论文部分内容阅读
据CMJ报道,华中科技大学同济医学院附属同济医院甄国华医师的研究表明,一氧化碳(CO)气体分子有抑制肺动脉高压发病的作用。同一氧化氮(NO)类似,CO也是具有生物活性的气体小分子,尽管CO是造成大气污染的重要因素。慢性支气管炎、哮喘等慢性阻塞性肺疾病导致肺泡缺氧,进而引起肺血管收缩和血管重构,是发生肺源性心脏病的主要原因。通过对缺氧大鼠及肺动脉平滑肌细胞的研究,发现机体自身产生的CO对缺氧导致的肺血管重构有抑制作用。使用促进CO产生的试剂可以部分地防止缺氧大鼠肺动脉高压的形成,为肺动脉高压及肺源性心脏病的防治提供了新的线索。
According to the CMJ report, Dr. Zhenhua Guo from Tongji Hospital affiliated to Tongji Medical College of Huazhong University of Science and Technology has shown that carbon monoxide (CO) gas molecules can inhibit the pathogenesis of pulmonary hypertension. Like nitric oxide (NO), CO is also a biologically active gas small molecule, although CO is an important contributor to air pollution. Chronic bronchitis, asthma and other chronic obstructive pulmonary disease leading to alveolar hypoxia, which in turn lead to pulmonary vasoconstriction and vascular remodeling, is the main cause of pulmonary heart disease. Through the study of hypoxic rat and pulmonary artery smooth muscle cells, found that the body’s own production of CO hypoxia-induced pulmonary vascular remodeling inhibited. The use of agents that promote CO production may partially prevent the formation of pulmonary hypertension in hypoxic rats and provide new clues for the prevention and treatment of pulmonary hypertension and pulmonary heart disease.