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Cited by 232Congenital heart defects researchCongenital Heart Disease StudiesCardiac electrophysiology and arrhythmias

Unilateral Vitelline Vein Ligation Alters Intracardiac Blood Flow Patterns and Morphogenesis in the Chick Embryo

Hogers, B., DeRuiter, M.C., Gittenberger-de Groot, A.C., Poelmann, R.E.·1997·Circulation Research
DOI 10.1161/01.res.80.4.473
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Abstract

Abstract To study the role of blood flow in normal and abnormal heart development, an embryonic chicken model was developed. The effect of altered venous inflow on normal intracardiac blood flow patterns was studied by visualization of blood flow with India ink. At stage 17, India ink was injected into a capillary or small venule within a specific yolk sac region. After determination of the normal intracardiac flow pattern, the right lateral vitelline vein was ligated, and the new intracardiac flow pattern was studied. Ligation resulted in disturbance of normal intracardiac flow patterns, which was most obvious in the conotruncus. The long-term effect of these abnormal intracardiac flow patterns on the development of the heart and pharyngeal arch arteries was investigated by permanent ligation in ovo with a microclip at stage 17 and subsequent evaluation at stages 34, 37, and 45. These experiments revealed anomalies of the vascular system in 58 of the 91 ligated embryos studied. We observed intracardiac malformations consisting of subaortic ventricular septal defects (n=52), semilunar valve anomalies (n=19), atrioventricular anomalies (n=7), and pharyngeal arch artery malformations (n=32). It is concluded that abnormal intracardiac blood flow, resulting from hampered venous inflow, may result in serious intracardiac and pharyngeal arch artery malformations comparable to defects observed in embryonic chicken models subjected to neural crest ablation, cervical flexure experiments, and excessive retinoic acid treatment.

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  • The vitelline and allantoic vascular beds offer mechanical resistance to blood flow, and their inadequate growth promotes mechanical signals in the heart that result in structural defects.

    “These vascular beds offer mechanical resistance to blood flow, and there is increasing evidence that their inadequate growth promotes mechanical signals in the heart that result in structural defects (218, 260, 341, 379).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [260]

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Authors
Hogers, B., DeRuiter, M. C., Gittenberger-de Groot, A. C., & Poelmann, R. E.
Affiliations
  • Leiden University (NL)
  • From the Department of Anatomy and Embryology, Leiden University (the Netherlands).
ORCID
Venue
Circulation Research
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1997-04
Volume
80
Issue
4
Pages
473-481
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
DOI
10.1161/01.res.80.4.473
OpenAlex
W2150258518
Cited by
232
References
71
Citations by year
2026: 7 · 2025: 7 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 7 · 2019: 5 · 2018: 10 · 2017: 11 · 2016: 5 · 2015: 13 · 2014: 9 · 2013: 9 · 2012: 15
FWCI
2.96
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
  • Health Sciences › Medicine › Epidemiology › Congenital Heart Disease Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
intracardiac blood flow, cardiac morphogenesis, chick embryo, ventricular septal defect, congenital heart disease
MeSH terms
Animals, Blood Volume, Branchial Region, Chick Embryo, Heart, Heart Defects, Congenital, Ligation, Microscopy, Electron, Scanning, Regional Blood Flow, Yolk Sac

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