Intramuscular injection of the 15-methyl analogue of prostaglandin F2α (15-me-PGF2α) is being used to initiate second trimester abortion. The natural prostaglandin F2α (PGF2α) is a known pulmonary pressor agent but there is little information about the cardiovascular effects of the analogue. Consequently, we compared the hemodynamic responses to the two forms in twenty-three anesthetized dogs. Given I.M. or I.V. 15-me-PGF2α produced a greater and more sustained rise in pulmonary arterial pressure than PG F2α. Intramuscular 15-me-PGF2α also elicited a more prolonged increase in pulmonary vascular resistance than prostaglandin F2α given I.M. or I.V. The methyl analogue (I.M. or I.V.) causes a greater initial fall in systemic arterial oxygen tension and cardiac output, and a greater increase in systemic resistance than I.M. PG F2α Breathlessness seen during abortion induced by prostaglandin F2α or its methyl analogue may be caused by acute pulmonary hypertension in addition to bronchoconstriction.
Bibliographical noteFunding Information:
This work was supported by grants #HL 14985 and HL 05973 from the National Institutes of Health, and a generous grant from the Upjohn Company, Kalamazoo, Michigan. Dr. Weir is the recipient of a Fulbright scolarship. Dr. Grover is the recipient of an NIH Research Career Development Award, #HL 29237. We are grateful for the assistance of R. Glas, B. Kaplan, M. Munroe, D. Smith, E. Toyos, S. Hofmeister and D. Jackson. We would like to thank Dr. G.O. Zerbe for statistical advice. Prostaglandins F2e and methyl F2e were kindly provided by the Upjohn Company.
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