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复方褐毛甘西鼠尾对大鼠离体心肌缺血再灌注损伤的保护作用
http://www.100md.com 《时珍国医国药》 2007年第3期
心肌缺血,再灌注损伤;,保护作用;,褐毛甘西鼠尾,,心肌缺血,再灌注损伤;,保护作用;,褐毛甘西鼠尾,1材料,2方法[7],3结果,4讨论,参考文献:
     摘要:目的与复方丹参注射液(丹参+三七)比较,探讨复方褐毛甘西鼠尾(褐毛甘西鼠尾+三七)对大鼠离体心肌缺血再灌注损伤的保护作用及其在抗心肌缺血再灌注损伤方面替代丹参的可行性。方法采用离体Langendorff缺血再灌注模型,低灌15min复灌30min。实验后检测灌流液中MDA含量及LDH,CK,SOD,GSHPx活性,实验过程全程记录冠脉流量、心率和心肌收缩力。结果复方褐毛甘西鼠尾注射液能显著降低离体缺血再灌注后MDA,CK,LDH水平,升高SOD和GSHPx,且作用强度相似于复方丹参;褐毛甘西鼠尾复方注射液能明显增加冠脉流量,增强再灌注期间的心肌收缩力;此两药均减慢缺血再灌注过程。结论 复方褐毛甘西鼠尾有较好的抗心肌缺血再灌注损伤作用,褐毛甘西鼠尾可在抗心肌再灌注损伤方面替代丹参。其机制可能与抗氧自由基损伤有关。

    关键词:心肌缺血/再灌注损伤; 保护作用; 褐毛甘西鼠尾

    The Protective Effect of Compounded Injection Made from Sanqi and Hemaoganxishuwei Native to Yunnan on Isolated Myocardial Ischemia/Reperfusion in Rats

    DUAN Weigang, LI Huilan, ZHANG Rongping, SU Yanhong, ZHENG Chunlan*

    (Department of Pharmacology of Kunming Medical College,Kunming 650031, China)

    Abstract:Objective To investigate the cardial protection induced by the compounded injections made from SPM+PN during ischemia/reperfusion in rats in vitro.MethodsThe Langendorff model in vitro was introduced, we perfused the heart at a low flow rate with Kreb's solution for 15min at first, then followed normal perfusion for 30min. We examined the contents of maleic dialdehyde (MDA) and the activities of lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD), and glutathione peroxidase (GSHPx) in the flow of effluent after reperfusion. Contractile force, perfusion flow, and rhythm were recorded during experiment. ResultsInjection of SPM+PN was able to decrease the contents of MDA, CK, LDH, increase actmcties of SOD and GSH-Px in vitro, and the effect was similar to that of SM+PN; The injection of SPM+PN was able to enhance ventrical contractile force, increase coronary flow, and slacken heart rate. ConclusionThe compounded injection from SPM+PN possesses cardial protective effect against ischemia/perfusion injury, which is not less powerful than the injection from SM+PN, and which suggests SPM can be a likely replacer for SM to protect myocardium from ischemia/reperfusion injury. The mechanisms of which may be associated with deactivating oxygen free radicles. ......

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