Background/aims: Although the cardiac output is increased in liver cirrhosis, some degree of cardiac failure could coexist as suggested by human investigations showing cardiac enlargement in cirrhosis and by animal studies describing a limited response to fluid loading in the cirrhotic rat. Endotoxemia induces similar hemodynamic changes during the septic shock. This septic cardiomyopathy has been attributed to an increased secretion of nitric oxide by the myocytes. In this study, we aimed to verify if cirrhotic cardiomyopathy was present in the rat with biliary cirrhosis, and if it could be related to abnormal nitric oxide secretion.
Methods: We therefore compared the coronary pressure, the systolic ventricular pressure and the peak rate of rise of the left ventricular pressure obtained from isolated hearts perfused with a modified Langendorff apparatus in control rats and in cirrhotic rats obtained by bile duct ligation. The variations occurring after inhibition of nitric oxide synthesis by the addition of NG monomethyl-L-arginine (10(-6)M) to the perfusing Krebs-Ringer solution were also studied in both groups.
Results: We found that the coronary pressure and the contractility of the cirrhotic hearts decreased significantly when compared to the controls. Inhibition of the nitric oxide synthesis increased those values significantly when the hearts were obtained from cirrhotic animals. This was not observed in the control group.
Conclusions: Our data suggest that the cardiac modifications induced by the cirrhosis in the studied parameters are related to nitric oxide.