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Drug Therapy for Portal Hypertension

WILLIAM G. RECTOR Jr., M.D.
[+] Article and Author Information

▸Requests for reprints should be addressed to William G. Rector, Jr., M.D.; Department of Medicine, Box 4000, Denver General Hospital, 777 Bannock Street; Denver, CO 80204-4507.


Denver, Colorado


© 1986 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1986;105(1):96-107. doi:10.7326/0003-4819-105-1-96
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Drugs used to treat portal hypertension cause constriction of mesenteric arterioles, reducing inflow to the portal venous system, portal pressure, and flow through portasystemic collaterals (such as esophageal varices). Vasopressin and somatostatin are direct vasoconstrictors. Propranolol acts by blocking vasodilatory betai receptors and reducing cardiac output. A major side effect of vasopressin therapy is impaired cardiac performance secondary to coronary vasoconstriction and increased work against high arterial pressure. Infusion of vasopressin together with a cardiac inotrope or a vasodilator, and administration of vasopressin as an inactive "hormonogen" from which it is slowly released in vivo, may lessen adverse effects. Somatostatin appears to act selectively in the mesenteric circulation. Controlled trials indicate that vasopressin may be useful for controlling hemorrhage from esophageal varices and that somatostatin works at least as well as vasopressin. Propranolol treatment has been used to prevent variceal bleeding; however, controlled trials of its effectiveness have produced conflicting results.

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