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心肌缺血预处理的抗血小板活化和内皮保护作用的实验研究
引用本文:肖滨,惠杰. 心肌缺血预处理的抗血小板活化和内皮保护作用的实验研究[J]. 浙江医学, 2010, 32(1): 62-64,67
作者姓名:肖滨  惠杰
作者单位:1. 浙江省新昌县人民医院心内科
2. 苏州大学附属第一医院心内科,苏州,215006
摘    要:
目的探讨心肌缺血预处理(MIP)对缺血-再灌注期血小板活化和血管内皮细胞功能的影响。方法将45只成年新西兰大白兔随机分为对照组(23只)和MIP组(25只),分别在试验的不同时间段行血细胞计数,并测定血浆可溶性P-选择素、血栓烷B2(TXB2)和6-酮-前列腺素F1α(6-keto—PGF1α)的含量。同时行心脏血管内皮细胞P-选择素表达的免疫组化分析。结果(1)两组实验动物的白细胞计数在再灌注期均明显升高(P〈0.05),MIP组缺血前的计数值也升高,但在再灌注期同一时间点均明显低于对照组(P〈0.05)。(2)较之基础状态时,MIP组再灌注60、120min时可溶性P-选择素明显升高、6-Keto—PGF1α明显下降(均P〈0.05),而且整个再灌注期TXB。水平均明显高于基础状态(P〈0.05);对照组自缺血40min起,可溶性P-选择素及。rX82水平均明显升高、6-Keto—PGF1α明显下降(均P〈0.05)。与对照组同一时间点比较,MIP组再灌注120min的可溶性P-选择素以及缺血后的TXB。水平均明显降低、再灌注60、120min的6-Keto—PGF1α明显升高(均P〈0.05)。结论MIP可以有效抑制缺血-再灌注期血小板活化,从而保护病变区域血管内皮细胞功能。

关 键 词:心肌缺血预处理  缺血-再灌注  血小板  内皮细胞

Myocardial ischemic preconditioning in inhibiting platelet activation and preventing endothelial injury during ischemia-reperfusion
XIAO Bin,HUI Jie. Myocardial ischemic preconditioning in inhibiting platelet activation and preventing endothelial injury during ischemia-reperfusion[J]. Zhejiang Medical Journal, 2010, 32(1): 62-64,67
Authors:XIAO Bin  HUI Jie
Affiliation:. (Department of Cardiology, the First Affiliated Hospital of Suzhou University, Suzhou 215006, China)
Abstract:
Objective To evaluate the effects of myocardial ischemic preconditioning (MIP)on platelet activation and endothelial function changes during ischemia-reperfusion (I/R). Methods Forty New Zealand white rabbits were divided into control group and MIP group randomly. Plasma soluble P-selectin (sP-selectin), thromboxane B2 (TXB2), 6-keto-PGF1α were measured and blood cell counts were examined at different time points. P-selectin IH was detected in heart specimens. Results Blood white cells increased in all animals during I/R (MIP group also increased at pre-occlusion), but compared with control group, MIP group had lower blood cell counts. MIP group had higher sP-selectin level at reperfusion 60min and 120min, lower 6-keto-PGF1α level at the same time; and higher TXB2 level in all the reperfusion times. Control group had higher sP-selectin, TXB2, but lower 6-keto-PGF1α level from reperfusion 40min during the reperfusion periods. Compared with control group, MIP group showed lower TXB2 level after the coronary artery occlusion, lower sP-selectin level at reperfusion 120min, and higher 6-keto-PGF1α level at reperfusion 60min and 120min. Conclusion MIP can effectively inhibit platelet activation and protect endothelial function during the I/R periods.
Keywords:Myocardial ischemic preconditioning Ischemia-Reperfusion Platelet Endothelium
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