论文部分内容阅读
目的：为阐明“二次打击”假说在创伤／休克后内源性感染发病中的病理意义，本研究探讨了低血容量性休克对轻度门静脉源性内素素血症的影响。方法：１８只动物分３组，即低血容量性休克组、脂多糖（ＬＰＳ）组和低血容量性休克＋ＬＰＳ组。结果：①输注完ＬＰＳ后，低血容量性休克＋ＬＰＳ组动物的血压持续下降，且明显低于单纯ＬＰＳ或单纯低血容量性休克组动物；而后两组动物的血压无明显变化。②休克后２４小时，低血容量性休克＋ＬＰＳ组动物全部死亡，而其余两组动物全部存活。③低血容量性休克＋ＬＰＳ组动物的血浆乳酸和β葡萄糖醛酸酶（βＧ）水平在输入ＬＰＳ后也显著升高，并明显高于单纯低血容量性休克组和单纯ＬＰＳ组。结论：低血容量性休克具有增加机体对内毒素敏感性的作用，继发于休克后的轻度内毒素血症在休克后器官功能损害中的作用不容忽视
Objective: To elucidate the pathological significance of the “second strike” hypothesis in the pathogenesis of endogenous infection after trauma / shock, this study investigated the effect of hypovolemic shock on mild portal venous endogenous hyperoxia. Methods: Eighteen animals were divided into three groups, namely hypovolemic shock group, lipopolysaccharide (LPS) group and hypovolemic shock + LPS group. Results: ① After LPS infusion, the blood pressure of hypovolemic shock + LPS group continued to decline, and was significantly lower than that of pure LPS or hypovolemic shock group. No significant changes were observed in the blood pressure of the two groups. 24 hours after shock, hypovolemic shock + LPS animals all died, while the remaining two groups of animals all survived. ③ The levels of plasma lactate and β-glucuronidase (βG) in hypovolemic shock + LPS group were significantly increased after LPS administration, and were significantly higher than those in hypovolemic shock group and LPS alone group. Conclusions: Hypovolemic shock can increase the body’s sensitivity to endotoxin. The role of mild endotoxemia secondary to shock in post-shock organ dysfunction should not be ignored