tailieunhanh - Báo cáo y học: "Thrombospondin-1 null mice are resistant to hypoxia-induced pulmonary hypertension"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Thrombospondin-1 null mice are resistant to hypoxia-induced pulmonary hypertension. | Ochoa et al. Journal of Cardiothoracic Surgery 2010 5 32 http content 5 1 32 JOURNAL OF CARDIOTHORACIC SURGERY RESEARCH ARTICLE Open Access Thromblospondin-1 null mice are resistant to hypoxia-induced pulmonary hypertension Cristhiaan D Ochoa Lunyin Yu Essam Al-Ansari Charles A Hales and Deborah A Quinn Abstract Background and objective Chronic hypoxia induces pulmonary hypertension in mice. Smooth muscle cell hyperplasia and medial thickening characterize the vasculature of these animals. Thrombospondin-1 null TSP-1- - mice spontaneously develop pulmonary smooth muscle cell hyperplasia and medial thickening. In addition TSP-1 produced by the pulmonary endothelium inhibits pulmonary artery smooth muscle cell growth. Based on these observations we sought to describe the pulmonary vascular changes in TSP-1- - mice exposed to chronic hypoxia. Methods We exposed TSP-1- - and wild type WT mice to a fraction of inspired oxygen FiO2 of for up to six weeks. Pulmonary vascular remodeling was evaluated using tissue morphometrics. Additionally right ventricle systolic pressures RVSP and right ventricular hypertrophy by right ventricle left ventricle septum ratios RV LV S were measured to evaluate pulmonary hypertensive changes. Finally acute pulmonary vasoconstriction response in both TSP-1- - and WT mice was evaluated by acute hypoxia and U-46619 a prostaglandin F2 analog response. Results In hypoxia TSP-1- - mice had significantly lower RVSP RV LV S ratios and less pulmonary vascular remodeling when compared to WT mice. TSP-1- - mice also had significantly lower RVSP in response to acute pulmonary vasoconstriction challenges than their WT counterparts. Conclusion TSP-1- - mice had diminished pulmonary vasoconstriction response and were less responsive to hypoxia-induced pulmonary hypertension than their wild type counterparts. This observation suggests that TSP-1 could play an active role in the pathogenesis of pulmonary hypertension .

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