SPLANCHNIC VASODILATION AND RENAL VASOCONSTRICTION - A KEY TO THE HEPATORENAL-SYNDROME

Systemic, femoral and renal hemodynamics were evaluated in 7 control subjects and 20 cirrhotic patients with ascites, 14 of them without (group A) and 6 with (group B) functional renal failure. Hyperdynamic systemic circulation, increased plasma volume, and hyperreninism were present in groups A and B. These changes were more severe in group B, which showed, as compared with group A, lower total vascular resistances and mean arterial pressure together with increased cardiac index and plasma renin activity. Significant differences in regional hemodynamics were also observed between groups. In A, femoral and renal fractions of cardiac output were respectively increased and reduced as compared with controls. By contrast, group B, both fractions of cardiac output were reduced as compared with controls. By contrast, in group B, both fractions of cardiac output were reduced when compared either with controls or with group A. In the entire patient group there was a close direct correlation between femoral and renal fractions of cardiac output (r = 0.88; p < 0.001) and both of them correlated independently with total vascular resistances (r = 0.79; p < 0.001 in both cases). These results indicate that, in nonazotemic cirrhotics with ascites, vasodilation in extrasplanchnic areas contributes to the genesis of the hyperdynamic circulation. The presence in group B of a reduced flow to extrasplanchnic territories, in association with an increase of the hyperdynamic circulatory status, suggests that exacerbation of splanchnic vasodilation is involved in the development of the hepatorenal syndrome. Finally, in cirrhosis, the changes that occur in systemic hemodynamics appear to influence renal function and renal function and renal blood flow.