川芎嗪对离体大鼠心肌缺血再灌注损伤的影响

作者	单位
傅春景	河南医科大学病理生理教研室郑州 450052
赵根尚	河南医科大学病理生理教研室郑州 450052
张建芳	河南医科大学病理生理教研室郑州 450052
李光泽	第一军医大学广州 510515

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中文摘要:

本实验用改良的langendorff模型灌流离体大鼠心脏,探讨心肌细胞本身或血管内皮细胞,是否在缺血再灌注时也参与了血栓素A₂（TXA₂）的释放,并探讨川芎嗪对TXA₂的影响。结果显示心肌缺血后再灌注时冠脉回流液中TXB₂含量增多,6-酮-前列腺素F_1α(6-keto-PGF_1α)相对减少,TXB₂/6-keto-PGF_1α比值增高,乳酸脱氢酶（LDH）释放增多。说明川芎嗪能促进6-keto-PGF_1α的产生,且能够抑制TXB₂和LDH的释放。

英文摘要:

In recent years, it is believed by some scholars that the injury of myocardial ischemic reperfusionis correlated to the thromboxane A₂（TXA₂） released by platelets. In order to explore that whetherthe myocardial and hemangio-endothelial cells participate in the TXA₂ production during the processof reperfusion, the modified Langendorff method was used to establish the model of reperfusing theisolated rat heart. On the other hand, this experiment was also intended to observe the effect ofligustrazine on the injury of myocardial ischemic reperfusion. The results revealed that the level ofthromboxane B₂ （metabolite of TXA₂） and lactic dehydrogenase （LDH） in coronary sinus refluxfluid increased during the process of reperfusion, while the level of 6-keto-PGF1α in the same fluidrelatively decreased （P<0.05）. The ratio of TXB₂/6-keto-PGF1α was raised. The ligustrazineinhibited the release of TXB₂ and LDH, but promoted the production of 6-keto-PGF1α （P<0.05）. Theresults also proved that the myocardial and hemangio-endothelial cells could synthesize TXA₂, andthe amount of TXA₂ released increased during the reperfusion of ischemic myocardium, which waslikely to be the major factor of the injury of ischemic myocardial reperfusion. Ligustrazine playsan important role in protecting the myocardium.

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