Fetal lamb pulmonary hypoplasia: Pulmonary vascular and myocardial abnormalities

Neonatal pulmonary hypoplasia resulting from a congenital diaphragmatic hernia (CDH) produces hemodynamic changes and morphologic abnormalities of the pulmonary vasculature. To characterize the myocardial and pulmonary vascular status of the fetus with pulmonary hypoplasia, we studied four chronically instrumented, near-term fetal lambs with pulmonary hypoplasia, induced by producing a diaphragmatic hernia. We found an elevation in the pulmonary arterial pressure (control 43.8 ± 5.9 mm Hg; CDH, 58.8 ± 9.1 mm Hg; p < 0.05), an elevation in the systemic arterial pressure (control, 43.8 ± 0.48 mm Hg; CDH, 58.6 ± 6.7 mm Hg; p < 0.05), and an elevation in the pulmonary vascular resistance (control, 0.47 ± 0.11; CDH, 3.87 ± 1.9; p < 0.05). In addition, though the total pulmonary blood flow was reduced (control, 83.5 ± 32.9 mL/min; CDH, 22.2 ±17.6 mL/min; p < 0.05), the blood flow reduction was proportional to the reduction in the lung mass (control, 79.8 ± 28.1 Cin flow per 100-g lung weight]; CDH, 85.4 ±71.7). The increase in the pulmonary vascular resistance in relation to the unit lung mass (control, 0.55 ± 0.33; CDH, 0.99 ± 0.5) was not as pronounced as its increase in relation to the total pulmonary blood flow. Myocardial enlargement occurred (control weight, 5.2 ± 0.8 g; CDH weight, 8.4 ± 0.4 g; p < 0.05) and right ventricular wall thickness was increased (control, 0.96 ± 0.31 mm; CDH, 1.78 ± 0.53 mm; p < 0.05), possibly resulting from increased myocardial wall stress, as indicated by an increased aubepicardial-subendocardial blood flow ratio (control, 1.4 ± 0.29; CDH, 1.7 ± 0.13; p < 0.05).