Morphologic development of the pulmonary vascular bed in experimental coarctation of the aorta.
Although electrocardiographic evidence of right ventricular hypertrophy is considered common in newborn infants with coarctation of the aorta, the reason for this finding is not well established. Investigations of the pulmonary vascular bed of these infants have resulted in variable findings, probably due to the differences in morphometric techniques, coexisting cardiac defects, and variable postnatal age at time of death. To study more carefully the pulmonary vascular bed, we produced coarctation of the aorta in fetal lambs at 103--126 days gestation. Twelve to 32 days later the fetuses were reoperated on and systemic and pulmonary arterial blood pressures, and arterial blood gas tensions were determined to be normal. At autopsy, juxtaductal coarctations extended a mean of 2.8 mm into the aortic lumen and occupied 9.5 mm of the aortic circumference. The fifth-generation pulmonary resistance vessels had increased medial width (p less than 0.01), decreased external diameter (p less than 0.001), and increased medial width/external diameter ratios (p less than 0.001) compared with vessels from control fetuses. The number of small muscular pulmonary vessels/cm2 lung tissue was significantly reduced (p less than 0.01) in the study animals compared with the control animals. These alterations of the pulmonary vascular bed were not due to fetal pulmonary arterial hypertension or fetal hypoxemia. These pulmonary vascular changes may explain the occurrence of pulmonary hypertension and right ventricular hypertrophy in newborn infants with coarctation of the aorta.
D000818:Animals; D001017:Aortic Coarctation / Q000196:embryology* / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure; D001808:Blood Vessels / Q000473:pathology; D005318:Fetal Heart / Q000473:pathology; D008168:Lung / Q000098:blood supply* / Q000196:embryology; D011651:Pulmonary Artery / Q000196:embryology* / Q000473:pathology; D012756:Sheep