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目的:探求急性心肌缺血再灌注后,抗凝护心Ⅱ号减轻炎症反应的机理和疗效。方法:48只wistar大鼠随机分为6组,建立急性心肌梗死缺血再灌注模型。一组为假手术组,其余分别给予生理盐水、抗凝护心Ⅱ号低剂量、中剂量、高剂量和噻氯吡啶,取大鼠心肌组织行HE染色观察炎性细胞浸润程度,并用酶联免疫吸附试验检测大鼠血浆P选择素水平。结果:抗凝护心Ⅱ号低剂量组、中剂量组和高剂量组均可明显降低血浆P选择素水平(P<0.01),且给药浓度增加该作用增强。组织学观察表明,抗凝护心Ⅱ号可减轻再灌注后心肌组织炎性细胞浸润。结论:抗凝护心Ⅱ号可减轻由心肌缺血再灌注引起的炎症反应及相应的病理改变。
Objective: To investigate the mechanism and effect of anticoagulant heart-protecting Ⅱ on reducing inflammatory reaction after acute myocardial ischemia-reperfusion. Methods: Forty-eight Wistar rats were randomly divided into 6 groups to establish an acute myocardial infarction model of ischemia-reperfusion. One group was sham operation group, the rest were given saline, anticoagulant heart II low dose, medium dose, high dose and ticlopyridine, the myocardial tissue of rats were observed by HE staining of inflammatory cell infiltration, and with enzyme linked Immunosorbent assay was used to detect plasma P-selectin levels in rats. Results: The anticoagulant protect heart Ⅱ low dose group, medium dose group and high dose group can significantly reduce plasma P-selectin level (P <0.01), and the drug concentration increased the role of enhanced. Histological observation showed that anticoagulant heart protection Ⅱ can reduce inflammatory cell infiltration after myocardial reperfusion. Conclusion: Anticoagulation and Protection of Heart No. Ⅱ can reduce the inflammatory reaction caused by myocardial ischemia and reperfusion and the corresponding pathological changes.