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Vasodilators and Prostaglandin Inhibitors in Primary Pulmonary Hypertension

JAMES B. HERMILLER, M.D.; DENNIS BAMBACH, M.D.; MICHAEL J. THOMPSON, M.D.; PATRICIA HUSS, R.N.; MARY E. FONTANA, M.D.; RAYMOND D. MAGORIEN, M.D.; DONALD V. UNVERFERTH, M.D.; and CARL V. LEIER, M.D.
[+] Article and Author Information

Grant support: supported by the James D. Casto Cardiovascular Research Fund and the S. J. Roessler Foundation.

▸Requests for reprints should be addressed to Carl V. Leier, M.D.; Room 653 Means Hall, Ohio State University Hospitals; Columbus, OH 43210.


Columbus, Ohio


© 1982 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1982;97(4):480-489. doi:10.7326/0003-4819-97-4-480
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Ten women with primary pulmonary hypertension had resting hemodynamic measurements taken before and after the nonparenteral administration of various vasodilators and prostaglandin inhibitors. Only sublingual isoproterenol, alone or combined with sublingual isosorbide dinitrate, effected a substantial (greater than 20%) drop in pulmonary vascular resistance; this decrease was accompanied by little change in pulmonary artery pressure. Isosorbide dinitrate was the only drug that elicited any reduction in pulmonary artery pressure; pulmonary vascular resistance decreased modestly. The oral administration of diazoxide, hydralazine, phentolamine, and tolazoline elicited little change in pulmonary artery pressure or resistance. Except for tolazoline, all these agents significantly decreased systemic blood pressure and resistance. Prostaglandin inhibition by indomethacin (acute and chronic dosing) increased pulmonary and systemic vascular resistances and reduced cardiac output. Aspirin combined with dipyridamole elicited no changes. The vasodilators and prostaglandin inhibitors studied evoked little improvement in resting pulmonary hemodynamic abnormalities in primary pulmonary hypertension.

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