Abstract
Delayed closure of the ductus arteriosus (DA) after birth has been observed in newborn infants with critical pulmonic stenosis (PS) and in lambs with experimental PS. This delayed closure may be the result of decreased ability to contract when exposed to oxygen or to increased production of or sensitivity to the endogenous DA vasodilator, prostaglandin(PG)E2. To determine if the abnormal hemodynamic pattern during fetal life associated with PS alters the responsiveness of the DA, we operated on 10 fetal lambs of gestational ages 70-77 days(term is 145 days) and placed a band around the pulmonary artery. Catheterization at 137-142 days showed severe pulmonic stenosis with RV pressure significantly higher in the experimental lambs (110 ± 8, ± SEM, n=10) than RV pressure in control lambs (61 ± 7, n=4, p<.001). We then studied isolated rings of DA from these lambs. The oxygen-induced increase in tension in rings of DA from lambs with PS was significantly decreased (2.55 ± 0.38, n=10) compared to rings from control lambs (4.03 ± 0.51, n=6, p<.03). There was no difference between the 2 groups in either the amount of PGE2 released or in the sensitivity (ED50) of the rings to PGE2. There was also no difference in the increase in tension when endogenous PGE2 was inhibited by indomethacin. We conclude that delayed closure of the DA in experimental PS is not caused by increased sensitivity to and production of PGE2 in the DA (as it is in premature lambs) but rather is the result of a diminished ability of the DA to contract when exposed to oxygen.
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Mahony, L., Clyman, R. & Heymann, M. DECREASED CONTRACTILITY OF THE DUCTUS ARTERIOSUS IN EXPERIMENTAL PULMONIC STENOSIS. Pediatr Res 18 (Suppl 4), 127 (1984). https://doi.org/10.1203/00006450-198404001-00203
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DOI: https://doi.org/10.1203/00006450-198404001-00203