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首页> 外文期刊>American Journal of Physiology >Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus.
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Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus.

机译：PGHS-2的阻滞抑制绵羊胎儿对脑灌注不足的下丘脑-垂体-肾上腺轴的反应。

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摘要

Decreases in fetal blood pressure stimulate homeostatic stress responses that help return blood pressure to normal levels. Fetal hypothalamus-pituitary-adrenal (HPA) axis responses to hypotension are mediated by chemoreceptor and baroreceptor reflexes and ischemia of the fetal central nervous system. Indomethacin, a nonselective inhibitor of prostaglandin endoperoxide synthase (PGHS)-1 and -2, attenuates the HPA response to hypotension in the fetus. The present study was designed to test the hypothesis that selective inhibition of PGHS-2 also inhibits the HPA response to cerebral hypoperfusion. We studied 13 chronically catheterized fetal sheep (126-136 days gestation). Five fetal sheep were subjected to intracerebroventricular infusion of nimesulide (0.01 mg/day), a specific inhibitor of PGHS-2, and eight were treated with vehicle (DMSO in water) for 5 days. Each fetus was subjected to a 10-min period of brachiocephalic occlusion, which decreased carotid arterial pressure approximately 75% and reflexively increased fetal plasma concentrations of ACTH, POMC, cortisol, and femoral arterial pressure, and decreased fetal heart rate. Nimesulide significantly inhibited the ACTH response to the BCO, while significantly augmenting the reflex cardiovascular response and altering fetal heart rate variability consistent with increased sympathetic nervous system activity. The results of this study demonstrate that the activity of PGHS-2 in the brain is a necessary component of the fetal HPA response to cerebral hypoperfusion in the late-gestation fetal sheep. These results are consistent with those of recent study, in which we demonstrated that the preparturient increase in fetal ACTH secretion depends upon PGHS-2 activity within the fetal brain.
机译：胎儿血压降低会刺激体内稳态压力反应，从而使血压恢复正常水平。胎儿下丘脑-垂体-肾上腺（HPA）轴对低血压的反应是由化学感受器和压力感受器反射以及胎儿中枢神经系统缺血介导的。消炎痛是前列腺素内过氧化物合酶（PGHS）-1和-2的非选择性抑制剂，可减轻HPA对胎儿低血压的反应。本研究旨在检验以下假设：PGHS-2的选择性抑制也抑制了HPA对脑灌注不足的反应。我们研究了13例经慢性导尿的胎羊（妊娠126-136天）。对五只胎羊进行脑室内脑内输注尼美舒利（0.01 mg /天），PGHS-2的特异性抑制剂，并对八只胎羊进行溶媒（DMSO水溶液）处理5天。每个胎儿都要经历10分钟的头颅脑阻塞，这会使颈动脉压降低约75％，并反过来增加胎儿血浆ACTH，POMC，皮质醇和股动脉压的浓度，并降低胎儿心率。尼美舒利显着抑制对BCO的ACTH反应，同时显着增强反射性心血管反应并改变与交感神经系统活动一致的胎儿心率变异性。这项研究的结果表明，大脑中PGHS-2的活性是妊娠晚期胎羊对胎儿脑灌注不足的胎儿HPA反应的必要组成部分。这些结果与最近的研究结果一致，在该研究中，我们证明了胎儿ACTH分泌的产前增加取决于胎儿脑内PGHS-2的活性。

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