CARDIAC MODIFICATIONS OCCURRING IN THE ASCITIC RAT WITH BILIARY-CIRRHOSIS ARE NITRIC-OXIDE RELATED

Background/Aims: Although the cardiac output is increased in liver cir rhosis, some degree of cardiac failure could coexist as suggested by h uman investigations showing cardiac enlargement in cirrhosis and by an imal studies describing a limited response to fluid loading in the cir rhotic rat. Endotoxemia induces similar hemodynamic changes during the septic shock. This septic cardiomyopathy has been attributed to an in creased secretion of nitric oxide by the myocytes. In this study, we a imed to verify if cirrhotic cardiomyopathy was present in the rat with biliary cirrhosis, and if it could be related to abnormal nitric oxid e secretion. Methods: We therefore compared the coronary pressure, the systolic ventricular pressure and the peak rate of rise of the left v entricular pressure obtained from isolated hearts perfused with a modi fied Langendorff apparatus in control rats and in cirrhotic rats obtai ned by bile duct ligation. The variations occurring after inhibition o f nitric oxide synthesis by the addition of N-G 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 cont ractility of the cirrhotic hearts decreased significantly when compare d to the controls. Inhibition of the nitric oxide synthesis increased those values significantly when the hearts were obtained from cirrhoti c animals. This was not observed in the control group. Conclusions: Ou r data suggest that the cardiac modifications induced by the cirrhosis in the studied parameters are related to nitric oxide.