Phenytoin‐induced cleft palate: Evidence for embryonic cardiac bradyarrhythmia due to inhibition of delayed rectifier k⁺ channels resulting in hypoxia–reoxygenation damage

Abstract

PHT-induced cleft palate was preceded by embryonic dysrhythmia and hemorrhage in the orofacial region. Embryonic heart rhythm was phase specifically affected, as described for selective I(Kr) channel blockers, at clinically relevant concentrations. The results support the idea that PHT teratogenicity is a consequence of pharmacologically induced dysrhythmia and hypoxia-related damage.