肝门阻断后细菌及内毒素移位的研究

Translocation of bacteria and endotoxin after portal triad clamping: Experimental and clinical study

细菌感染仍然是肝脏外科常见的并发症。为了了解其发生机理,通过阻断猪的肝门45分钟,松钳观察60分钟,造成肝缺血和内脏瘀血的动物模型,观察肠菌移位和血中内毒素含量,以及远端小肠粘膜的改变。结果发现:①阻断松解后门静脉血中内毒素含量明显高于阻断前和对照组;②实验组6只动物有4只出现肠菌移位;③实验组动物肠粘膜发生明显损伤。同时在16例肝切除病人的研究中也观察到有肠菌和内毒索移位现象。结果表明:肝门阻断可引起肠菌及内毒素移位及肠粘膜损伤;静脉内使用单一剂量的抗菌素不能完全杀灭进入周围血中的细菌,也不足以阻止肠菌移位。

An animal model of hepatic ischemia and gut congestion were established by clamping the portal triad in order to investigate the translocation of bacteria and endotoxin as well as the change of intestinal mucosa. The level of endotoxin was significantly in creased in the blood of portal vein and femoral artery after portal trias clamping (PIC) as compared with those of ore-clamping (P<0.05) and sham group (P<0.05). Among the 6 animals with portal triad clamping, 4 had bacterial translocations, while the culture of lymph nodes and blood in sham group were germ-free (P=0.0714). The intestinal mucosa had conspicuous damage (P<0.05) after the PTC was released. In clinical study, 16 patients who underwent hepatectomies with PTC were investigated. The results showed that the plasma endotoxin was markedly increased in traoperatively than that of the day before operation (P<0.01), and the bacterial translocations were observed in the blood and liver tissue. The present study suggests that PTC can result in intestinal mucosal damage and bacterial and endotoxin translocation. Prophylactic intravenous cephradine could not eradicate bacteria in the blood of peripheral circulation and could not prevent the bacterial translocation