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Free access | 10.1172/JCI109098

Indomethacin is a Placental Vasodilator in the Dog: THE EFFECT OF PROSTAGLANDIN INHIBITION

John G. Gerber, Robert A. Branch, Walter C. Hubbard, and Alan S. Nies

Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Division of Clinical Pharmacology, Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Find articles by Gerber, J. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Division of Clinical Pharmacology, Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Find articles by Branch, R. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Division of Clinical Pharmacology, Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Find articles by Hubbard, W. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Division of Clinical Pharmacology, Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Find articles by Nies, A. in: PubMed | Google Scholar

Published July 1, 1978 - More info

Published in Volume 62, Issue 1 on July 1, 1978
J Clin Invest. 1978;62(1):14–19. https://doi.org/10.1172/JCI109098.
© 1978 The American Society for Clinical Investigation
Published July 1, 1978 - Version history
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Abstract

The effect of 8 mg/kg of indomethacin on uterine blood flow, prostaglandin production, and intraamniotic fluid pressure was examined in late pregnant dogs. Uterine blood flow was measured with 15 μm radiolabeled microspheres. Because we found that a significant percentage of the microspheres shunted through the placental circulation into the lungs, we calculated placental blood flow by adding the shunted microspheres through the placenta to the nonshunted microspheres in the placenta. Total uterine blood flow significantly increased from 271±69 ml/min during control period to 371±72 ml/min (P < 0.01) 30 min after indomethacin. This increase was attributable to the change in blood flow to the placental circulation (222±58 to 325±63 ml/min; P < 0.01). Associated with these hemodynamic changes we found an almost complete suppression of uterine prostaglandin E2 production (1,654±305 to 51±25 pg/ml; P < 0.01) as measured by gas chromatography-mass spectrometry. In addition, we found that indomethacin treatment resulted in uterine relaxation as measured by intraamniotic fluid pressure changes (11.2±1.3 mm Hg to 8.5±1.2 mm Hg; P < 0.001).

We conclude that indomethacin causes an increase in placental blood flow without any change in flow to the rest of the uterus, and that this dose of the drug inhibits greater than 95% of uterine prostaglandin production. In addition, indomethacin is responsible for uterine relaxation. The increase in placental blood flow after indomethacin is probably a result of uterine relaxation, which is secondary to prostaglandin synthesis inhibition.

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