Prenatal ethanol alters development of cardiac ornithine decarboxylase response to adrenergic agents in rat. I. Continuous exposure.

The maturation of cardiac sympathetic nerve function has been studied in developing rats exposed continuously to ethanol from the 13th day of gestation. Adrenergic development was determined by stimulation of cardiac ornithine decarboxylase (ODC) activity in response to sympathetic activation induced by nicotine, isoproterenol or insulin. In control rats, a significant cardiac ODC response to isoproterenol was first observed at 5 days of postnatal age whereas the response to nicotine was observed at 7 days of age. Cardiac ODC response to insulin-induced hypoglycemia was maximal between 3 and 12 days of postnatal age in the controls. Chlorisondamine pretreatment blocked insulin-induced cardiac ODC response starting from 7 days of postnatal age indicating that the induction in the activity was mediated via central stimulation of sympathetic nerves at this age. In contrast, pups exposed to ethanol throughout development showed decreased cardiac responses to sympathetic stimulation induced by isoproterenol and insulin with increasing postnatal age. Nicotine response was delayed also until 10 days of age in these ethanol-treated animals. Withdrawal at birth did not prevent abnormal maturation of cardiac sympathetic nerve function. These results suggest that maternal ethanol intake slows the development of sympathetic innervation to the heart of the offspring, more particularly the developement of cardiac beta-adrenergic receptors response to isoproterenol.