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β‐Blockade with propranolol and hepatic artery blood flow in patients with cirrhosis
Author(s) -
Mastai Ricardo,
Bosch Jaime,
Bruix Jordi,
Navasa Miguel,
Kravetz David,
Rodés Juan
Publication year - 1989
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840100302
Subject(s) - propranolol , blockade , cirrhosis , medicine , blood flow , cardiology , artery , receptor
In patients with cirrhosis and portal hypertension, propranolol administration reduces heart rate and cardiac output and diminishes portal pressure and collateral eral blood flow. However, there is little information on the possible effects of propranolol on hepatic artery blood flow. The present study addressed this question in 12 cirrhotic patients with end‐to‐side portacaval shunt, in whom all of the liver blood flow represents the hepatic artery blood flow. Hepatic artery blood flow (continuous infusion of indocyanine green), cardiac output (thermal dilution), heart rate and mean arterial pressure were measured before and 20 min after the intravenous infusion of 10 to 15 mg of propranolol. β‐Adrenergic blockade caused a significant reduction of cardiac output (from 9.1 ± 2.1 to 7.1 ± 1.4 liters per min, p < 0.001) (mean ± S.D.) and heart rate (from 85 ± 10 to 71 ± 7 beats per min, p < 0.001), and a significant increase of systemic vascular resistance (from 9.0 ± 2.1 to 11.7 ± 2.7 mmHg per liter per min, p < 0.001), whereas mean arterial pressure did not change (77 vs. 78 mmHg). Propranolol significantly reduced hepatic artery blood flow (from 0.65 ± 0.20 to 0.55 ± 0.14 liters per min, p < 0.01). However, reduction of hepatic artery blood flow (‐12.9 ± 7.3%) was significantly less than reduction of cardiac output (‐21.1 ± 5.2%, p < 0.01). As a result, the fraction of the cardiac output delivered to the liver was significantly greater after propranolol (8.0 ± 1.7%) than before (7.3 ± 1.7%, p < 0.05). Similarly, increase in hepatic vascular resistance (14 ± 7%) was less pronounced than increase in systemic vascular resistance (27 ± 10%, p L< 0.05). Our results show that despite a redistribution of the cardiac output to the hepatic artery, propranolol causes a significant reduction of hepatic artery flow in cirrhosis.