Right lung ischemia induces contralateral pulmonary vasculopathy in an animal model.

摘要: Objective The study objective was to determine whether the vasculopathy seen in nonobstructed lung regions chronic thromboembolic pulmonary hypertension is induced by local blood flow increase or factors released ischemic lung. Methods Three groups of 10 piglets were studied 5 weeks after right artery ligation, pneumonectomy, dissection (sham). Pulmonary vascular resistance, arterial vasoreactivity, and morphometry measured, gene expressions involved smooth muscle cell proliferation quantified. Results Left similarly increased pneumonectomy ligation. Compared with ligation resulted left resistance ( P  = .0009), medial hypertrophy distal  = .013) endothelial nitric oxide synthase expression  = .041). These values similar sham pneumonectomy. In lung, for insulin-like growth factor  = .034), platelet-derived  = .0006),  = .0105) compared sham. Whereas endothelin-1 not affected, receptors A B downregulated  = .048  = .039, respectively)  = .033  = .028, respectively). Conclusions absent remaining but developed suggesting that remodeling contralateral This endocrine process may involve release proliferation.