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本文引用的文献

1
The effect of adrenalectomy on the cardiac response to subacute fetal anemia.肾上腺切除术对亚急性胎儿贫血心脏反应的影响。
Can J Physiol Pharmacol. 2011 Feb;89(2):79-88. doi: 10.1139/y10-108.
2
Cardiac remodelling as a result of pre-term birth: implications for future cardiovascular disease.早产儿心脏重构:对未来心血管疾病的影响。
Eur Heart J. 2010 Aug;31(16):2058-66. doi: 10.1093/eurheartj/ehq104. Epub 2010 May 7.
3
Cardiomyocyte enlargement, proliferation and maturation during chronic fetal anaemia in sheep.绵羊慢性胎儿贫血时心肌细胞的增大、增殖和成熟。
Exp Physiol. 2010 Jan;95(1):131-9. doi: 10.1113/expphysiol.2009.049379. Epub 2009 Aug 21.
4
Effect of fetal anaemia on myocardial ischaemia-reperfusion injury and coronary vasoreactivity in adult sheep.胎儿贫血对成年绵羊心肌缺血再灌注损伤及冠状血管反应性的影响。
Acta Physiol (Oxf). 2008 Dec;194(4):325-34. doi: 10.1111/j.1748-1716.2008.01892.x. Epub 2008 Sep 20.
5
Myocyte enlargement, differentiation, and proliferation kinetics in the fetal sheep heart.胎羊心脏中的心肌细胞增大、分化及增殖动力学
J Appl Physiol (1985). 2007 Mar;102(3):1130-42. doi: 10.1152/japplphysiol.00937.2006. Epub 2006 Nov 22.
6
Sequential growth of fetal sheep cardiac myocytes in response to simultaneous arterial and venous hypertension.胎儿绵羊心肌细胞对同时发生的动脉和静脉高血压的顺序性生长反应。
Am J Physiol Regul Integr Comp Physiol. 2007 Feb;292(2):R913-9. doi: 10.1152/ajpregu.00484.2006. Epub 2006 Oct 5.
7
The mitogen-activated protein kinases and Akt are developmentally regulated in the chronically anemic fetal sheep heart.丝裂原活化蛋白激酶和Akt在慢性贫血胎羊心脏中受到发育调控。
J Soc Gynecol Investig. 2006 Apr;13(3):157-65. doi: 10.1016/j.jsgi.2006.01.004.
8
Regulation of myocardial glucose transporters GLUT1 and GLUT4 in chronically anemic fetal lambs.慢性贫血胎羊中心肌葡萄糖转运蛋白GLUT1和GLUT4的调节
Pediatr Res. 2005 Oct;58(4):713-8. doi: 10.1203/01.PDR.0000180546.42475.69.
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Myocardial vascular and metabolic adaptations in chronically anemic fetal sheep.慢性贫血胎羊的心肌血管和代谢适应性变化
Am J Physiol Regul Integr Comp Physiol. 2005 Dec;289(6):R1736-45. doi: 10.1152/ajpregu.00278.2005. Epub 2005 Aug 25.
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Dilated cardiomyopathy presenting during fetal life.胎儿期出现的扩张型心肌病。
Cardiol Young. 2005 Aug;15(4):409-16. doi: 10.1017/S1047951105000855.

慢性贫血胎儿羊输血对心肌细胞生长和增殖的影响。

Transfusion effects on cardiomyocyte growth and proliferation in fetal sheep after chronic anemia.

机构信息

Department of Pediatrics, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA.

出版信息

Pediatr Res. 2011 Jun;69(6):485-90. doi: 10.1203/PDR.0b013e3182181e01.

DOI:10.1203/PDR.0b013e3182181e01
PMID:21386752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3090539/
Abstract

Chronic fetal anemia results in significant cardiac remodeling. The capacity to reverse these effects is unknown. We examined the effects of transfusion on cardiomyocyte adaptations after chronic anemia in fetal sheep subjected to daily hemorrhage beginning at 109-d GA (term ∼145 d). After 10 d of anemia, one group was killed for comparison with age-matched controls. A separate group of anemic fetuses was transfused with red blood cells at 119-d GA for comparison with controls at 129-d GA. Anemia significantly increased the heart-to-body weight ratio, an effect partially ameliorated after transfusion. Cardiomyocyte dimensions were similar among all groups, suggesting an absence of hypertrophy. The percentages of mono- and binucleated cardiomyocytes were similar between groups at 119-d GA, although the percentage of binucleated cells was significantly less in transfused fetuses compared with controls at 129-d GA. Protein levels of mitogen-activated protein kinases and protein kinase B were similar between controls and their respective intervention groups, except for a significant increase in phosphorylated c-Jun N-terminal kinase 1/2 in transfused fetuses. Thus, cardiomyocyte proliferation but not hypertrophy contributes to cardiac enlargement during fetal anemia. Transfusion results in slowing but not cessation of cardiac growth after anemia.

摘要

慢性胎儿贫血会导致显著的心脏重构。目前尚不清楚是否能够逆转这些影响。我们研究了在 109 天龄 GA(足月约 145 天)的胎儿羊每日出血导致慢性贫血后,输血对心肌细胞适应性的影响。在贫血 10 天后,一组被处死,与同龄对照组进行比较。另一组贫血胎儿在 119 天龄 GA 时输血,并与 129 天龄 GA 的对照组进行比较。贫血显著增加了心脏与体重的比值,输血后部分改善了这种情况。心肌细胞尺寸在所有组之间相似,表明没有肥大。在 119 天龄 GA 时,各组之间单核和双核心肌细胞的百分比相似,但在 129 天龄 GA 时,输血胎儿的双核细胞百分比明显低于对照组。除了转铁蛋白胎儿中磷酸化 c-Jun N-末端激酶 1/2 显著增加外,对照组及其各自干预组之间的有丝分裂原激活蛋白激酶和蛋白激酶 B 的蛋白水平相似。因此,心肌细胞增殖而不是肥大导致胎儿贫血时心脏扩大。输血导致贫血后心脏生长减缓但未停止。