Obstructive jaundice impairs hepatic sinusoidal endothelial cell function and renders liver susceptible to hepatic ischemia/reperfusion

Background/Aims: Obstructive jaundice is associated with increased surgical morbidity and mortality. While parenchymal injury has been defined in obst ructive jaundice, the pathogenesis of hepatic sinusoidal endothelial cell i njury in obstructive jaundice is unclear. The aims of this study were to in vestigate hepatic sinusoidal endothelial cell injury in obstructive jaundic e by determining serum hyaluronic acid levels, purine nucleoside phosphoryl ase/alanine aminotransferase ratios, and hyaluronic acid elimination rate, and also to determine whether hepatic parenchymal cell injury in obstructiv e jaundice is induced more than in normal liver after hepatic ischemia/repe rfusion. Methods: Male Wistar rats underwent ligation and division of the common bil e duct (obstructive jaundice group) or sham operation (Sham group), Serum h yaluronic acid levels and purine nucleoside phosphorylase/alanine aminotran sferase ratios in both groups were examined at intervals up to 21 days afte r surgery. Hepatic blood flow, permeability, neutrophil accumulation, and h yaloronic acid elimination rates in both groups were measured 14 days after surgery, Changes in serum hyaluronic acid and alanine aminotransferase con centrations were determined after 15 min of hepatic ischemia followed by re perfusion, Results: Serum hyaluronic acid levels remained elevated after bile duct lig ation, Hepatic sinusoidal endothelial cell swelling was observed by electro n microscopy, and hepatic permeability was increased 14 days after bile duc t ligation in association with neutrophil accumulation. Hepatic blood flow in obstructive jaundice remained unchanged, but hyaluronic acid elimination capacity was less than that in the Sham group, After hepatic reperfusion, the disappearance rate of serum hyaluronic acid in obstructive jaundice was lower, and serum alanine aminotransferase levels were higher than those in the Sham group. Conclusions: Our findings suggest that obstructive jaundice impairs sinusoi dal endothelial cells and that sinusoidal endothelial cell damage in associ ation with sinusoidal deterioration during obstructive jaundice renders liv er susceptible to ischemia/reperfusion relative to normal liver.