A Quantitative Study of the Ventricular Myoarchitecture in the Stage 21?29 Chick Embryo Following Decreased Loading

Abstract

During the early developmental period, ventricular myoarchitecture undergoes a transition from a smooth-walled cardiac tube, to left and right ventricular chambers filled with a sponge-like network of trabecular struts. We measured the quantitative changes of ventricular myocardium properties in normal stage 21-29 chick embryos and after chronic verapamil suffusion, which is known to decrease work load and decelerate ventricular growth. The morphologic parametres (compact layer thickness, ventricular wall composition, porosity of different layers and trabecular orientation) were determined from scanning electron micrographs of transversely dissected perfusionfixed hearts. A vascular bed of stage 21 chick embryos was suffused with 1 ng of verapamil at 1 pl per hour up to stages 24, 27 and 29 via a miniosmotic pump. From stage 24, the thickness of the compact myocardium in the left ventricle was greater than that of the right. The increase in thickness was minimal between stages 24 and 27, while the predominantly radially arranged trabeculae comprised up to 75% of total myocardial mass. The ratio of intertrabecular spaces to trabeculae (local porosity) decreased from the ventricular center (70%) towards the compact myocardium (0%). In verapamil-treated embryos, the hearts were smaller and showed delayed development. The compact myocardium was thinner than normal, and the proportion of trabeculae was higher than in controls. The local porosity values were similar in control and experimental groups. Decreased load resulted in delayed growth and morphogenesis, expressed as a persistence of trabeculae and a thinner compact myocardium. Embryonic heart pumping function is largely based on extensively developed trabeculation with regionally different properties.

Morphomechanics: transforming tubes into organs

“…For example, the embryonic heart has the ability to adapt to changes in loading conditions in ways that parallel the mature heart, e.g., pressure overload triggers ventricular hypertrophy [35,36]. Moreover, perturbing pressure and flow leads to abnormalities in patterns of myocardial trabeculation, septation, and valve formation [7,30*,32,37,38,39,40]. Experiments have linked fluid shear (drag) to the regulation of these processes, possibly through changes in gene expression [41,42,43,44,45].…”

High‐frequency ultrasonographic imaging of avian cardiovascular development

“…Additional considerations have to be taken for the calculated parameters, such as cardiac output. Internal structure of the embryonic ventricle resembles a sponge, with the proportion of the actual lumen being only ϳ37% of the epicardial area (Sedmera et al, 1998), so the volumes derived from tracking the epicardial contour, both on video or echo recordings, over-estimate the actual values.…”

Quantitative volumetric analysis of cardiac morphogenesis assessed through micro‐computed tomography

“…Additional hearts of identical stages were processed and analyzed using SEM (Sedmera et al, 1997(Sedmera et al, , 1998 and serial section reconstruction. Serial section reconstruction was performed on HH17, HH24, and HH30 staged hearts using frontal plane sections at 50-m intervals.…”