Splanchnic and systemic hemodynamics and plasma levels of aldosterone, glucagon and plasma renin were investigated in 12 patients with advanced cirrhosis before and 2 wk (14.6 f 2.8 days) and 2 mo (60.8 f 10.5 days) after orthotopic liver transplantation. Liver transplant was followed by significant (p < 0.01) changes in systemic hemodynamics at 2 wk, with a marked reduction in cardiac index (4.9 rt-0.8 vs. 3.7 rt-0.7 L/min -m2) and increases in mean arterial pressure (79 f 8 vs. 101 rt-11 mm Hg) and peripheral vascular resistance (721 f 149 vs. 1,274 f 253 dynsec * cm-9.
Two months after liver transplant, we saw further significant increases in peripheral vascular resistance (1,700 f 341 dyn * seccm-6; p < 0.05) without changes in cardiac index. Hepatic venous pressure gradient, very high before transplantation, was normal 2 wk after liver transplant (18.7 f 3.0 vs. 2.1 f 0.8 mm Hg; p < 0.01). Hepatic blood flow rose markedly from 1.03 rt-0.46 to 2.25 rt-0.79 L/min (p < 0.01) and was still elevated at 2 mo (1.84 rt-0.74 Wmin). Azygos blood flow had not changed after 2 wk with respect to pretransplant values (0.65 5 0.26 vs. 0.69 f 0.39 Wmin) but had decreased significantly at 2 mo (0.39 rt-0.16 L/min; p < 0.05). The elevated aldosterone, plasma renin and glucagon levels found in our cirrhotic patients before transplantation decreased to nearnormal values 2 wk after the procedure. These results suggest that most of the hemodynamic and humoral abnormalities characteristic of advanced cirrhosis are reversed after liver transplant. However, azygos blood flow remains high early after liver transplant but is decreased at 2 mo, indicating that the closure of portocollateral vessels occurs slowly despite the rapid normalization of portal pressure. The increase in hepatic blood flow after liver transplant may be a consequence of hepatic denervation. (HEPATOLOGY 1993;17:355-360.) Portal hypertension is a major complication of cirrhosis and is responsible for many of the clinical