Murine Model of Pulmonary Artery Overflow Vasculopathy Revealed Macrophage Accumulation in the Lung.

摘要: Chronic thromboembolic pulmonary hypertension (CTEPH) develops as a consequence of unresolved embolism or clots in the arteries. The obstruction not only reduces area vascular bed, but also elicits high pressure and shear stress spared unobstructed Subsequent overflow small arteries induces remodeling, termed vasculopathy (OV). While development OV significantly contributes to occurrence hypertension, its precise molecular mechanisms are yet be determined.We established novel murine artery (PAOV) model, which we resected left lung induced redistribution cardiac output remaining right lung. At 21 days after operation, mice showed an increase media area, indicating arterial remodeling. In addition, ventricular hypertrophy was detected PAOV model. Intriguingly, marked accumulation F4/80-positive monocytes/macrophages visualized high-flow arteries, implying role inflammatory process pathogenesis overflow-induced