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目的 探讨葡萄糖 胰岛素 钾极化液 (GIK)对心肌缺血 /再灌 (MI/R)后心肌细胞死亡(坏死和凋亡 )及心脏功能的影响 ,并比较和分析GIK各组分在其中的作用。方法 制备大鼠MI/R模型 ,分别用生理盐水、GIK、葡萄糖 钾液 (GK)或胰岛素干预分组。观察动脉血压、血糖、左室压等的变化 ,再灌注结束后检测心肌梗死或提取DNA检测心肌细胞凋亡。结果 MI/R造成明显的心脏功能障碍、心肌梗死和缺血区细胞凋亡。GIK与胰岛素 (而非GK)具有相似的减轻再灌注心肌损伤作用 ,包括减少心肌梗死范围 [(41 3± 8 3) %和 (39 6± 8 6) %比对照组 (54 4± 1 0 4) % ,q =4 34和q=4 90 ,P值均 <0 0 5]、减弱DNA梯带形成及促进再灌后心脏收缩 /舒张功能恢复。结论 GIK可减少心肌梗死、促进缺血心脏功能恢复 ,胰岛素可能通过抑制缺血心肌细胞凋亡在GIK心肌保护中发挥关键作用。
Objective To investigate the effect of GIK on cardiomyocyte death (necrosis and apoptosis) and cardiac function after myocardial ischemia / reperfusion (MI / R) and to compare and analyze the effect of GIK on effect. Methods The rat MI / R model was prepared and divided into groups according to the intervention of physiological saline, GIK, GK or insulin. Arterial blood pressure, blood glucose, left ventricular pressure and other changes were observed. Myocardial infarction or DNA extraction was detected after reperfusion to detect cardiomyocyte apoptosis. Results MI / R caused significant cardiac dysfunction, myocardial infarction and ischemic cell apoptosis. GIK and insulin, but not GK, had similar effects of reducing myocardial reperfusion injury, including reducing the extent of myocardial infarction (41 3 ± 8 3% vs 39 6 ± 8 6% vs 54 4 ± 10% 4)%, q = 4 34 and q = 4 90, all P <0 05], attenuated DNA ladder formation and promoted systolic / diastolic function recovery after reperfusion. Conclusion GIK can reduce myocardial infarction and promote the recovery of ischemic heart function. Insulin may play a key role in myocardial protection of GIK by inhibiting the apoptosis of ischemic myocardium.