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Morphine-induced fetal malformations. 3. Possible mechanisms of action.

Abstract: The teratogenic effects exerted by morphine sulfate in CF-1 mice on Days 8 and 9 appear, from indirect evidence, not to be attributable to cholinesterase inhibition. The anticholinergic drug, atropine, when used in combination with morphine, resulted in the potentiation of morphine-induced defects, exencephaly and axial skeletal fusions. In addition, both atropine and morphine, either alone or in combination, produced constriction of the placental vessels. Morphine administration on Days 8 and 9 resulted in an increase in blood sugar regardless of the dose employed. Previously reported similarities produced by atropine and morphine on the placental vessels, the knowledge that both drugs decrease oxygen tension, the resemblance of hypoxic-induced malformations to the defects observed in this study, the effects of hypoxia on carbohydrate metabolism, and the reported involvement of carbohydrate metabolism in the morphogenesis of the embryonic neural tube all suggest that the malformations observed following morphine administration are related to the reduced oxygen concentration as well as the hyperglycemia produced subsequent to its administration in gravid mice.