Portal and systemic hemodynamic responses to a very low dose of nitroglycerin in cirrhotic patients with portal hypertension.

Portal and systemic hemodynamic responses to a very low dose of nitroglycerin were studied in patients with portal hypertension and cirrhosis, and compared with those to a high dose of this compound. A 0.15 mg dose of nitroglycerin was given sublingually to 10 patients (LDG), and 0.3 mg to another 10 (HDG). Hemodynamic measurements were performed by means of hepatic venous and right cardiac catheterization before and 5 min after nitroglycerin administration. The wedged hepatic venous pressure decreased after dosing by 7.9% (p < 0.01) in LDG, and by 15.3% (p < 0.01) in HDG. Hepatic blood flow with ICG did not change in either group. In LDG, azygos blood flow remained unchanged, in contrast to a significant decrease by 10.1% (p < 0.05) in HDG. Mean arterial pressure fell by 3.6% (p < 0.05) in LDG and by 18.6% (p < 0.01) in HDG. Cardiac index did not change in LDG, but decreased by 11.4% (p < 0.05) in HDG. In both groups, mean pulmonary arterial pressure and pulmonary capillary wedge pressure fell significantly by the same amount. In HDG, a significant correlation between changes in wedged hepatic venous pressure and azygos blood flow (r = 0.70, p < 0.05) was observed. This suggested that splanchnic vasoconstriction mediated by a high-pressure, rather than a low-pressure, baroreceptor reflex was the main contributor to a decrease in portal venous blood flow, resulting in a reduction in wedged hepatic venous pressure; whereas a slight but significant fall of wedged hepatic venous pressure induced by a very low dose of nitroglycerin might have been due to venodilatation in the portal system and the hepatic vascular bed. These data suggest that, even with a very low dose of nitroglycerin, partial improvement of the hepatic circulation can be expected with minimal change in the systemic circulation in patients with cirrhosis and portal hypertension.