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Biphasic Remodeling of Alveolar Capillaries in Idiopathic Pulmonary Fibrosis*

Masahito Ebina, MD, PhD; Minoru Shimizugawa, MD; Takashi Suzuki, MD; Shigefumi Fujimura, MD, FCCP; Tohru Takahashi, MD; Masahiro Kohzuki, MD; Toshihiro Nukiwa, MD
Author and Funding Information

*From the Department of Respiratory Oncology and Molecular Medicine (Drs. Ebina, Shimizugawa, and Nukiwa), the Department of Pathology (Drs. Suzuki and Takahashi), the Department of Surgery (Dr. Fujimura), Institute of Development, Aging, and Cancer, and the Department of Internal Medicine (Dr. Kohzuki), Tohuku University, Sendai, Japan.

Correspondence to: Masahito Ebina, MD, PhD, Department of Respiratory Oncology and Molecular Medicine, Institute of Development, Aging, and Cancer, Tohuku University, 4-1 Seiryomachi Aoba-ku, Sendai 980-8575 Japan



Chest. 2001;120(1_suppl):S59-S60. doi:10.1378/chest.120.1_suppl.S59
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Extract

To clarify apparent contradictions in vascular remodeling in patients with idiopathic pulmonary fibrosis (IPF), we evaluated the vascular density (VD), the relative ratio of the vascular area with CD34-positive endothelial cells to the total area of alveolar walls with variegated fibrosis in the lungs of seven patients with IPF and three normal control subjects. Our results showed VD was significantly higher at low grades of fibrosis (23.4 ± 1.17) than that of control lungs (12.3 ± 1.62; p < 0.0001). In contrast, VD gradually decreased as the degree of fibrosis increased, and was lower than that of the control lungs in the most extensively fibrous lesions (5.10 ± 0.54; p < 0.0001). An augmented expression of angiotensin-converting enzyme was observed in the increased capillary endothelial cells in the early lesions. The efficacy of an angiotensin II type 1 receptor antagonist (p = 0.02) was proved against fibrosis in bleomycin-treated mouse lung as estimated by reduction of hydroxyproline content. These results revealed that vascular remodeling is biphasic in the fibrotic process of IPF, and suggested the involvement of angiogenesis in the early pathogenesis of pulmonary fibrosis.

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