缺血后处理与大鼠心肌能量代谢的关系

Relationship between ischemia postconditioning and rat myocardial energy metabolism

目的:探讨缺血后处理对大鼠体外心脏缺血再灌注损伤的作用。方法:48只Wistar大鼠,随机均分为2组;缺血后处理组、缺血再灌注组(对照组)。采用大鼠体外心脏Langendorff灌流模型,缺血后处理组全心缺血30 min后,再灌注30 s后,缺血30 s,反复3次,然后持续灌注57 min;对照组全心缺血30 min,再灌注60 min。TTC染色观察心肌梗死面积,高压液相色谱仪(HPLC)分析心肌组织中ATP的含量、灌流液腺苷(adenosine,ADO)含量,测定超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)活性。结果:缺血后处理可减少心肌梗死面积[(15.32±2.05)%],与对照组比较[(40.21±3.24)%],差异有统计学意义(P<0.05);减少ATP降解[(3.32±0.63)μmol/g],与对照组比较[(4.73±0.59)μmol/g]差异有统计学意义(P<0.05);心肌冠状动脉流出液中ADO清除速率[(4.33±1.87)nmol.min-1.g-1]小于对照组[(6.17±1.80)nmol.min-1.g-1],P<0.05;心肌SOD、CAT和GR酶活性均高于对照组(P<0.05),有更大的抗氧化能力。结论:缺血后处理可延缓ADO清除,减少ATP的降解,减轻活性氧的损伤作用而发挥心肌保护作用。

Objective：To investigate the effect of ischemic postconditioning （postcon） on myocardial ischemia/ reperfusion （I/R） injury of isolated rat heart. Method： Forty eight adult male Wistar rats were randomly divided into 2 groups （n= 24） ：control group and postcon group. In control group, isolated rabbit hearts were perfused according to the Langendorff technique and subjected to 30 minutes of isehemia and 60 minutes of reperfusion. In posteon group, ischemic postcon was performed （3 cycles of 30 second reperfusion/ischemia followed by 57 minutes of continuing reperfusion）, after 30 minutes of ischemia. The infarct size was measured by the triphenylte trazolium （TTC） staining. The content of ATP from myocardiol tissue was measured by HPLC. Adenosine （ADO） from perfusate was also measured by HPLC. Activities of SOD, CAT and GR were determined by spectrophotography. Result： The in{act size was reduced in postcon compared to control （[15.32 ± 2.05]% vs [40. 21±3.24]%,P〈0.05, the concentrations of ATP postcon were greater （[4.73±0.59 ]vs [3.32±0. 63]μmol/g,P〈0. 05）, and the associated levels were higher （[6. 17± 1.80]vs [4.33±1.87] nmol·min^-1·g^-1,P〈0.05） suggesting that intravascular adenosine retained longer in postcon. Activities of SOD, CAT and GR were all decreased in control. Conclusion.. These data suggest that postcon involves endogenous activation of adenosine receptor. This activation may be linked to the delay in washout of intravascular ADO postconditioning. ADO is known as a precursor for purine salvage pathways in the myocardial protection, and it is also advantageous to ATP production.