Pulmonary artery remodeling and pulmonary hypertension after exposure to hyperoxia for 7 days. A morphometric and...

This study shows by morphometric and hemodynamic techniques that exposure to hyperoxia at normobaric pressure causes rapid structural remodeling of rat pulmonary arteries and pulmonary hypertension. After 7 days of 90% O2, pulmonary artery cross-sectional area is reduced by a striking loss of intraacinar arteries (control, 13 +/- 1 sq mm; exposed, 8 +/- 1 sq mm; P less than 0.001), the ratio of arteries to alveoli being 4:100 in control rats and 2.5:100 after hyperoxia. The lumen of preacinar and intraacinar arteries is narrowed by a reduction of vessel external diameter (ED) and an increased medial wall thickness (MT). There is a significant reduction in the percent medial thickness [( 2 X 100 X MT]/ED) in both regions. The proportion of muscular and partially muscular intraacinar arteries increases at the expense of nonmuscular ones (P [chi 2] less than 0.01), and fully muscular arteries appear in the alveolar wall where they are not normally found. Intimal thickening occurs in 19% of alveolar duct and 34% of alveolar wall nonmuscular arteries. Right ventricular hypertrophy occurs, the ratio of the left ventricle plus the septum to the right ventricle being significantly reduced (control, 4.07 +/- 0.26; exposed, 3.23 +/- 0.10; P less than 0.02). After 3 days of 87% O2, pulmonary artery pressure is still normal (17.0 +/- 0.9 mmHg) but after 7 days it is significantly increased (26.2 +/- 0.9 mmHg; P less than 0.01), as is pulmonary vascular resistance (control, 0.033 +/- 0.003; exposed, 0.065 +/- 0.015 U/kg; P less than 0.05). Return to air breathing (after 7 days at 87% O2) causes pulmonary vasoconstriction and a further rise of the pulmonary artery pressure (to 38.3 +/- 3.3 mmHg after 60 minutes).