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目的 应用改良离体做功鼠心模型 ,探讨外源性磷酸肌酸 (CP)抗心肌缺血再灌注损伤的作用机制。方法将 72只鼠分为 5组 ,将 5组 L angendorff灌注鼠心在 37℃下缺血 40分钟后恢复灌注 2 0分钟。A组不灌注 St.Thom as液 ;B组和 C组于缺血开始灌注 St.Thomas液 ,C组的 St.Thom as液中加入 CP(10 mmol/L ) ;D组和 E组于缺血 15分钟后灌注 St.Thomas液 ,E组的 St.Thomas液中加入 CP(10 mm ol/L)。测定心脏做功指数、冠状动脉流量、心肌三磷酸腺苷 (ATP)和丙二醛 (MDA)含量以及尼克酰胺腺嘌呤二核苷酸 (NADH)的动态变化 ;进行线粒体半定量分析和心肌超微结构观察。 结果 E组复灌后心脏做功指数和冠状动脉流量分别高于 D组 (P<0 .0 5 ) ,同时心肌 ATP含量增高 (P<0 .0 5 ) ;B组与 C组比较无差异 ;C组和 E组复灌后 MDA,NADH分别较 B组和 D组下降 (P<0 .0 5 ) ,且缺血末 ATP与复灌 2 0分钟 MDA的生成无相关关系 ;而 B组和 D组呈负相关 (r=- 0 .6 43,P<0 .0 5 ) ;线粒体半定量分析表现出与MDA生成相应的变化。 结论 外源性 CP对心肌缺血再灌注损伤有较好的保护作用 ,其机制可能与其对线粒体结构和氧化磷酸化功能的保护以及核苷酸池的保存、减少氧自由基的产生有关。
Objective To investigate the mechanism of exogenous creatine phosphate (CP) against myocardial ischemia-reperfusion injury in a rat heart model. Methods Seventy-two mice were divided into five groups. Five groups of Langentorff perfusion rat hearts were reperfused for 20 minutes after ischemia at 37 ℃ for 40 minutes. St.Thom as fluid was not infused in group A, St.Thomas solution was infused in ischemic group in group B and group C, and CP (10 mmol / L) in group St.Thom as in group C. In group D and group E, Blood was infused St.Thomas fluid 15 minutes later, and St. Thomas liquid of group E CP (10 mm ol / L). The indexes of cardiac work index, coronary flow, myocardial ATP content, malondialdehyde (MDA) content and nicotinamide adenine dinucleotide (NADH) were measured. Semi-quantitative analysis of mitochondria and myocardial ultrastructure were performed. Results After reperfusion in Group E, cardiac work index and coronary flow were higher than those in Group D (P <0. 05) and ATP in myocardium (P <0.05). There was no difference between Group B and Group C; There was no correlation between MDA and NADH in group C and group E compared with those in group B and group D (P <0.05), and there was no correlation between ATP in ischemic group and MDA in 20 min after reperfusion D group was negatively correlated (r = - 0.363, P <0.05). Semi-quantitative analysis of mitochondria showed a corresponding change with MDA. Conclusions Exogenous CP can protect myocardium from ischemia-reperfusion injury. Its mechanism may be related to the protection of mitochondrial structure and oxidative phosphorylation, the preservation of nucleotide pool and the reduction of oxygen free radicals.