Abstract
Anticonvulsant drug treatment during pregnancy is associated with an increased incidence of developmental disorders. The finding that anticonvulsant treatment can induce hyponatraemia prompted us to study the role of this parameter in the induction of malformations. Rats were treated orally with the anticonvulsants phenytoin, phenobarbitone, carbamazepine and valproic acid, and their sera were used as media in cultures of post-implantation (day 10) rat embryos. Sodium concentrations in the media were adjusted by mixing sera with 25% tissue-culture medium with or without sodium chloride. We found that low sodium concentrations caused retardation of development and enhanced the sensitivity of embryos to the retardant effects of anticonvulsants. These results show that apart from the direct effects of drugs and their metabolites secondary factors may be important in the aetiology of maldevelopment.
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