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慢性胎儿胎盘栓塞后胎羊对持续性低氧应激的内分泌反应。

Fetal sheep endocrine responses to sustained hypoxemic stress after chronic fetal placental embolization.

作者信息

Gagnon R, Murotsuki J, Challis J R, Fraher L, Richardson B S

机构信息

Department of Obstetrics and Gynaecology, University of Western Ontario, London, Canada.

出版信息

Am J Physiol. 1997 May;272(5 Pt 1):E817-23. doi: 10.1152/ajpendo.1997.272.5.E817.

Abstract

The purpose of this study was to determine the endocrine and circulatory responses of the ovine fetus, near term, to sustained hypoxemic stress superimposed on chronic hypoxemia. Fetal sheep were chronically embolized (n = 7) for 10 days between 0.84 and 0.91 of gestation via the descending aorta until arterial oxygen content was decreased by approximately 30%. Control animals (n = 8) received saline only. On experimental day 10, both groups were embolized over a 6-h period until fetal arterial pH decreased to approximately 7.00. Regional distribution of lower body blood flows was measured on day 10, before and at the end of acute embolization. On day 10, the chronically embolized group had lower arterial oxygen content (P < 0.05), Po2 (P < 0.01), and placental blood flow (P < 0.05) than controls and higher prostaglandin E2 (PGE2) and norepinephrine plasma concentrations (both P < 0.05). In response to a superimposed sustained hypoxemic stress, there was a twofold greater increase in PGE2 in the chronically embolized group than in the control group (P < 0.05). However, the increase in fetal plasma cortisol in response to superimposed hypoxemic stress was similar in both groups, despite significantly lower adrenocorticotropic hormone and adrenal cortex blood flow responses in the chronically hypoxemic group (both P < 0.05). We conclude that PGE2 response to a sustained superimposed reduction in placental blood flow, leading to metabolic acidosis, is enhanced under conditions of chronic hypoxemia and may play an important role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.

摘要

本研究的目的是确定近足月绵羊胎儿对叠加于慢性低氧血症之上的持续性低氧应激的内分泌和循环反应。在妊娠0.84至0.91之间,通过降主动脉对胎羊进行为期10天的慢性栓塞(n = 7),直至动脉氧含量降低约30%。对照动物(n = 8)仅接受生理盐水。在实验第10天,两组均在6小时内进行栓塞,直至胎儿动脉pH值降至约7.00。在急性栓塞前和结束时的第10天,测量下肢血流的区域分布。在第10天,慢性栓塞组的动脉氧含量(P < 0.05)、氧分压(P < 0.01)和胎盘血流量(P < 0.05)均低于对照组,而前列腺素E2(PGE2)和去甲肾上腺素血浆浓度均高于对照组(均P < 0.05)。对叠加的持续性低氧应激的反应中,慢性栓塞组的PGE2增加量是对照组的两倍(P < 0.05)。然而,尽管慢性低氧血症组的促肾上腺皮质激素和肾上腺皮质血流反应明显较低(均P < 0.05),但两组对叠加低氧应激的胎儿血浆皮质醇增加量相似。我们得出结论,在慢性低氧血症条件下,对导致代谢性酸中毒的胎盘血流量持续叠加减少的PGE2反应增强,这可能对维持胎儿对叠加急性应激发作的皮质醇反应起重要作用。

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