Fetal cardiovascular morphology of truncus arteriosus with or without truncal valve insufficiency in the rat.

Author:

Momma K1,Ando M1,Takao A1,Miyagawa-Tomita S1

Affiliation:

1. Department of Pediatric Cardiology, Heart Institute of Japan, Tokyo Women's Medical College.

Abstract

BACKGROUND Recent advances in fetal echocardiography have necessitated further study on fetal in situ cardiovascular morphology of truncus arteriosus and the effects of truncal valve insufficiency. METHODS AND RESULTS We studied 55 fetal rats with truncus arteriosus among 300 fetuses from 40 virgin females treated with 200 mg fertilysin on the 10th day of pregnancy. After rapid whole-body freezing on the 21st day, the fetuses were studied by means of serial cross-sectional photographs of the frozen thorax. Thirty-five fetuses with a normal heart treated with fertilysin served as controls. Truncus arteriosus was characterized by a large ventricular septal defect, a solitary artery (truncus arteriosus) overriding the ventricular septum, the right and left pulmonary arteries originating from the truncus arteriosus with or without a common trunk (main pulmonary artery), and absent ductus arteriosus. Fetuses with truncal valve insufficiency had thick truncal valves, a large truncus arteriosus, and large ventricles. The subgroup of 12 fetuses with a large truncus (truncal diameter greater than 160% of the ascending aorta diameter in the controls) showed significantly greater values for right ventricular volume (200% of control) and mass (120% of control), left ventricular volume (170% of control) and mass (110% of control), right (120% of control) and left (110% of control) atrial volume, and pericardial fluid (140% of control) than the controls. These changes were less prominent and ventricular volumes were not increased in the remaining subgroup with a truncal diameter of 160% or less of aorta diameter in the controls. CONCLUSIONS In fetal truncus arteriosus, truncal valve insufficiency was associated with increased ventricular volume load and incomplete cardiac compensation in rats.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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