Blood flow dynamics reflect degree of outflow tract banding in Hamburger–Hamilton stage 18 chicken embryos

Altered blood flow during embryonic development has been shown to cause cardiac defects; however, the mechanisms by which the resulting haemodynamic forces trigger heart malformation are unclear. This study used heart outflow tract banding to alter normal haemodynamics in a chick embryo model at HH1...

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Veröffentlicht in:Journal of the Royal Society interface 2014-11, Vol.11 (100), p.20140643-20140643
Hauptverfasser: Midgett, Madeline, Goenezen, Sevan, Rugonyi, Sandra
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Sprache:eng
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Zusammenfassung:Altered blood flow during embryonic development has been shown to cause cardiac defects; however, the mechanisms by which the resulting haemodynamic forces trigger heart malformation are unclear. This study used heart outflow tract banding to alter normal haemodynamics in a chick embryo model at HH18 and characterized the immediate blood flow response versus the degree of band tightness. Optical coherence tomography was used to acquire two-dimensional longitudinal structure and Doppler velocity images from control (n = 16) and banded (n = 25, 6–64% measured band tightness) embryos, from which structural and velocity data were extracted to estimate haemodynamic measures. Peak blood flow velocity and wall shear rate (WSR) initially increased linearly with band tightness (p < 0.01), but then velocity plateaued between 40% and 50% band tightness and started to decrease with constriction greater than 50%, whereas WSR continued to increase up to 60% constriction before it began decreasing with increased band tightness. Time of flow decreased with constriction greater than 20% (p < 0.01), while stroke volume in banded embryos remained comparable to control levels over the entire range of constriction (p > 0.1). The haemodynamic dependence on the degree of banding reveals immediate adaptations of the early embryonic cardiovascular system and could help elucidate a range of cardiac adaptations to gradually increased load.
ISSN:1742-5689
1742-5662
DOI:10.1098/rsif.2014.0643