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目的 :研究慢性缺氧环境下NO及NOS在肺循环适应机制中的作用 ;方法 :Wistar大鼠从 2 2 6 0m带到 3780m的高原饲养 30天后进行肺动脉压及血液学、组织学观察 ,并和当地的适应动物高原鼠兔进行比较 ;结果 :缺氧 30天的大鼠血清NO的水平及NOS的活性均低于高原鼠兔 ,两者分别为 5 5 .40 μmol/L± 3.76 μmol/L、87.49μmol/L±5 .74μmol/L,和 1 .33u/ml± 0 .1 2u/ml、1 .99u/ml± 0 .1 3u/ml,肺动脉压增高 ,左右心室比重高原鼠兔为 0 .2 3,而Wis tar大鼠为 0 .47;高原鼠兔的肺动脉壁非常薄 ,而且没有平滑肌层 ,而大鼠同样大小的肺动脉在内外层的弹力纤维中间有一较厚的平滑肌层 ,肺动脉中层的厚度 ,鼠兔为 9.3% ,大鼠为 2 8.4% ,肺动脉增厚程度与NO的水平呈负相关 ;结论 :低氧环境下NO及NOS的代谢异常 ,既导致了大鼠的缺氧性肺血管收缩反应 ,又参与了肺血管的结构改建过程 ,高原鼠兔无低氧性肺血管收缩 ,NO在维持其张力方面起到了一重要作用。
Objective: To investigate the role of nitric oxide synthase (NO) and nitric oxide synthase (NOS) in pulmonary circulation adaptation mechanism in chronic hypoxic environment. Methods: The pulmonary arterial pressure and hematological and histological observation were performed in Wistar rats from 22 60 m to 3780 m plateau, The results showed that the level of NO and the activity of NOS of rats in hypoxia for 30 days were lower than those in plateau pikas, which were respectively 55.40 μmol / L ± 3.76 μmol / L , 87.49μmol / L ± 5.74μmol / L, and 1.33u / ml ± 0.12u / ml, 1.99u / ml ± 0.13u / ml, increased pulmonary arterial pressure, 0.23, while Wis tar rats were 0.47; plateau pika rabbit pulmonary artery wall is very thin, and there is no smooth muscle layer, and rat pulmonary artery of the same size in the inner and outer elastic fibers in the middle of a thicker smooth muscle layer, The thickness of the middle pulmonary artery was 9.3% in rats and rats, and 8.4% in rats. The thickening of pulmonary artery was negatively correlated with the level of NO. CONCLUSION: The abnormal metabolism of NO and NOS in hypoxia not only resulted in the lack of rats Oxygen pulmonary vasoconstrictor response, but also involved in the process of pulmonary vascular remodeling, plateau pika no hypoxic pulmonary vasoconstriction Reduced, NO played an important role in maintaining its tension.