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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The effect of adrenalectomy on the cardiac response to subacute fetal anemia.
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The effect of adrenalectomy on the cardiac response to subacute fetal anemia.

机译：肾上腺切除术对亚急性胎儿贫血的心脏反应的影响。

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The mechanisms that stimulate fetal heart growth during anemia are unknown. To examine the hypothesis that adrenal hormones contribute to this process, we determined the effects of adrenalectomy (Adx) on heart growth and the activation of cardiac mitogen-activated protein kinases (MAPKs) in the presence and absence of fetal anemia. To identify mechanisms contributing to the initiation of cardiac growth, the duration of anemia was limited to a period shorter than that previously described to result in increased cardiac mass. Four groups of fetal sheep were studied (Adx-Anemic, Adx-Control, Intact-Anemic, Intact-Control). Anemia was created by daily controlled hemorrhage for 5 days; hearts were collected for analysis at 133 d gestation (term 145 d). Cardiomyocyte morphometry, immunohistochemistry for Ki-67 (proliferation marker), and Western blotting for protein levels of MAPKs and proliferating cell nuclear antigen (PCNA) were performed. Blood pressure, heart rate, heart weight-to-body weight ratio, and cardiomyocyte length and width remained similar among groups throughout the study. PCNA levels in the Adx-Anemic group were twice as high as in any other group (both ventricles, p < 0.05). Levels of phosphorylated extracellular signal-regulated kinase (ERK) were ~60% higher in the Intact-Anemic and Adx-Anemic groups, compared with the Intact-Control and Adx-Control groups (p < 0.02). These results suggest that adrenal hormones may attenuate fetal cardiomyocyte proliferation in response to anemia (as evidenced by the increased PCNA in Adx-Anemic fetuses) and that phosphorylation of myocardial ERK results from fetal anemia, irrespective of the status of the fetal adrenal gland.
机译：贫血期间刺激胎儿心脏生长的机制尚不清楚。为了检查肾上腺激素促成这一过程的假说，我们确定了在存在和不存在胎儿贫血的情况下，肾上腺切除术（Adx）对心脏生长和心脏促丝裂原活化蛋白激酶（MAPK）活化的影响。为了确定促成心脏生长的机制，将贫血的持续时间限制在比先前所述的更短的时间以导致心脏质量增加。研究了四组胎羊（Adx-贫血，Adx-对照，完整-贫血，完整-对照）。每天控制出血5天可导致贫血。在第133天（第145天）收集心脏进行分析。进行心肌细胞形态测定，Ki-67的免疫组织化学（增殖标记物）以及MAPKs和增殖细胞核抗原（PCNA）蛋白质水平的蛋白质印迹分析。在整个研究中，各组之间的血压，心率，心脏体重与体重比以及心肌细胞的长度和宽度保持相似。 Adx-贫血组的PCNA水平是任何其他组的两倍（两个心室，p <0.05）。与完整对照组和Adx对照组相比，完整贫血组和Adx贫血组的磷酸化细胞外信号调节激酶（ERK）水平高约60％（p <0.02）。这些结果表明，肾上腺激素可能响应贫血而减弱胎儿心肌细胞的增殖（如Adx-贫血胎儿PCNA的增加所证明），并且心肌ERK的磷酸化是由胎儿贫血导致的，而与胎儿肾上腺的状态无关。

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