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缓激肽对兔血浆、组织丙二醛含量及超氧化物歧化酶活性的延迟性影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2001年第2期
页码:
109-111
栏目:
论著
出版日期:
2001-03-01

文章信息/Info

Title:
The influences of bradyklnin to plasma or myocardial MDA level and SOD activity in rabbits with acute myocardial infarction
作者:
汝磊生李 飞贾国良张荣庆
第四军医大学西京医院心内科,陕西西安710032
Author(s):
RU Lei-shengLI FeiJIA Guo-liangZHANG Rong-qing
Department of Cardiology,Xijing Hospital,Fourth Military Medical University,Xi'an Shaanxi 710032,China
关键词:
心肌缺血再灌注缓激肽超氧化物歧化酶
Keywords:
myocardial ischemia-reperfusionbradykininsuperoxide dismutase
分类号:
R542.22
DOI:
-
文献标识码:
A
摘要:
目的 观察缓激肤(BK)对血浆、组织超氧化物歧化酶(SOD)活性的影响,探讨BK对心肌保护作用的机制。方法 采用兔缺血再灌注模型,分别给予缺血再灌注、缺血再灌注加BK、缺血再灌注加BK及HOE140处理。测定处理后24 h的血浆、组织丙二醛(MDA)含量及SOD的活性。结果 与对照组相比,BK组MDA含量明显降低,Mn-SOD活性明显升高。结论 BK能够增强24 h后兔血浆、组织SOD活性,从而对缺血再灌注心肌具有保护作用。
Abstract:
AIM To investigate the influence of bradykinin(BK)to plasma or myocardial malondialdehyde (MDA)1eve1 or superoxide dismutase(S0D)activity in rabbits with acute myocardial infarction,and to study the protection mechanism of BK to myocardium .METHODS The ischemia-reperfusion anima1 models were constructed and the animal were given BK,HOE140 or BK+H0El40 respectively.After 24 h, plasma or myocardial MDA 1eve1 and S0D activity were measured.RESULTS Contrasting with those in control group,in BK group the plasma MDA level decreased significantly and MnSOD activity increased significantly.CONCLUSION BK can reduce plasma and myocardial MDA level and augment MnSOD activity.

参考文献/References

[1]李 飞,贾国良,吴丹宁.缓激肽对家兔心肌延迟性的保护作用的实验研究[J].中国病理生理杂志.1999,15(11):997.

[2]李飞,贾国良,李伟杰.缓激肽对缺血预适应兔心肌延迟相的保护怍用[J].解放军医学杂志,2000,25(2):l34.

[3] Martorana PA, Kecten buch B,Breiponl G.Reduction of infarc size local angiotnension converting enzyme inhibition is abolished by a bradykinin antagonist[J].Eur J Pharmacol.1990,182:399.

[4]Watt TM, Sheehy R, Hartman JC Role of bradykinin myocardua1 preconditioning [J].J Pharmac Exp Ther,1994,270(2):681.

[5]Iweierlt L.Measurement of superoxide-derived free radicals in the reperfused heart:evidence for a free radical mechanism of reperfusion injury[J]. J Biol Chem.l988,263:1353.

备注/Memo

备注/Memo:
收稿日期:2000-09-22.
更新日期/Last Update: 2001-03-01