Constriction of the Fetal Ductus Arteriosus Induced by Oxygen, Acteylcholine, and Norepinephrine in Normal Dogs and those Genetically Predisposed to Persistent Patency

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Abstract
Functional closure of the isolated perfused ductus arteriosus was studied in normal dog fetuses and in fetuses receiving various known proportions of their genes from dogs with patent ductus arteriosus (PDA). Constriction of the ductus in response to O2, acetylcholine (ACh), and norepinephrine (NE) was evaluated by plotting changes in input conductance against time. Ductuses from the control (normal dog) fetuses constricted in response to high PO2, ACh, and NE, indicating that in the dog the response of the ductus arteriosus to these agents is qualitatively similar to that in other mammals. Hypoxia relaxed the O2 constricted ductus. After two to three cycles of oxygenation and hypoxia, the ductus became refractory to O2 but remained responsive to ACh and NE. Ductuses from PDA-related fetuses tended to be more widely patent when hypoxic and did not respond to O2, ACh, and NE to a degree comparable to the control fetuses. Both the proportion of subnormal ductal responses and degree of abnormality in the PDA-related group increased as the degree of relationship to dogs with PDA increased. These experimental results are consistent with the polygenic mode of inheritance previously demonstrated for canine PDA. It is suggested that the liability to defective ductal closure in the dog results from a quantitatively inherited inability of the ductus to constrict.