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Pulmonary vascular changes in bronchopulmonary dysplasia: a clinicopathologic correlation in short- and long-term
M Gorenflo1, M Vogel, M Obladen
1Department of Neonatology, Free University of Berlin, Germany.
Insights
Infants with bronchopulmonary dysplasia (BPD) show altered pulmonary arteries. Reduced arterial density and abnormal vessel muscularization contribute to pulmonary hypertension in BPD.
Area of Science:
- Neonatal Medicine
- Pediatric Pathology
- Pulmonary Hypertension
Background:
- Pulmonary vascular findings in infants with bronchopulmonary dysplasia (BPD) are inconsistent.
- Previous studies lack detailed histomorphometric analysis of pulmonary vasculature in BPD.
Purpose of the Study:
- To compare pulmonary vascular histology in infants with BPD versus controls.
- To investigate the influence of oxygen and ventilation on arterial density in BPD.
- To elucidate the pathogenesis of pulmonary hypertension in BPD.
Main Methods:
- Histologic examination and quantitative histomorphometry of lung slices from infants with BPD and controls.
- Comparison of arterial density and vessel wall thickness.
- Analysis of the impact of oxygen concentration and positive pressure ventilation.
Main Results:
- Infants with early BPD (Group I) showed increased arterial density compared to controls.
- Infants with later BPD (Group II) and cor pulmonale had decreased arterial density and increased vessel wall thickness.
- Total oxygen dose significantly reduced arterial density; abnormal muscularization of peripheral arteries was observed.
Conclusions:
- Reduced cross-sectional perfusion area and abnormal muscularization of peripheral vessels are key in BPD-associated pulmonary hypertension.
- Oxygen exposure is a major factor influencing reduced arterial density in BPD.
- Histomorphometric analysis provides crucial insights into BPD pulmonary vascular changes.
Abstract:
Pulmonary vascular findings in infants with bronchopulmonary dysplasia (BPD) are inconsistent. We compared five infants who fulfilled histologic criteria of BPD (group I; survival up to 1 month) with five controls who died of severe neonatal infection without having been ventilated. Nine infants who survived up to 7 months also fulfilled clinical criteria of BPD (group II). These were compared with three term infants who died of nonpulmonary causes. Lung slices were examined qualitatively and by quantitative histomorphometry. The influence of oxygen concentration and positive pressure ventilation on arterial density was studied. Arterial concentration in group I [2.43 (0.63) vessels/mm2, mean +/- SD] increased significantly compared with the controls [1.64 (0.49) vessels/mm2, mean +/- SD]. Most infants in group II who had cor pulmonale at autopsy had decreased arterial density when compared with normal term infants. Postmortem pulmonary angiography was also consistent with this finding. Total oxygen dose was the factor with the greatest influence on reduced arterial density. Relative wall thickness of vessels less than 75 microns in diameter was not significantly reduced in group I (p greater than .05). Infants from group II with cor pulmonale had an increased wall thickness compared with their controls. The proportion of fully muscularized arteries less than 100 microns in diameter was reduced in group I but increased in group II. We conclude that the reduction of cross-sectional perfusion area and abnormal muscularization of more peripheral vessels are important in the pathogenesis of pulmonary hypertension in infants with BPD.