Hemodynamic changes and compensatory mechanisms during early cardiogenesis after neural crest ablation in chick embryos

L Leatherbury, DM Connuck, HE Gauldin, ML Kirby - Pediatric research, 1991 - nature.com
L Leatherbury, DM Connuck, HE Gauldin, ML Kirby
Pediatric research, 1991nature.com
Microcinephotography was used to study early heart development in chick embryos with
ablations of the neural crest known to result in persistent truncus arteriosus with associated
aortic arch anomalies. The premigratory neural crest destined for the 3rd and 4th pharyngeal
arches and the aorticopulmonary septum were ablated. When the embryos reached the
looped cardiac tube stage (stage 18), 15 experimental and 15 control embryos were filmed
at 100 frames/s under controlled environmental conditions. End-diastolic and end-systolic …
Abstract
Microcinephotography was used to study early heart development in chick embryos with ablations of the neural crest known to result in persistent truncus arteriosus with associated aortic arch anomalies. The premigratory neural crest destined for the 3rd and 4th pharyngeal arches and the aorticopulmonary septum were ablated. When the embryos reached the looped cardiac tube stage (stage 18), 15 experimental and 15 control embryos were filmed at 100 frames/s under controlled environmental conditions. End-diastolic and end-systolic dimensions were determined for the conotruncus and presumptive right ventricle that together compose the bulbus cordis. The results showed that the shortening fractions and ejection fractions were significantly depressed in the experimental embryos. The experimental embryos exhibited dilation and decreased emptying of the ventricle. There was no difference in heart rate or stroke volume between the control and experimental embryos. Thus, the calculated cardiac output was the same in the control and experimental groups. It appeared that the experimental embryos compensated for decreased contractility by ventricular dilation. These functional compensations in very early cardiac development may play an etiologic role in the subsequent development of structural heart defects.
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