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出 处:《中华航海医学与高气压医学杂志》2003年第2期100-102,共3页Chinese Journal of Nautical Medicine and Hyperbaric Medicine
摘 要:目的 探讨一氧化氮 (NO)和超氧化物歧化酶 (SOD)含量在减压病发病过程中的变化及其在发病机制中的意义。方法 将 16只实验兔放入加压舱中 ,于 5 min内用压缩空气加压至 0 .5 MPa,停留 6 0 min,然后于 5 m in内再减至常压。分别于进舱前、出舱后即刻和出舱后 2 4 h,应用心内穿刺方法采血 2 m l,分离血清 ,避免溶血。应用硝酸还原法和改良亚硝酸法分别及时测定血清 NO含量和 SOD活性。结果 (1)血清中 NO含量在减压出舱后即刻 [(112 .73± 15 .74 ) μm ol/ L]及出舱后 2 4 h[(117.6 0±16 .0 7) μm ol/ L],与进舱前自身对照 [(85 .33± 12 .6 8) μmol/ L]比较 ,明显增高 (P<0 .0 1)。 (2 )血清中SOD活性在出舱后即刻 [(6 5 .97± 16 .5 2 ) NU/ ml]与出舱后 2 4 h[(6 3.0 1± 16 .10 ) NU/ m l],与进舱前[(85 .84± 16 .6 8) NU/ ml]比较 ,均明显降低 (P<0 .0 5 )。结论 NO含量的增加和 SOD活性的降低可导致自由基生成增加 ,这可能在减压病的继发性损伤中起着重要作用。Objective To investigate the changes of nitric oxide(NO) level and superoxide dismutase(SOD) activity in the serum of rabbits with experimental decompression sickness (DCS) and to evaluate their role in the pathogenesis of DCS.Methods 16 rabbits were put into the hyperbaric chamber.The pressure was increased to 0.5 MPa within using compressed ait and maintained at 0.5 MPa for 60 min,and then was decompressed to normal pressure within 5 min.All blood samples were collected through endocardial puncture.The blood samples were collected before compression,immediately after compression and 24 hours after decompression respectively.NO level and SOD activity were measured in time.Results Compared with those before compression,NO levels [(85.33±12.68) μmol/L] in the serum of rabbits were increased significantly immediately after decompression [(112.73±15.74) μmol/L] and 24 hours after decompression[(117.60±16.07) μmol/L](P<0.01),and SOD activites [(85.84±16.68) NU/ml] in the serum of rabbits were decreased significantly immediately after decompression [(65.97±16.52) NU/ml] and 24 hours after decompression [(63.01±16.10) NU/ml](P<0.05).Conclusions The increase of NO level and the decrease of SOD activity can play an important role in the secondary injury of DCS.
关 键 词:实验 减压病 兔 血清 NO SOD 含量 一氧化氮 超氧化物歧化酶
分 类 号:R84[医药卫生—航空、航天与航海医学]
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