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The hypothesis that early vascularization of the embryonic heart is improved after bolus injections of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) into the vitelline vein before the start of myocardial vasculogenesis was investigated. Findings showed that enhancement of bFGF or VEGF before myocardial vascularization increases vascular growth, the effects of these growth factors on vascular volume and numerical density are temporarily dependent, and bFGF affects ventricular modeling aside from its effects on the coronary vasculature.

The embryonic vascular system responds to changes in the volume of circulating blood by maintaining constant blood pressure levels. The artificial reduction of blood circulation increases the peripheral resistance of the blood vessels and produces constant levels of hydraulic pressure. This reaction is due to the efficient utilization of energy necessary for vascular development in the embryonic vasculatory system. The embryonic vasculature is also regulated by vasoactivators in the absence of autonomic control.

Measurement of atrial and ventricular blood pressure by micropressure system reveals a positive atrioventricular (AV) pressure gradient across the ventricular filling. The atrioventricular orifice and endocardial cushions act as flow resistance sites for diastolic pressure gradient. Ventricular end-diastolic pressure increases linearly from 0.18 + or - 0.03 to 0.55 + or - 0.04 mm Hg and the peak atrial pressure increases from 0.38 + or - 0.03 to 1.21 + or - 0.17 mm Hg. AV pressure gradient from 16-21 stage in terms of increasing AV flow reveals a reduction in AV orifice resistance.

Objective: We tested the hypothesis that the degree of coronary microvessel formation in the embryonic heart is regulated by the magnitude of myocardial growth. Methods: The outflow tract of Hamburger–Hamilton stage 21 chicken hearts (prior to the onset of coronary vasculogenesis) was constricted in ovo with a loop of 10-0-nylon suture, and the hearts were studied at stages 29 and 36. Results: At stage 29 ventricular mass was 64% greater in the pressure-overloaded than in the hearts of sham-operated controls, but vascular volume density and numerical density, determined by electron microscopic morphometry, were identical. As demonstrated by histological morphometric evaluation, the compact region of the left ventricle at stage 29 was 43% thicker than the shams. However, by stage 36 heart mass, thickness of the compact region, and overall wall thickness (demonstrated by scanning electron microscopy) were significantly less than in the sham group of this stage, but vascular volume density was virtually identical in the two groups. Formation of the two main coronary arteries was clearly impeded in the banded hearts, i.e., the coronaries were stunted in their development or failed to completely form coronary ostia. Conclusions: Vascular growth is proportional to myocardial growth in the embryonic, overloaded heart, but the persistence of the pressure overload results in a failure of or severe limitations in coronary artery development. These data support the hypothesis that vascular growth during this period of development is regulated, at least in part, by the rate and magnitude of myocardial growth. [ABSTRACT FROM PUBLISHER]

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 perfusion-fixed hearts. A vascular bed of stage 21 chick embryos was suffused with 1 ng of verapamil at 1 µl 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. [ABSTRACT FROM AUTHOR]