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The Journal of Thoracic and Cardiovascular Surgery, Vol 103, 733-741, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Prostaglandin synthesis inhibition prevents placental dysfunction after fetal cardiac bypass

JF Sabik, RS Assad and FL Hanley
Department of Cardiovascular Surgery, Children's Hospital of Boston, Harvard Medical School, Mass.

Surgical therapy of certain congenital heart lesions in utero may have advantages over postnatal repair or palliation. For fetal heart operations to be done, it will be necessary to devise a method of fetal cardiac bypass. Previous studies in which standard cardiopulmonary bypass techniques were used have reported fetal death resulting from increased placental vascular resistance, which causes decreased placental blood flow and depressed respiratory gas exchange. The mechanism responsible for this increase in placental vascular resistance has remained unknown. In a series of 10 fetal cardiac bypass experiments we examined the role of prostaglandins as the mediators of this response. Observations were made during a 1-hour prebypass period, a 30-minute bypass period, and a 2-hour postbypass period. The cardiac bypass circuit consisted of a centrifugal pump, and bypass flows were adjusted to equal a normal fetal cardiac output of 400 ml/min/kg. In six of the experiments indomethacin (3 mg/100 ml) was added to the pump priming to block prostaglandin synthesis. By means of the microsphere technique, fetal cardiac output, placental blood flow, individual organ blood flow, and placental vascular resistance were determined at five times during the experiments: presternotomy, poststernotomy, during cardiac bypass, at 5 minutes after cessation of bypass, and 30 minutes after cessation of bypass. Fetal arterial blood gas measurements were made every 15 to 30 minutes. When indomethacin was used to inhibit prostaglandin synthesis, placental vascular resistance did not increase, placental blood flow did not decrease, and fetal blood gases remained at normal prebypass levels during and after fetal cardiac bypass. We propose that production of vasoactive prostaglandins is responsible for the increased placental vascular resistance and decreased placental blood flow observed after fetal cardiac bypass. An understanding of the mechanism responsible for the increased placental vascular resistance seen after fetal cardiac bypass will be an important first step before clinical application.

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