Premium
Pravastatin for thioacetamide‐induced hepatic failure and encephalopathy
Author(s) -
Huang HuiChun,
Chang ChingChih,
Wang SunSang,
Chan ChoYu,
Lee FaYauh,
Chuang ChiaoLin,
Hsin IFan,
Teng TzuHua,
Lin HanChieh,
Lee ShouDong
Publication year - 2012
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2011.02566.x
Subject(s) - thioacetamide , pravastatin , medicine , fulminant hepatic failure , bilirubin , hepatic encephalopathy , endocrinology , hyperammonemia , encephalopathy , cirrhosis , gastroenterology , cholesterol , liver transplantation , transplantation
Eur J Clin Invest 2011 Abstract Background Nitric oxide (NO) inhibition aggravates hepatic damage and encephalopathy and increases mortality in rats with thioacetamide (TAA)‐induced acute liver failure. Statins enhance NO production but whether they influence the above parameters are unknown. Material and methods Male Sprague‐Dawley rats were used. In the first series, TAA (350 mg/kg per day, i.p. for 3 days) was administered to induce acute liver failure. Control rats received saline. Rats received distilled water or pravastatin (20 mg/kg per day, p.o.) from 2 days before to 3 days after TAA or saline injection. In the second series, liver cirrhosis was induced by common bile duct ligation (BDL). Sham‐operated rats served as controls. Rats received distilled water or pravastatin for 5 or 14 days until the 42nd day after operation. On the last day of treatment, survival, motor activities, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, ammonia and brain histology were evaluated. Results Thioacetamide and BDL rats showed higher ALT, AST, bilirubin and ammonia levels and lower motor activity counts compared with their corresponding control groups. In TAA rats, pravastatin elicited higher total and ambulatory motor activity counts and lower AST and total bilirubin levels. Survival was improved, whereas brain H&E staining was not significantly different in TAA rats with or without pravastatin treatment. In BDL groups, rats with or without pravastatin treatment were not different in motor activity counts and liver biochemistry. Conclusions Pravastatin ameliorates hepatic encephalopathy and liver biochemistry and improves survival in rats with acute liver failure, but not in those with cirrhosis.