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目的 :揭示地奥心血康 (DK)对心肌缺血再灌注损伤的抗氧化作用与机制。方法 :用成年杂种犬复制心肌缺血再灌注损伤模型。多道生理记录仪监测心功能指标 ;酶法测定AST、CK、LDH含量 ;荧光法测血清与心肌细胞膜MDA含量 ;电子自旋共振 (ESR)记录微分谱线进行体外羟自由基捕捉实验。结果 :①生理盐水对照 (NS)组随着缺血再灌注时间的延长 ,LVSP ,±dp/dtmax呈进行性下降 ;而DK组缺血再灌注后LVSP和±dp/dtmax虽有下降 ,但显著高于NS组 (P <0 0 5 ) ;②血清中AST ,CK ,LDH含量随缺血 /再灌时间延长均增高 ,于再灌 12 0min后DK显著低于NS组 (P <0 0 5 ) ;③血清MDA含量于再灌注 2 4 0min时DK组显著低于NS组 (P <0 0 5 ) ;④DK组心肌细胞膜MDA含量也显著地低于NS组 (P <0 0 5 ) ;⑤在DK浓度为 0 71%、1 4 3%和 2 14 %时 ,羟自由基强度分别减少 6 6 %、80 %和10 0 %。结论 :DK对心肌缺血再灌注损伤犬的心功能和心肌细胞膜有明显的保护作用 ,其很强的清除羟自由基的功能是实现这种保护效应的重要机制。
Objective : To reveal the antioxidation and mechanism of Dioxinxuekang (DK) on myocardial ischemia-reperfusion injury. METHODS: Myocardial Ischemia-reperfusion injury models were replicated in adult mongrel dogs. Multiple physiological recorders were used to monitor cardiac function parameters; enzymatic assays were used to determine AST, CK, and LDH levels; serum levels of MDA and myocardial cell membranes were measured by fluorescence spectrometry; electron-spin resonance (ESR) recordings of differential lines were used to capture hydroxyl radicals in vitro. RESULTS: 1 With the prolongation of ischemia-reperfusion time in the saline control (NS) group, the LVSP and ±dp/dtmax were progressively decreased; while the LVSP and ±dp/dtmax were decreased in the DK group after ischemia-reperfusion. The levels of AST, CK, and LDH in serum increased with the prolongation of ischemia/reperfusion time, and the DK was significantly lower than that of NS group after reperfusion for 120 min (P<0 0). 5) MDA content was significantly lower in the DK group than in the NS group (P < 0.05) at 24 minutes after reperfusion, and the MDA content in the 4DK group was also significantly lower than that in the NS group (P <0 05). 5 When the DK concentration was 0 71%, 134%, and 214%, the hydroxyl radical intensity decreased by 66%, 80%, and 100%, respectively. Conclusion: DK has a significant protective effect on heart function and myocardial cell membrane in dogs with myocardial ischemia-reperfusion injury. Its strong ability to scavenge hydroxyl radicals is an important mechanism to achieve this protective effect.