Open AccessProstacyclin inhibition by indomethacin aggravates hepatic damage and encephalopathy in rats with thioacetamide-induced fulminant hepatic failure
Author(s) -
ChiJen Chu,
Ching-Chin Hsiao,
Teh-Fang Wang,
ChoYu Chan,
Fa-Yauh Lee,
FullYoung Chang,
YiChou Chen,
HuiChun Huang,
Sun-Sang Wang,
ShouDong Lee
Publication year - 2005
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v11.i2.232
Subject(s) - thioacetamide , fulminant hepatic failure , medicine , hepatic encephalopathy , hyperdynamic circulation , encephalopathy , endocrinology , prostacyclin , nitric oxide , intraperitoneal injection , pathogenesis , portal hypertension , cirrhosis , transplantation , liver transplantation
Vasodilatation and increased capillary permeability have been proposed to be involved in the pathogenesis of acute and chronic form of hepatic encephalopathy. Prostacyclin (PGI2) and nitric oxide (NO) are important contributors to hyperdynamic circulation in portal hypertensive states. Our previous study showed that chronic inhibition of NO had detrimental effects on the severity of encephalopathy in thioacetamide (TAA)-treated rats due to aggravation of liver damage. To date, there are no detailed data concerning the effects of PGI2 inhibition on the severity of hepatic encephalopathy during fulminant hepatic failure.