Effects of long-term propranolol and octreotide on postprandial hemodynamics in cirrhosis: A randomized, controlled trial

Postprandial increases in portal pressure may influence esophageal variceal rupture. The effects of chronic propranolol and octreotide (100 and 200 μg subcutaneously in a single dose) on postprandial hemodynamics were evaluated. First study: 36 cirrhotic patients were studied at baseline and 30 and 60 minutes after a standard meal and then treated with propranolol (139 ± 9 mg/d during 39 ± 2 days). Second study: After baseline measurements, patients were randomized into 3 groups: (1) placebo, (2) octreotide (100 μg), or (3) octreotide (200 μg) (n = 12 for each group). Thirty minutes postinjection a new base-line was established and measurements were repeated 30 and 60 minutes after the meal. First study: Baseline portal pressure was 18.1 ± 1.2 mm Hg, 30 and 60 minutes after the meal it was 21.5 ± 0.8 mm Hg and 20.5 ± 0.8 mm Hg, respectively (both P < 0.01 vs. baseline). Cardiac index (Cl) was 4.5 ± 0.2, 4.8 ± 0.2, and 4.9 ± 0.2 L · min−1 · m−2, respectively (both P < 0.05 vs. baseline). Peripheral vascular resistance was 1012 ± 56, 902 ± 51 (P = NS), and 884 ± 49 dynes · sec · cm−5 (P < 0.05 vs. baseline), respectively. Second study: Propranolol and placebo did not blunt postprandial increase in portal pressure. Octreotide (100 μg) partially ameliorated postprandial increase in portal pressure. Octreotide (200 μg) significantly enhanced the portal hypotensive effect of propranolol and blunted the postprandial increase in portal pressure. Octreotide blunts postprandial increase in portal pressure not prevented by long-term propranolol administration.