Experimental aortic stenosis in fetal lambs.

Morphologic analyses of lungs from infants who died of severe aortic stenosis shortly after birth have shown increased pulmonary vascular smooth muscle and an increased number of pulmonary resistance vessels. These findings have been thought to be caused by in utero pulmonary venous, pulmonary arterial or right ventricular hypertension. To study this problem in the fetus, we created aortic stenosis in 10 fetal lambs (97-115 days gestation). Fetuses were reoperated upon at 133-141 days gestation (mean 32.6 days aortic stenosis). The left ventricular-to-systemic arterial systolic blood pressure difference was measured in three fetuses and was abnormal (18, 22 and 22 mm Hg). Pulmonary arterial blood pressure was measured in three fetuses and was normal (54-58 mm Hg mean). At autopsy, aortic stenosis was severe and the aortic diameter reduced (1.7 ± 1.0 mm vs 6.1 ± 0.7 mm for controls,p < 0.01). Heart weight was greater in aortic stenosis (21.5 ± 8.8 g) compared with control (17.2 + 5.8 g, p < 0.01). This was the result of increased left ventricular free wall weight (aortic stenosis 9.79 ± 7.73 g vs control 5.46 ± 2.26 g, p < 0.01) and thickness (aortic stenosis 7.3 ± 1.5 mm vs control 5.1 + 1.7 mm, p < 0.05). Lungs of six fetuses were fixed by perfusion and 331 fifth-generation resistance vessels were measured. Medial width (m) was decreased in aortic stenosis (4.82 ± 0.66 g) compared with vessels from six control fetuses (6.19 ± 1.70 ,u, n = 529,p < 0.002). External diameter (d) was also decreased in aortic stenosis (22.18 ± 1.37 g) compared with control vessels (39.05 ±