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母体对热应激的内分泌反应及胎儿的代谢反应。

Maternal endocrine and fetal metabolic responses to heat stress.

作者信息

Dreiling C E, Carman F S, Brown D E

机构信息

Department of Biochemistry, University of Nevada, School of Medicine, Reno 89557.

出版信息

J Dairy Sci. 1991 Jan;74(1):312-27. doi: 10.3168/jds.S0022-0302(91)78175-7.

DOI:10.3168/jds.S0022-0302(91)78175-7
PMID:2030175
Abstract

Heat-stressed pregnant ewes deliver intrauterine growth-retarded lambs. Selected maternal and fetal changes were investigated during acute heat stress in order to elucidate the mechanism for this growth retardation. Uterine blood flow decreased 20 to 30% in pregnant ewes during 1 degree C increases in core temperature. The decreases were accompanied by 60 and 100% increases in serum oxytocin and antidiuretic hormone, respectively. These effects were mimicked by salt loading or injections of antidiuretic hormone or oxytocin, suggesting a role for either or both hormones in regulating uterine blood flow during pregnancy. Chronically heat-stressed pregnant ewes were delivered by Caesarean section. Their fetuses were approximately 20% smaller than thermoneutral controls. Within each pair of heat-stressed twins, one fetus weighted one-third less than its litter mate. No difference in weights were observed within the control twins. The livers and brains of the heat-stressed fetuses were disproportionate in size. The livers from the small heat-stressed twins contained only one-half the protein of the controls and one-fourth the protein of their litter mates. Muscle protein was decreased in the heat-stressed fetuses, and liver and muscle glycogen were elevated as were liver arginase, glutamate-pyruvate transaminase and muscle creatinine. These results are consistent with the following hypothesis: heat stress stimulates the release of maternal antidiuretic hormone or oxytocin, which reduces uterine blood flow and causes a shift in fetal metabolism from anabolic to catabolic pathways; one fetus of heat-stressed twins is more severely affected than its litter mate.

摘要

热应激的怀孕母羊产出子宫内生长受限的羔羊。为了阐明这种生长受限的机制,对急性热应激期间选定的母体和胎儿变化进行了研究。在核心温度每升高1摄氏度时,怀孕母羊的子宫血流量减少20%至30%。血流量减少的同时,血清催产素和抗利尿激素分别增加了60%和100%。盐负荷、注射抗利尿激素或催产素可模拟这些效应,表明这两种激素中的一种或两种在调节孕期子宫血流量中发挥作用。长期热应激的怀孕母羊通过剖腹产分娩。它们的胎儿比处于热中性状态的对照羊的胎儿小约20%。在每对热应激的双胞胎胎儿中,有一个胎儿的体重比其同窝胎儿轻三分之一。对照双胞胎胎儿的体重没有差异。热应激胎儿的肝脏和大脑大小不成比例。热应激的小双胞胎胎儿的肝脏所含蛋白质仅为对照胎儿的一半,为其同窝胎儿的四分之一。热应激胎儿的肌肉蛋白质减少,肝脏和肌肉糖原增加,肝脏精氨酸酶、谷丙转氨酶和肌肉肌酐也增加。这些结果与以下假设一致:热应激刺激母体抗利尿激素或催产素的释放,这会减少子宫血流量,并导致胎儿代谢从合成代谢途径转变为分解代谢途径;热应激双胞胎中的一个胎儿比其同窝胎儿受到的影响更严重。

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