Abstract
Multiple problems exisf with in vitro analysis of PDA reactivity. Accordingly, 42 studies were performed from 1 to 27 days postoperatively in 14 fetal lambs instrumented chronically with PDA sonomicrometer dimension crystals and with pressures determined in main pulmonary artery and ascending and descending aorta. The PDA was found to be dilated maximally in utero, but was not a passive channel. PDA diameter varied with hydrostatic alterations. Alpha and beta adrenergic agonists and adrenergic and cholinergic antagonists had no influence on ductal caliber. Similarly, angiotensin 1 and 2 and blockade of conversion to angio 2 with SQ20881 did not influence the PDA. In contrast, exquisite sensitivity was found to alterations in the PG milieu. Inhibition of PG synthesis by a single I.V. dose of as little as 0.005 mg/kg of indomethacin (indo.) caused profound PDA constriction. The latter responses were accompanied by striking reductions in circulating PGE levels, measured by radioimmunoassay, but reversal of constriction by infusion of PGE1 and 2 did not elevate circulating levels. Thus, ductal reactivity appeared to be associated with alterations in PG synthetase activity within the PDA. Of major interest was the finding of a direct correlation after fetal administration of indo. between fetal and maternal circulating levels of PG's. These findings suggest that PG's may directly influence PDA calibre and that past theories concerning the mechanism of spontaneous or delayed PDA constricticn must be revised.
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Stanley, E., Kirkpatrick, Morton, P. et al. PROSTAGLANDINS (PC's) AND THE FETAL DUCTUS ARTERIOSUS (PDA). Pediatr Res 11, 394 (1977). https://doi.org/10.1203/00006450-197704000-00147
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DOI: https://doi.org/10.1203/00006450-197704000-00147