Effects of Propranolol on Azygos Venous Blood Flow and Hepatic and Systemic Hemodynamics in Cirrhosis

TLDR

The study examined propranolol’s impact on gastroesophageal collateral blood flow and systemic/hepatic hemodynamics in 23 cirrhotic patients with portal hypertension, measuring azygos venous flow by continuous thermal dilution. Propranolol markedly reduced azygos venous blood flow by 34.2 % (from 544 ± 48 ml/min to 354 ± 34 ml/min), a greater decrease than cardiac output, hepatic venous pressure gradient, or hepatic blood flow, and this effect was not related to plasma norepinephrine levels, indicating that diminished collateral flow may underlie its benefit in preventing variceal bleeding.

Abstract

The effects of propranolol on blood flow through gastroesophageal collaterals and on systemic and hepatic hemodynamies were investigated in 23 cirrhotic patients with portal hypertension. Gastroesophageal collateral blood flow was evaluated by the measurement of azygos venous blood flow by continuous thermal dilution. Azygos venous blood flow was markedly increased in these patients (544 ± 48 ml per min, as compared with 132 ± 18 ml per min in subjects without portal hypertension (p < 0.001). Propranolol at doses achieving effective β-blockage (83 ± 5 mg) (mean ± S.E.M.) markedly reduced azygos venous blood flow (to 354 ± 34 ml per min, p < 0.001). Reduction of azygos venous blood flow (-34.2 ± 3.6%) was significantly greater (p < 0.01) than reductions in cardiac output (-22.6 ± 1.9%), hepatic venous pressure gradient (-11.5 ± 2.4%) and hepatic blood flow (-13.4 ± 7.4%). The hemodynamic effects of propranolol were not related to plasma norepinephrine levels. Reduction of gastroesophageal collateral blood flow may be the mechanism by which oral propranolol therapy reduces the risk of repeated episodes of variceal bleeding in cirrhotic patients with portal hypertension.