Binienda Z, Rosen E D, Kelleman A, Sadowsky D W, Nathanielsz P W, Mitchell M D
Laboratory for Pregnancy and Newborn Research, New York State College of Veterinary Medicine, Ithaca 14853.
Endocrinology. 1990 Dec;127(6):3047-51. doi: 10.1210/endo-127-6-3047.
Food deprivation during pregnancy leads to an increase in maternal and fetal prostaglandin (PG) production and increased uterine contractility. We investigated the effect of maintaining fetal normoglycemia during food withdrawal-induced maternal hypoglycemia on uterine 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) production and myometrial activity in late pregnant sheep. Pregnant sheep were surgically instrumented with fetal and maternal catheters and electromyogram leads under halothane anesthesia. Maternal and fetal blood plasma samples were obtained once a day at 0900 h, 24 h before (baseline sample) and after 48 h of food withdrawal. Food, but not water, was withdrawn from ewes in group I (n = 5). During food withdrawal in group II (n = 5), glucose was infused into a fetal vein to maintain fetal normoglycemia. All data were normalized to the concentration in the baseline sample in each animal as 100%. After 48 h of food withdrawal, maternal whole blood glucose fell by 42.2 +/- 4.4% (mean +/- SEM: group I) and 31.4 +/- 6.2% (group II). These values were not significantly different. Fetal blood glucose fell by 40.4 +/- 5.7% (group I). In group II, fetal blood glucose was maintained in the normal range (99.6 +/- 1.6% of baseline). Maternal uterine electromyogram activity, uterine venous estrone sulfate, and uterine veno-arterial difference in PGFM rose significantly during food withdrawal in group I ewes, but not in group II ewes. Maternal and fetal arterial plasma ACTH and cortisol did not change in group II animals. We conclude that maintenance of fetal normoglycemia during 48 h of food withdrawal in sheep prevents the increase in myometrial activity, maternal plasma estrogens, and uterine PGFM production during food withdrawal in late pregnancy.
孕期食物剥夺会导致母体和胎儿前列腺素(PG)生成增加以及子宫收缩力增强。我们研究了在食物戒断诱导的母体低血糖期间维持胎儿血糖正常对妊娠晚期绵羊子宫13,14 - 二氢 - 15 - 酮 - 前列腺素F2α(PGFM)生成及子宫肌层活动的影响。在氟烷麻醉下,对妊娠绵羊进行手术,植入胎儿和母体导管以及肌电图导联。在撤食前24小时(基线样本)及撤食48小时后,每天09:00采集母体和胎儿血浆样本。第一组(n = 5)母羊停止供应食物,但不限制饮水。在第二组(n = 5)撤食期间,将葡萄糖注入胎儿静脉以维持胎儿血糖正常。所有数据均以每只动物基线样本中的浓度为100%进行标准化。撤食48小时后,母体全血葡萄糖下降了42.2±4.4%(平均值±标准误:第一组)和31.4±6.2%(第二组)。这些值无显著差异。第一组胎儿血糖下降了40.4±5.7%。在第二组中,胎儿血糖维持在正常范围内(为基线的99.6±1.6%)。第一组母羊撤食期间,母体子宫肌电图活动、子宫静脉硫酸雌酮以及子宫静脉 - 动脉PGFM差值显著升高,而第二组母羊则未出现此现象。第二组动物的母体和胎儿动脉血浆促肾上腺皮质激素(ACTH)及皮质醇未发生变化。我们得出结论,在绵羊撤食48小时期间维持胎儿血糖正常可防止妊娠晚期撤食期间子宫肌层活动、母体血浆雌激素及子宫PGFM生成增加。