 组显著加重全身血流动力学异常改变和肝、肺、肠等器官功能损害(P<0.01)。而单纯 LPS 组或 I/R 组上述指标改变较轻或无明显异常。体外试验显示,当 LPS 刺激浓度≤10 ng/ml 时,抗 CD14单抗可显著抑制全血 TNF的诱生(P<0.05～0.01),且 I/R 组抗 CD14单抗对 LPS 诱导 TNF 的抑制率明显高于伤前值或假手术组(P<0.05～0.01)。结论 I/R 可显著提高机体对 LPS 攻击的敏感性,其机理与体内 CD14依赖途径的作用增强有关。
Objective To investigate the sensitizing effects of intestinal ischemia reperfusion injury (I / R) on endotoxin and its mechanism. Methods Rats in the superior mesenteric artery were occluded for 45 min and then fasted for reperfusion. Low-dose endotoxin (LPS, 1.5 mg / kg) was injected intravenously. Observe the function index of multiple organ of animals and induce the change of tumor necrosis factor (TNF) in vitro. Results The I / R + LPS group significantly aggravated the hemodynamic abnormalities and the functional impairment of liver, lung, intestine and other organs (P <0.01). The simple LPS group or I / R group, the above indicators changed little or no abnormality. In vitro experiments showed that anti-CD14 mAb significantly inhibited the induction of whole blood TNF (P <0.05 ~ 0.01) when LPS stimulation was less than 10 ng / ml, and anti-CD14 mAb of I / The inhibition rate was significantly higher than the pre-injury value or sham operation group (P <0.05 ~ 0.01). Conclusion I / R can significantly increase the body’s sensitivity to LPS challenge. The mechanism is related to the enhanced role of CD14-dependent pathway in vivo.