Karsten T M, van Gulik T M, Spanjaard L, Bosma A, van der Bergh Weerman M A, Dingemans K P, Dankert J, Gouma D J
Department of Surgery, Academic Medical Centre, Amsterdam, The Netherlands.
J Surg Res. 1998 Feb 1;74(2):125-30. doi: 10.1006/jsre.1997.5192.
The disruption of the hepatocyte tight junctions observed in biliary obstruction suggests altered permeability of the blood-bile barrier. In this study the role of biliary obstruction and increased biliary pressure on the translocation of bacteria from biliary tract to bloodstream and lymphatic system were evaluated.
Rats underwent distal bile duct ligation (BDL, n = 33) for two weeks or a sham celiotomy (n = 21). Seventeen of the 33 BDL rats underwent subsequent biliary decompression by a choledochojejunostomy (CJ). Two weeks after the final operation, a laparotomy was performed again and the CBD, the thoracic duct, and the caval vein were canulated. Next, a suspension containing 10(8) Escherichia coli/ml was retrogradely infused in the CBD for 5 min at 5 or 20 cm H2O above the secretory biliary pressure.
A higher biliary infusion pressure resulted in a significant increase of cfu E.coli per milliliter of blood in all the three groups (Sham, BDL, CJ). BDL rats showed significantly more bacterial translocation to the bloodstream than the shams. After biliary decompression, translocation normalized to the control levels. At 5 cm H2O infusion pressure only one lymph culture was positive (CJ group). At 20 cm H2O overpressure, nine lymph cultures were E.coli positive (P = 0.03). These were found mainly in groups with a nonobstructed bile duct (Sham and CJ 40% vs BDL 10%).
Translocation of bacteria from biliary tract to bloodstream increased at higher intrabiliary pressures. Longstanding bile duct obstruction was an independent determinant for cholangiovenous reflux. Bacterial translocation to the lymphatic system did not parallel translocation to the bloodstream, although in the nonobstructed biliary tract, increased bacterial translocation to the lymphatic system was pressure related.
在胆道梗阻中观察到的肝细胞膜紧密连接的破坏提示血-胆汁屏障通透性改变。本研究评估了胆道梗阻和胆道压力升高对细菌从胆道向血液和淋巴系统移位的作用。
大鼠接受远端胆管结扎术（BDL，n = 33）两周或假剖腹术（n = 21）。33只BDL大鼠中的17只随后通过胆总管空肠吻合术（CJ）进行胆道减压。末次手术后两周，再次进行剖腹术，插管至胆总管、胸导管和腔静脉。接下来，将含有10⁸/ml大肠杆菌的悬液在高于分泌性胆道压力5或20 cm H₂O的条件下逆行注入胆总管5分钟。
较高的胆道灌注压力导致所有三组（假手术组、BDL组、CJ组）每毫升血液中的大肠杆菌菌落形成单位（cfu）显著增加。BDL大鼠向血液中的细菌移位明显多于假手术组。胆道减压后，移位恢复至对照水平。在5 cm H₂O灌注压力下，仅1例淋巴培养阳性（CJ组）。在20 cm H₂O超压下，9例淋巴培养大肠杆菌阳性（P = 0.03）。这些主要见于胆管未梗阻的组（假手术组和CJ组为40%，BDL组为10%）。
在较高的胆道内压力下，细菌从胆道向血液的移位增加。长期胆管梗阻是胆管静脉反流的独立决定因素。细菌向淋巴系统的移位与向血液的移位并不平行，尽管在非梗阻性胆道中，细菌向淋巴系统的移位增加与压力有关。
