复方水蛭精胶囊对大鼠心肌缺血及再灌注损伤的保护作用

Expermental study of Fufangshuizhijing Capsule on injury induced by ischemia and reperfusion in rats

目的 :通过研究复方水蛭精胶囊 (水蛭 ,黄连 ,大黄 ,郁金 ,玉竹等 )对心肌缺血及再灌注损伤保护作用 ,观察其对经皮腔内冠状动脉成形术 (PTCA)后再狭窄的作用机制。方法 :大鼠左冠脉结扎造成心肌梗塞 ,观察心肌缺血和心律失常情况并检测血液流变学、血小板聚集性、血清过氧化物 (LPO)、超氧化物歧化酶 (SOD)、cAMP值、心肌梗塞的范围和心肌超微结构。结果 :复方水蛭精胶囊对心肌缺血及心肌梗塞后心电图ST段降低有明显的改善作用。实验表明 ,复方水蛭精胶囊能降低LPO ,升高血清SOD浓度 ,降低cAMP值 ,降低全血粘度 (ηb)、血浆粘度 (ηp) ,降低心肌梗塞范围 ,特别是减少左心室梗塞区面积与对照组比较有显著差异 (P <0 .0 1 )。结论 :复方水蛭精胶囊能拮抗心肌缺血及再灌注损伤和心律失常。对PTCA后再狭窄的作用机理可能是通过清除氧自由基、调节细胞第二信使、降低血液粘稠度 ,保护线粒体。

Objective: To investigate mechanism on the restenosis after percutaneous transluminal coronary angioplasty (PTCA) with FSZ (Hirudo, Rhizoma Coptidis, Radix et Rhizoma Rhei, Radix Curcumae, Rhizoma Polygonati Odoroti, etc) by studying the protective effects of FSZ on arrhythmia and injury induced by ischemia and reperfusion.Methods:Rats were randomly divided into four groups and administered orally with FSZ. Left coronary artery ligature was used to form ischemia and reperfusion model. Lipid peroxidation (LPO), superoxide dismutase (SOD), cyclic adenosine monophosphate (cAMP), area of myocardial infarction, myocyte ultrastructural injury and occurrence of arrhymia were investigated.Results: FSZ could improve the changes in ST segment. In rats treated with FSZ, the levels of SOD were elevated while cAMP, LPO, and the specific viscosity of whole blood or plasma and the aggregation of the platelet were lowered, keep to improving the hemorheological changes. It also could antagonize the myocardial damage by myocardial ischemia or reperfusion reduced the area of myocardial infarction. Especially, Fufangshuizhijing Capsule reduced the area of left ventricular (LV) compared with the control group remarkably.Conclusion: FSZ could obviously antagonize arrhythmia and the injury induced by the ischemia and reperfusion, FSZ may scavenge oxygen free radical, regulate the second messenger, remarkably improve the local circulation to reduce the specific viscosity of whole blood of plasma and the aggregation of the platelet in rats, protect mitochondria safeguard the cardiac myocyte to treat PTCA.