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目的:观察氟伐他汀预处理对血清白细胞介素8(IL8)及心肌梗死面积的影响,探讨其对心肌梗死再灌注损伤保护作用的可能机制。方法:健康新西兰白兔24只,随机分为3组:假手术组、对照组、氟伐他汀组(氟伐他汀10mg·kg-1·d-1),每组8只。除假手术组外,其余2组通过结扎冠状动脉前降支60min,然后松开180min建立心肌梗死再灌注动物模型。在实验终点采右心房血,分离血清,检查IL8、CKMB含量,处死动物取出心脏,用1%氯化三苯基四氮唑染色后计算梗死心肌面积,并检测梗死区心肌髓过氧化酶(MPO)含量。结果:对照组、氟伐他汀组IL8、MPO活性明显高于假手术组(均P<0.05),氟伐他汀组IL8、MPO活性低于对照组(均P<0.05)。对照组血清CKMB明显高于假手术组(P<0.01),氟伐他汀组CKMB也明显高于假手术组(P<0.05),但较对照组明显降低(P<0.05)。氟伐他汀组心肌梗死面积[(26.90±1.81)%]较对照组[(31.22±2.31)%]小(P<0.05)。结论:氟伐他汀能通过抑制IL8的合成,减少中性粒细胞的浸润,从而改善心肌缺血再灌注损伤。
Objective: To observe the effect of fluvastatin preconditioning on the serum levels of interleukin 8 (IL 8) and myocardial infarction, and to explore the possible mechanism of fluvastatin on myocardial infarction reperfusion injury. Methods: Twenty-four healthy New Zealand white rabbits were randomly divided into 3 groups: sham-operated group, control group and fluvastatin group (fluvastatin 10 mg · kg-1 · d-1) Except sham group, the other two groups were established by ligation of the anterior descending coronary artery 60min, then release 180min myocardial infarction reperfusion animal model. At the end of the experiment, the right atrial blood was taken, serum was separated, IL8 and CKMB levels were examined, the heart was sacrificed, the area of infarcted myocardium was counted with 1% triphenyltetrazolium chloride staining, and myocardial myeloperoxidase MPO) content. Results: The activity of IL8 and MPO in control group and fluvastatin group was significantly higher than that in sham operation group (all P <0.05). The activity of IL8 and MPO in fluvastatin group was lower than that of control group (all P <0.05). CKMB in control group was significantly higher than that in sham operation group (P <0.01). CKMB in fluvastatin group was also significantly higher than that in sham operation group (P <0.05), but lower than that in control group (P <0.05). The area of myocardial infarction in fluvastatin group [(26.90 ± 1.81)%] was smaller than that in control group [(31.22 ± 2.31)%] (P <0.05). Conclusion: Fluvastatin can improve myocardial ischemia-reperfusion injury by inhibiting IL8 synthesis and decreasing neutrophil infiltration.