缺氧冷损伤血管一氧化氮合酶活性的变化及其生物学意义

目的 观察缺氧寒冷损伤血管一氧化氮合酶(NOS)活性的变化,并研究超氧化物歧化酶(SOD)和维生素C(VC)对这种变化的影响,为缺氧寒冷损伤的防治开拓新的思路。方法 分离Wistar大鼠主动脉并使其暴露于缺氧或／和寒冷环境中,以全自动生化分析仪测定血管培养液中乳酸脱氢酶(LDH)活性,以Griess化学法观测血管NOS活性,以肾上腺素自氧化法测定血管SOD活性。结果 缺氧和寒冷损伤使血管NOS活性较对照组显下降,分别达18．2％和19．1％,缺氧寒冷复合损伤更使血管NOS活性下降达25．9％;NOS的这种变化具有明显的时间依赖性,并与相应血管培养液中IDH活性有显负相关关系;缺氧或／和寒冷损伤血管SOD活性亦显下降。当血管受到缺氧或／和冷冻后立即给与SOD(200u／m1)或VC(50mg／ml)可使缺氧或／和寒冷损伤血管NOS活性升高,SOD活性复升;对血管培养液中IDH的测定表明,SOD和VC对缺氧冷损伤血管具有一定的保护作用。结论 血管NOS活性的降低与缺氧冷损伤发生密切相关,可望通过抗氧化剂的使用,防止或减缓缺氧寒冷环境中机体损伤的发生。

Change of NOS activity in hypoxia and cold-induced blood vessels damage and its biological significance

Objectives To explore the therapeutic methods for hypoxia and cold induced blood vessel damage by observing the changes of NO synthase (NOS) activity in hypoxia and development of coldm induced blood vessels damage, and studying the effects of SOD and vitamin C on the changes of NOS activity. Methods The main artery was isolated from Wistar rats and exposed to hypoxia and /or cold environment in vitro. LDH activity was measured using an automatic biochemical analyzer and NOS and SOD activities in blood vessels were analyzed respectively by Griess assay and adrenaline autoxidantion method. Results NOS activity in hypoxia, cold and hypoxia cold damaged vessels decreased by 18 2%, 19 1% and 25 9% respectively after exposure as compared with the control vessels. The changes of NOS activity were time dependent. The NOS activity in damaged vessels was negatively correlated with LDH activity in the culture medium of the respective vessels. The SOD activity in hypoxia and /or cold damaged vessels also decreased significantly. Giving SOD (200 u/ml) or vitamin C (50 mg/ml) immediately after hypoxia and/or cold exposure increased the NOS activity and SOD activity in the damaged vessels significantly, as compared with the non treatment controls. Conclusions The decrease of NOS activity is closely related to the development of damage induced by hypoxia and/or cold injury. SOD and vitamin C could protect the blood vessels exposed to hypoxia and/or cold from damage, possibly by increasing NOS activity.