Short–Term Effects of Propranolol on Portal Venous Pressure

Hepatology - Tập 6 Số 1 - Trang 101-106 - 1986
Guadalupe García‐Tsao1, Norman D. Grace2, Roberto J. Groszmann3, Harold O. Conn1, Max Bermann1, Michael J. Patrick1, Steven S. Morse1, Jeanne Alberts1
1West Haven Veterans Administration Medical Center, West Haven, Connecticut 06516
2Yale‐New Haven Medical Centers and Yale University School of Medicine, New Haven, Connecticut 06510
3Faulkner and Lemuel Shattuck Hospitals and Tufts University School of Medicine, Boston, Massachusetts 02130

Tóm tắt

The present study was designed to investigate the effect of propranolol on portal pressure of patients with alcoholic cirrhosis and portal hypertension and to correlate these effects with clinical and laboratory parameters. The mean baseline hepatic venous pressure gradient in the 50 patients studied was of 18.2 ± 4.1 mm Hg. It decreased significantly2 hr after the oral administration of 40 mg of propranolol to 15.7 ± 4.2 mm Hg (a mean reduction of 13.4 ± 17%). This reduction in hepatic venous pressure gradient resulted mainly from a decrease in mean wedged hepatic venous pressure. There was no correlation between the decrease in hepatic venous pressure gradient and the decrease in heart rate. When results were analyzed individually, only 15 (30%) showed a large decrease in hepatic venous pressure gradient (>20%), 15 (30%) showed a moderate decrease (10 to 19%), and in 20 patients (40%) there was no reduction or an increase in hepatic venous pressure gradient. Comparison of “responders” (those that reduced hepatic venous pressure gradient >10%) and “nonresponders” (hepatic venous pressure gradient reduction <10%) showed no significant differences in baseline laboratory and hemodynamic parameters, in the severity of the liver disease, in theheart rate and blood pressure response to propranolol, nor in the propranolol plasma levels achieved 2 hr after propranolol administration. Propranolol plasma levels correlated with the reduction in heart rate but not with the reduction in hepatic venous pressure gradient. Of 14 nonresponders to 40 mg of propranolol who received additional doses, six showed a reduction inhepatic venous pressure gradient. We conclude that, although propranolol reduces the mean portal pressure in patients with alcoholic cirrhosis and portal hypertension, this response is not uniform. Twenty percent of cirrhotic patients do not show any reduction in portal pressure even after maximal doses of propranolol. There is no clear explanation for this variable response; pharmacologic and/or hemodynamic factors may be involved. Neither the heart rate response to propranolol nor the propranolol plasma concentrations were found to be useful in assessing the portal pressure response to propranolol.

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Thông tin xuất bản

Hepatology

Tập 6 Số 1

101-106

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