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首页> 外文期刊>American Journal of Physiology >High oxygen prevents fetal lethality due to lack of catecholamines
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High oxygen prevents fetal lethality due to lack of catecholamines

机译：由于缺乏儿茶酚胺，高氧可防止胎儿致死率

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First published July 16, 2008; doi:10.n52/ajpregu.00860.2007.-The catecholamine norepinephrine is required for fetal survival, but its essential function is unknown. When catecholamine-deficient [tyrosine hydroxylase (Th) null] mouse fetuses die at embryonic day (E)13.5-14.5, they resemble wild-type (wt) fetuses exposed to hypoxia. They exhibit bradycardia (28% reduction in heart rate), thin ventricular myocardium (20% reduction in tissue), epicardial detachment, and death with vascular congestion, hemorrhage, and edema. At E12.5, before the appearance of morphological deficits, catecholamine-deficient fetuses are preferentially killed by experimentally induced hypoxia and have lower tissue Po2 levels than wt siblings. By microarray analysis (http://www.ncbi.nlm.nih.gov/geo; accession no. GSE10341), hypoxia-inducible factor-1 target genes are induced to a greater extent in null fetuses than in wt siblings, supporting the notion that mutants experience lower oxygen tension or have an enhanced response to hypoxia. Hypoxia induces a 13-fold increase in plasma norepinephrine levels, which would be expected to increase heart rate, thereby improving oxygen delivery in wt mice. Surprisingly, increasing maternal oxygen (inspired O2 33 or 63%) prevents the effects of catecholamine deficiency, restoring heart rate, myocardial tissue, and survival of Th null fetuses to wt levels. We suggest that norepinephrine mediates fetal survival by maintaining oxygen homeostasis.
机译：2008年7月16日首次发布; doi：10.n52 / ajpregu.00860.2007.-儿茶酚胺去甲肾上腺素是胎儿存活所必需的，但其基本功能尚不清楚。当儿茶酚胺缺陷型[酪氨酸羟化酶（Th）无效]的小鼠胎儿在胚胎第（E）13.5-14.5天死亡时，它们类似于暴露于低氧状态的野生型（wt）胎儿。它们表现出心动过缓（心率降低28％），心室心肌薄（组织降低20％），心外膜脱离以及血管充血，出血和水肿死亡。在E12.5时，在形态学缺陷出现之前，儿茶酚胺缺乏的胎儿优先被实验诱导的缺氧杀死，并且与wt兄弟姐妹相比组织Po2含量更低。通过微阵列分析（http://www.ncbi.nlm.nih.gov/geo;保藏号为GSE10341），缺氧胎儿中的缺氧诱导因子-1靶基因的诱导程度要比wt兄弟姐妹更大。突变体的氧张力降低或对缺氧的反应增强的观点。缺氧导致血浆去甲肾上腺素水平增加13倍，这有望增加心率，从而改善wt小鼠的氧气输送。出乎意料的是，增加孕妇氧气（吸入的O2为33或63％）可防止儿茶酚胺缺乏，恢复心率，心肌组织以及Th胎儿存活至wt水平的影响。我们建议去甲肾上腺素通过维持氧稳态来介导胎儿存活。

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