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Am J Physiol Regul Integr Comp Physiol 282: R184-R190, 2002;
0363-6119/02 $5.00
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Vol. 282, Issue 1, R184-R190, January 2002

In utero indomethacin alters O2 delivery to the fetal ductus arteriosus: implications for postnatal patency

Seth H. Goldbarg1, Yasushi Takahashi1, Carolyn Cruz1, Hiroki Kajino1, Christine Roman1, Bao Mei Liu1, Yao Qi Chen1, Françoise Mauray1, and Ronald I. Clyman1,2

1 Cardiovascular Research Institute and 2 Department of Pediatrics, University of California, San Francisco, California 94143-0544

Indomethacin produces constriction and hypoxia of the fetal ductus arteriosus. This is associated with death of smooth muscle cells in the ductus wall and an increased incidence of patent ductus arteriosus in the newborn period. We used fetal sheep to determine which factors are responsible for indomethacin-induced hypoxic cell death. Cell death in the ductus wall is directly related to the degree of indomethacin-induced ductus constriction and is present at both moderate and marked degrees of constriction. Both moderate and marked degrees of ductus constriction reduce vasa vasorum flow to the ductus (moderate = 69 ± 25%; marked = 30 ± 16% of preinfusion values) and increase the thickness of the ductus wall. In contrast, ductus luminal blood flow is not affected by moderate degrees of constriction and is reduced only after marked constriction. Although indomethacin increases ductus tone, it has no effect on ductus oxygen consumption. These findings suggest that the hypoxic cell death that occurs during the early stages of indomethacin-induced constriction is primarily due to changes in vasa vasorum blood flow and muscle media thickness.

vasa vasorum; microspheres; cell death; oxygen consumption; tocolysis


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