Lung and Liver Changes Due to the Induction of Cirrhosis in Two Experimental Models

Abstract

-Context -To evaluate lung and liver changes in two experimental models using intraperitoneal carbon tetrachloride (CCl 4 ) and bile duct ligation (BDL). Methods -Twenty-four male Wistar rats were divided into a control group (CO) and an experimental group (EX). We evaluated the liver transaminases (AST, ALT, AP), arterial blood gases (PaO 2 , PCO 2 and SpO 2 ) and lipid peroxidation by TBARS (substances that react to thiobarbituric acid) and chemiluminescence. We also evaluated the antioxidant enzyme superoxide dismutase (SOD) and histology of lung tissue and liver. Results -There were significant differences in AST, ALT, ALP and PaO 2 between CO group and EX group (P<0.05). The levels of TBARS, chemiluminescence and activity of enzyme superoxide dismutase were increased to different degrees in the CCl 4 groups: CO and in the BDL -EX (P<0.05, respectively). In the lung histology, an increase in the wall thickness of the pulmonary artery and a diameter reduction in the CCl 4 animal model were observed: comparing CO group with EX group, we observed a reduction in thickness and an increase in the diameter of the artery wall lung. Conclusion -Both experimental models have caused liver damage and alterations in the artery wall that are associated with major changes in pulmonary gas exchange.

Antioxidant and anti-inflammatory action of melatonin in an experimental model of secondary biliary cirrhosis induced by bile duct ligation

“…Ferrari et al[40] demonstrated that rats with cirrhosis, whether induced by BDL or by CCl 4 , exhibit necrosis, fibrotic nodules, inflammatory infiltrate and cellular changes. Tieppo et al[14] also observed that rats subjected to BDL exhibit hepatic changes with ductular proliferation and fibrosis, findings that improved in cirrhotic rats treated with quercetin.…”

Impact of liver damage on blood-borne variables and pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats

“…Furthermore, high level of ROS may decrease the bioavailability of NO and lead to the constriction of pulmonary vessels [19]. Taken together, all these suggested mechanisms cannot be linked directly to POPH because of lacking an accepted animal model for POPH, and some limitations in human studies [20][21][22].…”

“…Although, POPH can be linked to portal hypertension, the increase in portal pressure by partial mechanical obstruction of the portal vein in animals does not lead to pulmonary hypertension [33]. In addition, the increase of pulmonary artery pressure following the injection of sephadex microsphere into the portal vein [22], creation of portosystemic shunt [21] and intraperitoneal administration of carbon tetrachloride [20] could not entirely create a condition like POPH in human.…”

Impact of liver damage on blood-borne variables and pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats

“…Although, POPH can be linked to portal hypertension, the increase in portal pressure by partial mechanical obstruction of the portal vein in animals does not lead to pulmonary hypertension [33]. In addition, the increase of pulmonary artery pressure following the injection of sephadex microsphere into the portal vein [22], creation of porto-systemic shunt [21] and intraperitoneal administration of carbon tetrachloride [20] could not entirely create a condition like POPH in human.…”