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Chronic ethanol exposure increases the non-dominant glucocorticoid, corticosterone, in the near-term pregnant guinea pig

机译：长期乙醇暴露会增加近期怀孕的豚鼠的非主要糖皮质激素皮质酮

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Maternal-fetal signaling is critical for optimal fetal development and postnatal outcomes. Chronic ethanol exposure alters programming of the fetal hypothalamic-pituitary-adrenal (HPA) axis, resulting in a myriad of neurochemical and behavioral alterations in postnatal life. Based on a recent study which showed that human intra-partum fetal stress increased fetal secretion of corticosterone, the non-dominant glucocorticoid, this investigation tested the hypothesis that an established model of HPA axis programming, chronic maternal ethanol administration to the pregnant guinea pig, would result in preferential elevation of corticosterone, which is also the non-dominant glucocorticoid. Starting on gestational day (GD) 2, guinea pigs received oral administration of ethanol (4 g/kg maternal body weight/day) or isocaloric-sucrose/pair-feeding. Each treatment was administered daily and continued until GD 45, 55, or 65 (approximately 3 days pre-term), when pregnant animals were euthanized and fetuses delivered by Caesarean section. Maternal and fetal plasma samples were collected. After sample preparation (protein precipitation and C-18 solid phase extraction), plasma cortisol and corticosterone concentrations were determined simultaneously by liquid chromatography coupled to tandem mass spectrometry. As predicted, chronic ethanol exposure increased both fetal and maternal plasma corticosterone concentration in late gestation. In contrast, plasma cortisol did not differ across maternal treatments in maternal or fetal samples. The plasma concentration of both maternal glucocorticoids increased with gestational age. Thus, corticosterone, the non-dominant glucocorticoid, but not cortisol, was elevated by chronic ethanol exposure, which may have effects on HPA function in later life.
机译：母胎信号对于最佳胎儿发育和产后结局至关重要。长期乙醇暴露会改变胎儿下丘脑-垂体-肾上腺（HPA）轴的程序，导致产后生活中发生无数的神经化学和行为改变。根据最近的一项研究表明，人类产时胎儿应激会增加胎儿皮质酮（非主要的糖皮质激素）的分泌，该研究检验了以下假设：建立的HPA轴编程模型，对怀孕的豚鼠进行长期母体乙醇给药，会导致皮质酮的优先升高，这也是非主要的糖皮质激素。从妊娠第2天（GD）开始，豚鼠口服乙醇（4 g / kg母体体重/天）或等热量蔗糖/配对喂养。每天给予每种治疗，并持续至GD 45、55或65（足月约3天），此时对安乐死的动物进行安乐死，并通过剖腹产来分娩胎儿。收集母体和胎儿血浆样品。样品制备（蛋白质沉淀和C-18固相萃取）后，通过液相色谱-串联质谱法同时测定血浆皮质醇和皮质酮浓度。如所预测的，在妊娠后期，慢性乙醇暴露会增加胎儿和母体血浆皮质酮的浓度。相反，在母体或胎儿样品中，血浆皮质醇在母体治疗之间没有差异。两种孕激素糖皮质激素的血浆浓度均随胎龄增加。因此，慢性乙醇暴露会升高皮质酮（一种非主要的糖皮质激素，而不是皮质醇），这可能对以后的HPA功能产生影响。

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