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心包内动脉干分隔在人胚心脏早期的发生。

Septation of the Intrapericardial Arterial Trunks in the Early Human Embryonic Heart.

机构信息

Department of Histology and Embryology, Shanxi Medical University, Taiyuan, Shanxi 030001, China.

出版信息

Chin Med J (Engl). 2018 Jun 20;131(12):1457-1464. doi: 10.4103/0366-6999.233956.

DOI:10.4103/0366-6999.233956
PMID:29893363
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6006820/
Abstract

BACKGROUND

Outflow tract (OFT) septation defects are a common cause of congenital heart disease. Numerous studies have focused on the septation mechanism of the OFT, but have reported inconsistent conclusions. This study, therefore, aimed to investigate the septation of the aortic sac and the OFT in the early embryonic human heart.

METHODS

Serial sections of 27 human embryonic hearts from Carnegie stage (CS) 10 to CS19 were immunohistochemically stained with antibodies against α-smooth muscle actin (α-SMA) and myosin heavy chain.

RESULTS

At CS10-CS11, the OFT wall was an exclusively myocardial structure that was continuous with the aortic sac at the margin of the pericardial cavity. From CS13 onward, the OFT was divided into nonmyocardial and myocardial portions. The cushion formed gradually, and its distal border with the OFT myocardium was consistently maintained. The aortic sac between the fourth and sixth aortic arch arteries was degenerated. At CS16, the α-SMA-positive aortopulmonary septum formed and fused with the two OFT cushions, thus septating the nonmyocardial portion of the OFT into two arteries. At this stage, the cushions were not fused. At CS19, the bilateral cushions were fused to septate the myocardial portion of the OFT.

CONCLUSIONS

Data suggest that the OFT cushion is formed before the aortopulmonary septum is formed. Thus, the OFT cushion is not derived from the aortopulmonary septum. In addition, the nonmyocardial part of the OFT is septated into the aorta and pulmonary trunk by the aortopulmonary septum, while the main part of the cushion fuses and septates the myocardial portion of the OFT.

摘要

背景

流出道(OFT)间隔缺损是先天性心脏病的常见原因。许多研究都集中在 OFT 的间隔机制上,但报告的结论不一致。因此,本研究旨在探讨早期胚胎人心主动脉窦和 OFT 的间隔。

方法

对来自卡内基阶段(CS)10 至 CS19 的 27 个人类胚胎心脏进行连续切片,并用抗α-平滑肌肌动蛋白(α-SMA)和肌球蛋白重链的抗体进行免疫组织化学染色。

结果

在 CS10-CS11,OFT 壁是一种纯粹的心肌结构,在心包腔边缘与主动脉窦连续。从 CS13 开始,OFT 分为非心肌和心肌两部分。心垫逐渐形成,其与 OFT 心肌的远端边界保持一致。第四和第六主动脉弓动脉之间的主动脉窦退化。在 CS16,α-SMA 阳性的主肺动脉隔形成并与两个 OFT 心垫融合,从而将 OFT 的非心肌部分分隔成两个动脉。在这个阶段,心垫没有融合。在 CS19,双侧心垫融合将 OFT 的心肌部分分隔开。

结论

数据表明,OFT 心垫在主肺动脉隔形成之前形成。因此,OFT 心垫不是来自主肺动脉隔。此外,OFT 的非心肌部分由主肺动脉隔分隔成主动脉和肺动脉,而心垫的主要部分融合并分隔 OFT 的心肌部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/0f2224d135dd/CMJ-131-1457-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/eb51a2f8d1fa/CMJ-131-1457-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/9a6347c34572/CMJ-131-1457-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/d43902dfcb47/CMJ-131-1457-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/64ac3f743d6a/CMJ-131-1457-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/1967fb6987e7/CMJ-131-1457-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/0f2224d135dd/CMJ-131-1457-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/eb51a2f8d1fa/CMJ-131-1457-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/9a6347c34572/CMJ-131-1457-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/d43902dfcb47/CMJ-131-1457-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/64ac3f743d6a/CMJ-131-1457-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/1967fb6987e7/CMJ-131-1457-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84de/6006820/0f2224d135dd/CMJ-131-1457-g006.jpg

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A Tubular Aortopulmonary Window: An Embryological Curiosity.管状主肺动脉窗:一种胚胎学上的罕见现象。
World J Pediatr Congenit Heart Surg. 2016 May;7(3):411-3. doi: 10.1177/2150135115596586. Epub 2016 Jan 21.
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Neural crest-derived SEMA3C activates endothelial NRP1 for cardiac outflow tract septation.神经嵴衍生的SEMA3C激活内皮细胞的NRP1以实现心脏流出道分隔。
J Clin Invest. 2015 Jul 1;125(7):2661-76. doi: 10.1172/JCI79668. Epub 2015 Jun 8.
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Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndrome.Wnt5a的缺失会破坏第二心脏区域细胞的部署,并可能导致DiGeorge综合征中的流出道畸形。
Hum Mol Genet. 2015 Mar 15;24(6):1704-16. doi: 10.1093/hmg/ddu584. Epub 2014 Nov 19.
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Evolutionary and developmental origins of the cardiac neural crest: building a divided outflow tract.心脏神经嵴的进化与发育起源:构建分隔的流出道。
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