TETRALOGY OF FALLOT, TRUNCUS ARTERIOSUS, AND ABNORMAL MYOCARDIAL ARCHITECTURE

暴露于双二胺的大鼠胚胎发生各种心血管疾病 反常现象。心脏畸形与主动脉病变的关系 对65只晚期用药大鼠的弓状动脉进行了定量分析。 解剖显微镜下的胎儿期。有26只大鼠(40%)患有 膜周部室间隔缺损14例 大鼠(22%)患有法洛四联症，4只(6%)有动脉干，以及 8例有相对较小的间隔缺陷，无其他重大异常。 在四只有主干的大鼠中，有两只在脑干上有残留的血管 主干根部和3个根部漏斗发育不全。44只大鼠(68%) 室间隔的中纬度肌束不是 与左心室游离壁相连，但与右心室相连 室壁游离壁。无论是孤立的还是联合的，都有一个替身 或右主动脉弓6只(9%)，迷走锁骨下动脉 右动脉管9例(14%)，右动脉管12例(18%)，发育不良 四个(6%)。导管的横截面积，经校正后为 47只大鼠(72%)的主动脉峡部面积异常小。那些老鼠 有室间隔缺陷和/或异常心肌结构的患者通常 有一条很小的导管；在患有糖尿病的大鼠中很小或没有 四部曲。据推测，该缺陷可能是异常的和 第六弓动脉发育减慢，这给人施加压力 胎儿右心室的负荷，可能导致了持续性 室间隔缺损作为一种宣泄和/或心肌形成 有利于右派产生压力的建筑 脑室。

Rat fetuses exposed to bis-diamine develop various cardiovascular anomalies. The relation between anomalies of the heart and the aortic arch arteries were quantitatively analyzed in 65 treated rats at a late fetal stage under a dissecting microscope. There were 26 rats (40%) with a ventricular septal defect in the perimembranous portion, of which 14 rats (22%) had tetralogy of Fallot, four (6%) had truncus arteriosus, and eight had relatively small septal defect with no other major anomalies. Of the four rats with truncus, two had a vestigial vasculature on the truncus root and three had a rudimentary infundibulum. In 44 rats (68%) the middle latitudinal muscle bundle of the ventricular septum was not continuous with the left ventricular free wall but rather with the right ventricular free wall. There were, isolated or in association, a double or right aortic arch in six rats (9%), aberrant subclavian arteries in nine (14%), right ductus arteriosus in 12 (18%), and agenetic ductus in four (6%). The cross-sectional area of the ductus, as corrected by that of the aortic isthmus, was abnormally small in 47 rats (72%). The rats with a septal defect and/or an abnormal myocardial architecture usually had a small ductus; it was very small or absent in the rats with tetralogy. It is speculated that the defect may be the anomalous and reduced development of the 6th arch arteries, which, imposing pressure load on the fetal right ventricle, may have led to the persistence of ventricular septal defect as a vent and/or to the formation of myocardial architecture favorable for the generation of pressure in the right ventricle.