Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1990;81:1047-1057

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Leatherbury, L.
Right arrow Articles by Kirby, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Leatherbury, L.
Right arrow Articles by Kirby, M. L.

Circulation, Vol 81, 1047-1057, Copyright © 1990 by American Heart Association


ARTICLES

Microcinephotography of the developing heart in neural crest-ablated chick embryos

L Leatherbury, HE Gauldin, K Waldo and ML Kirby
Department of Pediatrics, Medical College of Georgia, Augusta 30912.

Microcinephotography was used to study heart development in a neural crest model of heart defects, that is, persistent truncus arteriosus, interrupted aortic arch, double outlet right ventricle, or single ventricle and tricuspid valve anomalies. These defects were created in chick embryos by ablation of premigratory neural crest destined for the aorticopulmonary and truncal septa, as well as the third and fourth aortic arch arteries. When embryogenesis reached the looped cardiac tube stage of development (Hamburger-Hamilton stage 18), 19 experimental and 15 control embryos were filmed at 100 frames per second under controlled environmental conditions. Analysis of the microcinephotography films showed the following significant distinguishing characteristics of the developing heart in the experimental embryos: altered conotruncal shape in 100%, depressed contractility and dilation of the primitive ventricle in 84%, decreased emptying of the bulbus cordis in 79%, incompetent truncal cushions in 68%, incomplete looping of the cardiac tube in 58%, and fourth right aortic arch artery without blood flow and third right aortic arch artery with increased flow in 53%. These abnormal characteristics suggested that there were functional and morphological changes in the developing heart of experimental embryos before the time when the predicted structural heart defects would be apparent. It is proposed that the primitive ventricle might attempt to compensate for depressed contractility by ventricular dilation. The incompetent truncal cushions could be secondary to the depressed contractility or secondary to the neural crest ablation that is known to cause persistent truncus arteriosus, an interrupted aortic arch, or both. The absence of blood flow in the right fourth aortic arch artery that will become the definitive aorta correlates with the expected incidence of interrupted aortic arches in this neural crest-ablation model of heart defects. It is speculated that the incomplete looping of the cardiac tube might hinder normal developmental alignment of the outflow and inflow tracts, producing a spectrum of lesions of maldevelopment of the tricuspid valve and dextroposition of the aorta.


This article has been cited by other articles:


Home page
HypertensionHome page
B. Mersich, P. Studinger, Z. Lenard, K. Kadar, and M. Kollai
Transposition of Great Arteries Is Associated With Increased Carotid Artery Stiffness
Hypertension, June 1, 2006; 47(6): 1197 - 1202.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
T. M. Yelbuz, K. L. Waldo, D. H. Kumiski, H. A. Stadt, R. R. Wolfe, L. Leatherbury, and M. L. Kirby
Shortened Outflow Tract Leads to Altered Cardiac Looping After Neural Crest Ablation
Circulation, July 23, 2002; 106(4): 504 - 510.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
R. M. Payne, M. C. Johnson, J. W. Grant, and A. W. Strauss
Toward a Molecular Understanding of Congenital Heart Disease
Circulation, January 15, 1995; 91(2): 494 - 504.
[Abstract] [Full Text]