Sedmera D, Pexieder T, Rychterova V, Hu N, Clark E B
Institute of Physiology, Faculty of Medicine, University of Lausanne, Switzerland.
Anat Rec. 1999 Feb 1;254(2):238-52. doi: 10.1002/(SICI)1097-0185(19990201)254:2<238::AID-AR10>3.0.CO;2-V.
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.
成年心肌通过肥大或萎缩来适应不断变化的功能需求，而发育中的心脏则通过增生或发育不全做出反应。目前尚不清楚胚胎心肌结构如何适应实验性改变的负荷。我们对鸡胚心脏施加机械性改变的负荷，以研究其对心室肌结构的影响。对鸡胚心脏进行圆锥干束带术（增加后负荷模型），或左心房结扎或夹闭，创建右心室前负荷增加和左心室前负荷降低的联合模型。通过扫描电子显微镜和组织学形态计量学研究心肌结构的改变。在圆锥干束带组中，左心室有轻度至中度扩张、致密心肌和小梁增厚，小梁走行呈螺旋状。右房室瓣形态从正常的肌瓣变为双叶结构。左心房结扎或夹闭导致左心结构发育不全，右侧出现代偿性过度发育。发育不全的左心室心肌体积减小，小梁致密化加速。右心室容量负荷增加主要通过心室扩张伴小梁模式改变以及后期小梁增生和致密心肌增厚来代偿。在所有圆锥干束带组和25%的左心房结扎心脏中发现室间隔缺损。增加压力负荷是胚胎心肌生长的主要刺激因素，而增加容量负荷主要通过扩张来代偿。适当的负荷对正常心脏形态发生和典型心肌模式的发育很重要。
