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Oxidative Medicine and Cellular Longevity
Volume 2012 (2012), Article ID 486190, 8 pages
http://dx.doi.org/10.1155/2012/486190
Research Article

Oxidative Stress and Pulmonary Changes in Experimental Liver Cirrhosis

1Federal University of Rio Grande do Sul (UFRGS), 90035-903 Porto Alegre, RS, Brazil
2Laboratory of Hepatology and Experimental Gastroenterology, Hospital Clinics of Porto Alegre (HCPA), 90035-903 Porto Alegre, RS, Brazil
3Laboratory of Airway and Lung, Hospital Clinics of Porto Alegre (HCPA), 90035-903 Porto Alegre, RS, Brazil
4Graduate Program in Human Movement Sciences and Respiratory Sciences, UFRGS, 90035-903 Porto Alegre, RS, Brazil
5Lutheran University of Brazil (ULBRA), Canoas, Rs, Brazil

Received 10 September 2012; Revised 31 October 2012; Accepted 26 November 2012

Academic Editor: Oren Tirosh

Copyright © 2012 Renata Salatti Ferrari et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The use of carbon tetrachloride (CCl4) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI4 administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI4: G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-α and IL-1β in the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels.