Abstract:
These studies were designed to determine the effect of acute alcohol treatmenton gestational length and to probe for a mechanism underlying alcohol-inducedearly onset of parturition (EOP) in mice. Experiment 1:alcohol increases the incidence of EOP. Pregnant C57BL/6J mice were givenalcohol (0, 4, 5 or 6 g kg <emph type="7">-1 , i.g.) on Gestational Day(GD) 10, 15, 16, 17 or 18. Deliveries were monitored every 6 h from GD 18.Results indicated that 6 g kg <emph type="7">-1 alcohol treatment on GD17 or 18 increased the incidence of EOP. Experiment 2: prostaglandins (PGs)play roles in parturition. The purpose of Experiment 2was to determine whether PGs mediate alcohol-induced EOP in mice. The resultsindicated that pretreatment on GD 17 with aspirin, a prostaglandin synthesisinhibitor, prevented alcohol-induced EOP. These data suggest thatalcohol-induced EOP in mice may be mediated by PGs. Experiment 3: PGs areinfluenced by alcohol and are triggers of labour.Experiment3 measured uterine PGsassociated with the onset of alcohol-induced EOP in mice. Alcohol increaseduterine PGE and PGF<emph type="8">2a , with PGE levels higher thancontrol before labour, and elevated PGF<emph type="8">2a levelscorrelating with labour. Changes in gestational length have importantimplications for pregnancy outcome, as well as for normal fetal growth anddevelopment.