Remodeling of chick embryonic ventricular myoarchitecture under experimentally changed loading conditions

Abstract

Adult myocardium adapts to changing functional demands by hyper- or hypotrophy while the developing heart reacts by hyper- or hypoplasia. How embryonic myocardial architecture adjusts to experimentally altered loading is not known. We subjected the chick embryonic hearts to mechanically altered loading to study its influence upon ventricular myoarchitecture. Chick embryonic hearts were subjected to conotruncal banding (increased afterload model), or left atrial ligation or clipping, creating a combined model of increased preload in right ventricle and decreased preload in left ventricle. Modifications of myocardial architecture were studied by scanning electron microscopy and histology with morphometry. In the conotruncal banded group, there was a mild to moderate ventricular dilatation, thickening of the compact myocardium and trabeculae, and spiraling of trabecular course in the left ventricle. Right atrioventricular valve morphology was altered from normal muscular flap towards a bicuspid structure. Left atrial ligation or clipping resulted in hypoplasia of the left heart structures with compensatory overdevelopment on the right side. Hypoplastic left ventricle had decreased myocardial volume and showed accelerated trabecular compaction. Increased volume load in the right ventricle was compensated primarily by chamber dilatation with altered trabecular pattern, and by trabecular proliferation and thickening of the compact myocardium at the later stages. A ventricular septal defect was noted in all conotruncal banded, and 25% of left atrial ligated hearts. Increasing pressure load is a main stimulus for embryonic myocardial growth, while increased volume load is compensated primarily by dilatation. Adequate loading is important for normal cardiac morphogenesis and the development of typical myocardial patterns.

Dependence of Aortic Arch Morphogenesis on Intracardiac Blood Flow in the Left Atrial Ligated Chick Embryo

“…In the left atrial ligated embryo, the proportion of left to right ventricle is markedly changed including decreased trabeculae in favor of a more compact myocardium and lumen despite the unaltered heart size (Sedmera et al, 1999). Some cardiac malformations can be attributed to a lack of proper looping of the heart (Bouman et al, 1995).…”

“…We positioned the egg under the stereomicroscope, and removed the egg shell and its membrane to expose the embryo. The embryo was gently turned to the left-side-up position, and an overhand knot 10-0 nylon suture was placed around the left atrium (Sedmera et al, 1999;Tobita and Keller, 2000). We constricted the left atrioventricular orifice by tightening the knot, thus decreasing the effective volume of the left atrium.…”

“…Various experimental manipulations of blood volume, course, or rate of intracardiac blood flow produce cardiovascular anomalies and alter cardiomyocyte assembly (Clark et al, 1984;Hogers et al, 1997;le Noble et al, 2004). In the chick embryo, left atrial ligation before cardiac septation redistributes intracardiac blood flow and produces hypoplasia of left heart structures (Rychter et al, 1979;Sedmera et al, 1999;Tobita and Keller, 2000). Reducing blood flow through one side of the embryonic heart by diverting it to the other side results in underdevelopment or hypoplasia of all structures on the affected side, with a corresponding enlargement or hyperplasia of the side into which the flow is diverted.…”

“…The hemodynamic forces generated by blood flow within the developing heart also have a molding influence on cardiovascular development. The left atrial ligation technique is well established as a model to generate cardiac outflow tract abnormalities (Rychter and Rychterova, 1981;Sedmera et al, 1999). We use this model to test the hypothesis that the redistributed intracardiac blood flow alters aortic arch development.…”

High‐frequency ultrasonographic imaging of avian cardiovascular development

“…There was also an increase of 50% in the stroke volume, and 31% increase in the cardiac output. At Stages 24, 27, and 29, we performed imaging of embryos subjected to the experimental hemodynamic interventions of conotruncal banding (Clark et al, 1984Sedmera et al, 1999). In embryos banded 24 h before (at Stage 21), an outflow tract Doppler velocity gradient across the band (Fig.…”