Houdijk Alexander P J, Oosterling Steven J, Siroen Michiel P C, de Jong Sigrid, Richir M, Rijssenbeek Astrid L, Teerlink Tom, van Leeuwen Paul A M
Department of Surgery, Medical Center Alkmaar, Alkmaar, The Netherlands.
JPEN J Parenter Enteral Nutr. 2006 May-Jun;30(3):186-93. doi: 10.1177/0148607106030003186.
Surgery in obstructive jaundice is associated with complications related to gut-derived endotoxemia. The organs involved in these complications, including liver, kidneys, and gut, are important in the metabolism of taurine, which is implicated in bile acid conjugation and has antioxidative effects. Taurine organ metabolism and liver oxidative status were studied in bile duct-ligated rats (BDL) after laparotomy. Oral cholestyramine treatment inhibits gut-derived endotoxemia and was used to evaluate the role of endotoxin. In BDL rats, postoperative plasma taurine levels were higher compared with SHAM (p < .0001). Cholestyramine treatment reduced plasma taurine in BDL rats (p < .005), but levels remained higher compared with SHAM groups (p < .0001). In contrast to a liver uptake of taurine in SHAM rats, a release from livers of BDL rats was found (p < .005). Cholestyramine treatment in BDL rats resulted in a liver uptake of taurine (p < .05 vs BDL). A higher uptake of taurine by the kidneys was found in both BDL animals after surgery and SHAM controls (p < .005); however, cholestyramine had no effect. A release of taurine from the gut was found in the SHAM groups, which was reversed in both BDL groups (p < .01). Cholestyramine lowered the elevated levels of hepatic enzymes in BDL rats (ALT and AST: p < .05). Total liver glutathione levels were lower in BDL rats (p < .0001) compared with SHAM groups, and cholestyramine significantly attenuated this decrease (p < .01). Liver malondialdehyde levels were higher in BDL rats compared with SHAM (p < .01), whereas cholestyramine completely prevented this increase in lipid peroxidation (p < .0001). Hypertaurinemia in BDL rats after surgery is most likely explained by reduced bile acid conjugation and hepatocellular leakage. Cholestyramine treatment reduced hepatocellular damage by inhibiting gut-derived endotoxemia, and reversed the release of taurine from the jaundiced liver into an uptake and consequently lowered plasma taurine levels. This uptake may contribute to the improved antioxidant status in cholestyramine-treated BDL rats.
梗阻性黄疸手术与肠道源性内毒素血症相关的并发症有关。这些并发症所涉及的器官，包括肝脏、肾脏和肠道，在牛磺酸的代谢中起重要作用，牛磺酸参与胆汁酸结合并具有抗氧化作用。在剖腹术后的胆管结扎大鼠（BDL）中研究了牛磺酸的器官代谢和肝脏氧化状态。口服消胆胺治疗可抑制肠道源性内毒素血症，并用于评估内毒素的作用。在BDL大鼠中，术后血浆牛磺酸水平高于假手术组（p <.0001）。消胆胺治疗降低了BDL大鼠的血浆牛磺酸水平（p <.005），但与假手术组相比仍较高（p <.0001）。与假手术大鼠肝脏摄取牛磺酸相反，发现BDL大鼠肝脏释放牛磺酸（p <.005）。BDL大鼠接受消胆胺治疗后导致肝脏摄取牛磺酸（与BDL组相比，p <.05）。术后BDL动物和假手术对照组的肾脏对牛磺酸的摄取均较高（p <.005）；然而，消胆胺没有作用。在假手术组中发现肠道释放牛磺酸，而在两个BDL组中均逆转（p <.01）。消胆胺降低了BDL大鼠肝脏酶的升高水平（ALT和AST：p <.05）。与假手术组相比，BDL大鼠肝脏总谷胱甘肽水平较低（p <.0001），消胆胺显著减轻了这种下降（p <.01）。与假手术组相比，BDL大鼠肝脏丙二醛水平较高（p <.01），而消胆胺完全阻止了脂质过氧化的这种增加（p <.0001）。术后BDL大鼠高牛磺酸血症最可能的解释是胆汁酸结合减少和肝细胞渗漏。消胆胺治疗通过抑制肠道源性内毒素血症减少肝细胞损伤，并将黄疸肝脏中牛磺酸的释放逆转至摄取，从而降低血浆牛磺酸水平。这种摄取可能有助于改善消胆胺治疗的BDL大鼠的抗氧化状态。
