백서에서 간외폐쇄성 황달의 간손상 및 Ursodeoxycholic Acid의 예방 효과 = The Effect of Ursodeoxycholic Acid on Extrahepatic Cholestatic Liver Damage in the Rat백서에서 간외폐쇄성 황달의 간손상 및 Ursodeoxycholic Acid의 예방 효과

다국어 초록 (Multilingual Abstract)

Background/Aims: Generally many reports were known that the liver function was decreased with different forms of extrahepatic obstructive jaundice. To clarify the mechanism of these hepatic dysfunction in extrahepatic obstructive jaundice, we studied histologica] and biochemical alterations of experimental rats with obstructive jaundice induced by common bile duct(CBD) ligation at two time periocL(group I) and the limiting effects of administration of ursodeoxycholic acid(UDCA) or NSAID(lndomethacin) on the histological and biochernical alterations(group II). Methods: In control, lO rats underwent laparotomy without CBD-ligation(sham-operation). In group I, the CBD of 20 rats was ligated by laparotomy. Three(group Ia) and Four(group Ib) weeks aft=r ligation and 4 weeks after in case of control rats, the liver was isolated and microscopic examination was done. In group II, 40 rats with ligation of CBD were ramdomly assigned to receive UDCA(25 mg/kg/day) for 15 rats and NSAID(indomethacin, 4 mg/kg/day) for 15 rats and placebo for 10 rats. Results: In the study of group I, bi]e ducts proliferation was observed from portal tracts to porta] tracts and to hepatic lobules in group la, and hepatic ]obules were destroyed by severe prc>]iferation and fibrosis, and the area ratio of hepatocytes and sinusoid was decreased relatively in thie microscopic field in group lb. In the study of group II, the decreased area ratio of hepatocytes and sinusoid was limited in UDCA treoted group, but not in indomethacin group. Biochemical abnormalities(s-GPT, alkaline phosphatase, tota] bilirubin) were not limited significantly in both drug treated groups. Conclusions: Impairment of liver function of the rats with extrahepatic obstrutive jaundice may be due to relatively decreased hepatocytes and sinusoid ratio by bile duct proliferation and interstitial fibrosis and this alteration may be prevented by administration of UDCA. (Korean J Gastroenterol 1996; 28:232 240)