Abstract
To evaluate liver alterations caused by biliary obstruction and drainage. Thirty-nine male Wistar rats were randomly distributed in 4 groups: BO (n=18) bile duct ligation for 20 days, with a periodic evaluation of liver histological alterations, Doppler echography portal flow and measurements of NO and malondialdehyde (MDA); BO/DB (n=13) bile duct occlusion for 20 days followed by biliary drainage by choledochoduodenal anastomosis, 5 days follow-up, same BO group parameters evaluations; group CED (n=4) sham operation and portal flow evaluation trough 20 days; CHB (n=4) sham operation, with hepatic biopsy on 25th day and followed-up trough 25 days, by the same parameters of group BO, with exception of portal flow. Direct bilirubin (DB) and alkaline phosphatase (AP) were evaluated in the group BO, BO/DB and CHB. The bile duct ligation led to an increase of DB and AP, development of liver histological alterations, reduction of portal flow and increase of plasmatic NO and of MDA levels. The bile duct clearing resulted in a reduction of DB, AP, NO, MDA histological alterations and increase of portal flow. The biliary occlusion resulted in cholestasis and portal flow reduction, besides the increase of plasmatic NO and of hepatic MDA levels, and histological liver alterations, with a tendency of normalization after the bile duct clearing.
Highlights
Benign extra-hepatic cholestasis may lead to cholangitis and increased intra-canaliculi pressure, developing acute and chronic hepatic injuries[1,2] reduced portal flow,[3,4,5,6] increased serum nitric oxide (NO)[7,8,9] and triggering of liver lipid peroxidation.[10,11,12]
The accumulation of hydrophobic bile acids during cholestasis leads to mitochondrial free radicals (FR) generation in the liver, consisting of a major mechanism of injury and fibrosis due to the propagation of the lipid peroxidation chain after spontaneous reaction with oxygen.[11,16,17]
Doppler echography were performed on days 0, 15 and 20 to evaluate portal flow and obtain liver biopsy, whereby 650 and 900 mg pieces were removed for histology and for dosage of NO and malondialdehyde (MDA)
Summary
Benign extra-hepatic cholestasis may lead to cholangitis and increased intra-canaliculi pressure, developing acute and chronic hepatic injuries[1,2] reduced portal flow,[3,4,5,6] increased serum nitric oxide (NO)[7,8,9] and triggering of liver lipid peroxidation.[10,11,12] Surgical desobstruction is the elective treatment.Acute liver injuries results, among others, mainly in abscesses, ductal proliferation and reduced number of hepatocyte[2] while secondary biliary cirrhosis is aroused due to chronic injuries.[13]. Benign extra-hepatic cholestasis may lead to cholangitis and increased intra-canaliculi pressure, developing acute and chronic hepatic injuries[1,2] reduced portal flow,[3,4,5,6] increased serum nitric oxide (NO)[7,8,9] and triggering of liver lipid peroxidation.[10,11,12] Surgical desobstruction is the elective treatment. The accumulation of hydrophobic bile acids during cholestasis leads to mitochondrial FR generation in the liver, consisting of a major mechanism of injury and fibrosis due to the propagation of the lipid peroxidation chain after spontaneous reaction with oxygen.[11,16,17]
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