Abstract

BACKGROUND/AIMS:Primary biliary cirrhosis (PBC), an autoimmunedisease of the liver, is marked by slow progressive destruction of bile ducts.These patients with PBC often undergo orthotopic liver transplantation (OLT).Ischemic bile duct lesion (IBDL) is a major source of morbidity and evenmortality after OLT. Cirrhosis of the liver has a higher tolerance to ischemiathan a normal liver, but the mechanism remains unknown. Angiogenesis andproliferation of bile duct often responses in bile duct ischemia, which mayenhance ischemic tolerance in patients with cirrhosis.

METHODOLOGY:To test the hypothesis, a rat model with cirrhosiswas established. Biochemical indexes of ischemic severity were measuredincluding total bilirubin (TBIL) and direct bilirubin (DBIL).Immunohistochemical assay was performed for Ki67 (a biomarker for theproliferation of bile duct) and CD34 (a biomarker of angiogenesis).

RESULTS:The levels were lower for TBIL and DBIL in the bileduct from rat model with cirrhosis than that from a normal rat after ischemicsurgery (P < 0.05). The levels were higher for Ki67 and CD34 from a ratmodel with cirrhosis than that from a normal rat after ischemic surgery (P <0.05).

CONCLUSIONS:The results suggest that a liver with cirrhosis hasa better ischemic tolerance than a normal liver. Angiogenesis and proliferationof bile duct enhances ischemic tolerance in rats with cirrhosis. More researchon the pathogenesis of IBDLs is needed for developing more specific preventiveor therapeutic strategies.