Abstract- Cirrhosis has been related with hyperdynamic circulation, manifesting as increased cardiac output
and decreased systemic vascular resistance. In the present study we examined the cirrhosis outcome on
apoptosis of rat hearts. We also tried to explore the role of nitric oxide (NO) and oxidative stress in the
probable changed apoptosis of cirrhotic hearts. Twenty eight days after ligation of bile duct, heart tissues
were tested for apoptosis. The extent of malondialdehyde (MDA), and the activities of catalase (CAT),
glutathione peroxidase (GSHPx) and superoxide dismutase (SOD) have been calculated in heart tissues. The
cirrhotic hearts exhibited structural defects and greater apoptosis. Chronic treatment of cirrhotic rats with LNAME,
a non-selective inhibitor of NO synthase, inhibited heart structural defects and reduced apoptosis of
hearts. We also showed that cirrhotic rat hearts had an enhanced level of MDA and reduced activities of
CAT, GSHPx and SOD. When the animals were treated by L-NAME chronically, the MDA level reduced
and activities of CAT, GSHPx and SOD augmented in cirrhotic heart. In conclusion, increased apoptosis of
cirrhotic hearts probably happen due to NO overproduction and increased oxidative stress in hearts of
cirrhotic rats