不同血糖水平缺血后适应下心肌缺血再灌注损伤差异及其机制研究

目的探讨不同血糖水平对离体心脏缺血后适应下血流动力学、心梗面积的差异及其机制。方法12周龄C57／BI。雄性小鼠，利用Langendorff灌流装置建立小鼠心肌缺血后适应（IPC）模型。K—H缓冲液临用前配制，方案分正常葡萄糖水平组（NBG组）：11．1mmol／L和高葡萄糖水平组（HBG组）：22．2mmol／L，其他成分两组一致。IPC采用60min全心缺血，再灌注之前给予3次IPC循环，每次10S，再灌注120min。沿左心房置人顶端球囊测压导管进行心脏血流动力学检测；采用三苯基氯化四氮唑染色的方法确定心肌梗死范围；采用Western印迹检测心肌组织RISK信号通路。结果和NBG组比较，HBG组小鼠心脏血流动力学指标左心室收缩压（LVSP）显著下降，差异有统计学意义（P〈0．05），左室舒张末压（LVEDP）差异无统计学意义（P〉0．05），心肌梗死范围增加，差异有统计学意义（P〈0．01）；两组ERK1／2信号通路显著抑制，Akt信号通路表达无明显差异。结论正常水平血糖较高血糖状态下进行缺血后适应处理更能有效地减轻心肌缺血冉灌注损伤。

Research of injury differences and mechanisms of myocardial ischemia reperfusion under different blood glucose levels of ischemic postconditioning

Objective To explore the differences and mechanisms of hemodynamics and myocardial infarct size under different blood glucose levels of ischemic myocardial postconditioning in vitro. Methods Myo- cardial ischemia postconditioning （IPC） models were built with 12-weeks-old C57/BL male mice, by use of Langendorff perfusion device. K-H buffer was prepared before using. Two groups were divided according to protocal： normal blood glucose （NBG） group with 11.1 mmol/L, and high glucose （HBG） group with 22.2 mmol/L, other components were the same. The IPC model adopted 60min whole heart ischemia, 3 times IPC cycle were administered before reperfusion, each time for 10 s, and reperfusion for 120 min. In- sert top end saccule manometry catheter into the left atriam to detect cardiac hemodynamics. Triphenyl tet razolium staining method was used to determine the scope of myocardial infarction. Western blot was applied to detect the RISK signaling pathway of myocardial tissue. Results Left ventricular systolic pressure （I.VSP） of the cardiac hemodynamic parameters of HBG group mice decreased significantly, compared with NBG group （P 〈0.05） ; the left ventricular end-diastolic pressure （LVEDP） of two groups had no significant differences （P 〈0.05） ; and the scope of myocardial infarction of HBG group increased, corn pared with NBG group （P 〈0.05）. ERK1/2 signaling pathway was significantly inhibited, and there was no significant difference of the expression of AKT signaling pathway. Conclusion d glucose （HBG） group, the normal blood glucose （NBG） group can be more cardial ischemia-reperfusion injury by ischemic postconditioning treatment. Compared with the high effectively relieved my.