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Research Paper

The Endothelin-1 Pathway and the Development of Cardiovascular Defects in the Haemodynamically Challenged Chicken Embryo

Groenendijk B.C.W.a, d · Stekelenburg-de Vos S.b · Vennemann P.c · Wladimiroff J.W.b · Nieuwstadt F.T.M.c · Lindken R.c · Westerweel J.c · Hierck B.P.a · Ursem N.T.C.b · Poelmann R.E.a

Author affiliations

aDepartment of Anatomy and Embryology, Leiden University Medical Center, Leiden, bDepartment of Obstetrics and Gynaecology, Erasmus MC, University Medical Center, Rotterdam, cDepartment of Aero- and Hydrodynamics, Delft University of Technology, Delft, and dDepartment of Medical Biochemistry, Academic Medical Center, Amsterdam, The Netherlands

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J Vasc Res 2008;45:54–68

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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: March 24, 2007
Accepted: June 03, 2007
Published online: September 27, 2007
Issue release date: December 2007

Number of Print Pages: 15
Number of Figures: 8
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: https://www.karger.com/JVR

Abstract

Background/Aims: Ligating the right lateral vitelline vein of chicken embryos (venous clip) results in cardiovascular malformations. These abnormalities are similar to malformations observed in knockout mice studies of components of the endothelin-1 (ET-1)/endothelin-converting enzyme-1/endothelin-A receptor pathway. In previous studies we demonstrated that cardiac ET-1 expression is decreased 3 h after clipping, and ventricular diastolic filling is disturbed after 2 days. Therefore, we hypothesise that ET-1-related processes are involved in the development of functional and morphological cardiovascular defects after venous clip. Methods: In this study, ET-1 and endothelin receptor antagonists (BQ-123, BQ-788 and PD145065) were infused into the HH18 embryonic circulation. Immediate haemodynamic effects on the embryonic heart and extra-embryonic vitelline veins were examined by Doppler and micro-particle image velocimetry. Ventricular diastolic filling characteristics were studied at HH24, followed by cardiovascular morphologic investigation (HH35). Results: ET-1 and its receptor antagonists induced haemodynamic effects at HH18. At HH24, a reduced diastolic ventricular passive filling component was demonstrated, which was compensated by an increased active filling component. Thinner ventricular myocardium was shown in 42% of experimental embryos. Conclusion: We conclude that cardiovascular malformations after venous clipping arise from a combination of haemodynamic changes and altered gene expression patterns and levels, including those of the endothelin pathway.

© 2007 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: March 24, 2007
Accepted: June 03, 2007
Published online: September 27, 2007
Issue release date: December 2007

Number of Print Pages: 15
Number of Figures: 8
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: https://www.karger.com/JVR


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