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目的观察重组人胰岛素样生长因子-Ⅰ(rhIGF-I)对急性心肌缺血大鼠心功能的影响并探讨其作用机制。方法 24只8周龄雄性SD大鼠随机分为rhIGF-Ⅰ组(预先使用rhIGF-I,50μg/kg,腹腔注射)、缺血组和对照组(后两组预先腹腔注射等量生理盐水)。1 h后,前两组腹腔注射垂体后叶素(20 U/kg)建立心肌缺血模型,对照组注射等量生理盐水。Medlab生物信号采集处理系统测定注射垂体后叶素后即刻与60 min时大鼠左室收缩末压(LVESP)、左室舒张末压(LVEDP)、心室内压最大上升和下降速率(±dp/dtmax)。心肌缺血模型建立60 min时处死大鼠。测定血浆心肌肾素活性(RA)、血管紧张素Ⅱ(AngⅡ)及心肌细胞内环磷腺苷酸(cAMP)的含量;血清、动脉条中NOS活性及NO含量;心肌组织匀浆内钙离子含量。结果 rhIGF-Ⅰ组与缺血组相比LVESP、±dp/dtmax明显提高,LVEDP下降。血清和心肌中RA、AngⅡ降低;心肌细胞内cAMP,心肌Ca2+增加;NOS活性,NO含量增加。结论 rhIGF-Ⅰ可对急性心肌缺血后导致的心功能下降起到保护作用。减少心肌缺血大鼠体内AngⅡ含量;提高NOS活性、NO含量;增加心肌细胞内cAMP含量可能是其发挥心功能保护作用的机制。
Objective To observe the effect of recombinant human insulin-like growth factor-Ⅰ (rhIGF-I) on cardiac function in acute myocardial ischemia rats and to explore its mechanism. Methods Twenty-four male Sprague-Dawley rats of 8 weeks old were randomly divided into three groups: rhIGF-Ⅰ group (rhIGF-I, 50μg / kg, ip), ischemic group and control group . After 1 h, the first two groups were injected intraperitoneally with pituitrin (20 U / kg) to establish the model of myocardial ischemia, while the control group was injected with the same amount of normal saline. Medlab biological signal acquisition and processing system was used to measure LVESP, LVEDP, ± dp / dtmax). Rats were sacrificed 60 minutes after establishment of myocardial ischemia model. Serum levels of myocardial NOS and NO in serum and arteries were measured. The content of intracellular calcium (Ca (superscript 2 +)) in myocardium content. Results Compared with ischemia group, the LVESP, ± dp / dtmax in rhIGF-Ⅰ group increased significantly and the LVEDP decreased. Serum and myocardial RA, Ang Ⅱ decreased; myocardial cells cAMP, myocardial Ca2 + increased; NOS activity, NO content increased. Conclusion rhIGF-Ⅰ can protect cardiac function induced by acute myocardial ischemia. Reduce myocardial Ang Ⅱ content in rats with myocardial ischemia; increase NOS activity and NO content; and increase cAMP content in myocardial cells may be its mechanism of exerting cardioprotection.