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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 on myocardial ischemia-reperfusion injury in vitro. Methods: Forty-eight Wistar rats were randomly divided into two groups: ischemic postconditioning group and ischemia-reperfusion group (control group). The rat heart Langendorff perfusion model was used. After ischemia for 30 min, the rats in the ischemic postconditioning group were subjected to 30 s reperfusion for 30 s, min, reperfusion for 60 min. TTC staining was used to observe the area of myocardial infarction. The content of ATP and the content of adenosine (ADO) in myocardium were measured by high pressure liquid chromatography (HPLC). The contents of superoxide dismutase (SOD), catalase ), Glutathione reductase (GR) activity. Results: The ischemic postconditioning could reduce the area of myocardial infarction [(15.32 ± 2.05)%], compared with the control group [(40.21 ± 3.24)%], the difference was statistically significant (P <0.05) ± 0.63) μmol / g], compared with the control group [(4.73 ± 0.59) μmol / g] (P <0.05). The ADO clearance rate in the coronary artery effluent was (4.33 ± 1.87) nmol. min-1.g-1] was significantly lower than that of the control group [(6.17 ± 1.80) nmol.min-1.g-1], P <0.05; , Have greater antioxidant capacity. CONCLUSION: Ischemic postconditioning can delay ADO clearance, decrease ATP degradation and reduce the damage of reactive oxygen species.