The results of the study showed that the cardiovascular system of patients with hepatic cirrhosis and ascites tolerate acute hypervolemia better than patients with hepatic cirrhosis without ascites. It can be explained by a rapid transfer of surplus liquid into the abdominal cavity. Further, it was found that the low cardiac output at rest in patients with hepatic cirrhosis evidently indicated a latent cardiac insufficiency becoming manifest only after the volume exertion. In our control group, jaundice produced bradycardia and hypotension without cardiodepressive effects. Patients with cirrhosis and with or without ascites responded to furosemide probably associated with the elution of vasoconstrictive substances in the same way as the control group. Following acute volume expansion, no differences were found between the compensated and decompensated cirrhotic patients and the healthy control group, not even in the natriuretic hormone of the secretion. However, the relevant organs of each control group had a varied response to the elevated plasma level of natriuretic factor.