EARLY-ONSET OF PARTURITION INDUCED BY ACUTE ALCOHOL EXPOSURE IN C57BL6J MICE - ROLE OF UTERINE PGE AND PGF(2-ALPHA)/

These studies were designed to determine the effect of acute alcohol t reatment on gestational length and to probe for a mechanism underlying alcohol-induced early onset of parturition (EOP) in mice. Experiment I: alcohol increases the incidence of EOP. Pregnant C57BL/6J mice were given alcohol (0, 4, 5 or 6 g kg(-1), i.g.) on Gestational Day (GD) 1 0, 15, 16, 17 or 18. Deliveries were monitored every 6 h from GD 18. R esults indicated that 6 g kg(-1) alcohol treatment on GD 17 or 18 incr eased the incidence of EOP. Experiment 2: prostaglandins (PGs) play ro les in parturition. The purpose of Experiment 2 was to determine wheth er PGs mediate alcohol-induced EOP in mice. The results indicated that pretreatment on GD 17 with aspirin, a prostaglandin synthesis inhibit or, prevented alcohol-induced EOP. These data suggest that alcohol-ind uced EOP in mice may be mediated by PGs. Experiment 3: PGs are influen ced by alcohol and are triggers of labour. Experiment 3 measured uteri ne PGs associated with the onset of alcohol-induced EOP in mice. Alcoh ol increased uterine PGE and PGF(2 alpha), with PGE levels higher than control before labour, and elevated PGF(2 alpha) levels correlating w ith labour. Changes in gestational length have important implications for pregnancy outcome, as well as for normal fetal growth and developm ent.