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芪丹通脉片对心肌缺血再灌注犬血浆NO/ET, 6ketoPGF1α/TXB2的影响
http://www.100md.com 《第四军医大学学报》 2003年第5期
缺血再灌注,,缺血再灌注;缺血预处理;芪丹通脉片;血浆内皮素;一氧化氮;血栓素B2;6酮前列腺素,芪丹通脉片对心肌缺血再灌注犬血浆NO,ET,6ketoPGF1α,TXB2的影响,0引言,1材料和方法,2结果,3讨论,【参考文献】
     Effects of Qidantongmai tablets on the equilibrium between NO and ET, 6ketoPGF1αand TXB2 in plasma of dogs with myocardial ischemia reperfusion injury

    MA AiLing,WANG ZongRen, LI JunChang, HANG Li, ZHENG Jin, WANG Wen, LI JingHua

    Department of Traditional Chinese Medicine, Xijing Hospital, Fourth Military Medical University, Xian 710033, China

    【Abstract】 AIM: To investigate the effects of Qidantongmai tablet (QDTMT) on the equilibrium between ET and NO and the equilibrium between TXB2 and 6ketoPGF1αin the canine model of myocardial ischemia reperfusion injury (MIRI). METHODS: Twentyfour adult healthy crossbred canines were randomly assigned to four groups: Control group, ischemia preconditioning group, QDTMT low dosage group (QDTMTL) and QDTMT high dosage group (QDTMTH). Canines in all groups took QDTMT (or NS) orally for a week under the same condition. The model of MIRI was established by ligating levoanterior descending branch of coronary artery. The contents of ET, NO, TXB2 and 6ketoPGF1α in plasma were measured at four time points: Predrug (T1), 20 min after ligation (T2), 10 min (T3) and 30 min (T4) after reperfusion respectively and the equilibrium between NO / ET and that between 6ketoPGF1α/ TXB2 were analyzed. RESULTS: Compared with the control group, QDTMTL and QDTMTH reduced the level of ET and TXB2, promoted the expression level of NO, increased the activity of 6ketoPGF1α, and regulated the equilibrium between NO and ET and that between 6ketoPGF1α and TXB2 (P<0.05, P<0.01). There is no significant difference between QDTMT groups and the ischemia preconditioning group(P>0.05). CONCLUSION: Just as ischemia preconditioning, QDTMT has good protective effects on MIRI. The mechanism of protection relates to its function of decreasing the level of ET and TXB2, promoting the expression level of No, increasing the activity of 6ketoPGF1α, and regulating the equilibrium between NO and ET and the equilibrium between 6ketoPGF1α and TXB2. ......

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