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目的观察心肌缺血期处理后在体大鼠心肌缺血-再灌注损伤中中介素(Intermedin IMD)参与情况下的保护机制;研究IMD对心肌细胞的保护作用是否途经ATP敏感性钾通道(ATP-sensitive potassium channel,KATP),为探讨心肌保护机制提供临床思路。方法选取标准SD大鼠45只,随机分为缺血再灌注组(I/R组)、IMD治疗组(IMD组)、格列本脲+IMD治疗组(Gli+IMD组),每组15只。各组分别于再灌注末期分别抽取动脉血3ml,用比色法测定血清CK和LDH,用ELISA法测cTnI活性。取心尖部心肌组织,10%甲醛液固定,石蜡包埋,后在光镜下观察心肌损害程度。结果 IMD组与I/R组比较,P<0.01;Gli+IMD组与I/R组、IMD组比较,P<0.05。结论 IMD在心血管系统中具有保护作用且其机制可能与其激活了ATP敏感性钾通道相关。
Objective To observe the protective mechanism of Intermedin (IMD) involved in myocardial ischemia-reperfusion injury in rats after myocardial ischemia and to explore whether the protective effect of IMD on cardiomyocytes via ATP-sensitive potassium channel ATP-sensitive potassium channel, KATP) to provide clinical ideas for exploring myocardial protection mechanism. Methods Forty-five SD rats were randomly divided into two groups: ischemia reperfusion group (I / R group), IMD treatment group (IMD group), glibenclamide + IMD treatment group (Gli + IMD group) only. At the end of reperfusion, 3ml arterial blood was taken from each group, CK and LDH were measured by colorimetric method, and cTnI activity was measured by ELISA. Take the apex myocardial tissue, fixed in 10% formalin, embedded in paraffin, and observe the extent of myocardial damage under light microscope. Results IMD group and I / R group, P <0.01; Gli + IMD group and I / R group, IMD group, P <0.05. Conclusion IMD has a protective effect in cardiovascular system and its mechanism may be related to its activation of ATP-sensitive potassium channels.