the possible role of nitric oxide and oxidative stress in the enhanced apoptosis of cardiac cells in cirrhotic rats

cirrhosis is associated with hyperdynamic circulation, manifesting as increased cardiac output and decreased systemic vascular resistance. the aim of this study was to investigate the effect of cirrhosis on heart apoptosis and involvement of nitric oxide (no) and oxidative stress in the possible altered apoptosis of cirrhotic hearts. twenty-eight days after bile duct ligation, heart tissues were examined for apoptosis and the level of malondialdehyde (mda), and the activities of catalase (cat), glutathione peroxidase (gshpx), and superoxide dismutase (sod) were studied in cardiac tissues. the effect of treatment with l-name, a non-selective inhibitor of no synthase, on cirrhotic cardiac apoptosis, the level of mda and cat, sod and gshpx activities were also investigated. the hearts of cirrhotic rats showed structural abnormalities and enhanced apoptosis. chronic treatment of cirrhotic rats with l-name prevented cardiac structural abnormalities and decreased apoptosis of hearts. cirrhotic rat hearts also indicated an increased level of mda and decreased activities of cat, gshpx, and sod. by chronic l-name treatment the level of mda decreased and activities of cat, gshpx and sod increased in cirrhotic hearts. apoptosis in cirrhotic hearts might occur because of no excessive production, which could induce oxidative stress in hearts of cirrhotic rats.