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首页> 外文期刊>Circulation journal >Difference in the cardioprotective mechanisms between ischemic preconditioning and pharmacological preconditioning by diazoxide in rat hearts.
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Difference in the cardioprotective mechanisms between ischemic preconditioning and pharmacological preconditioning by diazoxide in rat hearts.

机译：大鼠心脏缺血预处理与药物预处理之间的心脏保护机制差异。

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BACKGROUND: Recent studies have implicated the opening of mitochondrial K(ATP) (mitoK(ATP)) channels and the production of reactive oxygen species (ROS) in the cardioprotective mechanism of ischemic preconditioning (IPC). METHODS AND RESULTS: The involvement of mitoK(ATP) channels and ROS in the cardioprotective effects of both IPC and the mitoK(ATP) channel opener diazoxide (DZ) was investigated in ischemic/reperfused rat hearts. The effects of IPC and DZ on myocardial high-energy phosphate concentrations and intracellular pH (pH(i)) were also examined using (31)P nuclear magnetic resonance spectroscopy. Although both the mitoK(ATP) channel inhibitor 5-hydroxydecanoate and the antioxidant N-acetylcysteine abolished the postischemic recovery of contractile function by DZ, neither of them inhibited that by IPC. IPC attenuated the decline in pHi during ischemia, but DZ did not (6.28+/-0.04 in IPC, p<0.05, and 6.02+/-0.05 in DZ vs 6.02 +/-0.06 in control hearts). DZ, but not IPC, reduced the decrease in ATP levels during ischemia (ATP levels at 20-min ischemia: 26.3+/-3.4% of initial value in DZ, p<0.05, and 8.1+/-3.0% in IPC vs 15.1+/-1.3% in control hearts). CONCLUSIONS: These results suggest that DZ-induced cardioprotection is related to ROS production and reduced ATP degradation during ischemia, whereas attenuated acidification during ischemia is involved in IPC-induced cardioprotection, which is not mediated through mitoK(ATP) channel opening or ROS production.
机译：背景：近期研究表明，在缺血预处理（IPC）的心脏保护机制中，线粒体K（ATP）（mitoK（ATP））通道的开放和活性氧（ROS）的产生。方法和结果：在缺血/再灌注大鼠心脏中研究了mitoK（ATP）通道和ROS参与IPC和mitoK（ATP）通道开放剂二氮嗪（DZ）的心脏保护作用。还使用（31）P核磁共振波谱检查了IPC和DZ对心肌高能磷酸盐浓度和细胞内pH（pH（i））的影响。尽管mitoK（ATP）通道抑制剂5-羟基癸酸酯和抗氧化剂N-乙酰半胱氨酸都消除了DZ缺血后收缩功能的恢复，但它们都没有被IPC抑制。 IPC减轻了缺血期间pHi的下降，但DZ没有（IPC为6.28 +/- 0.04，DZ为p <0.05，6.02 +/- 0.05，而对照心脏为6.02 +/- 0.06）。 DZ而非IPC减少了缺血期间ATP水平的降低（缺血20分钟时的ATP水平：DZ中初始值的26.3 +/- 3.4％，IPC中p <0.05,8.1％/ 3.0％vs 15.1）对照组为+/- 1.3％）。结论：这些结果表明，DZ诱导的心脏保护作用与缺血过程中ROS的产生和ATP降解的减少有关，而缺血过程中酸化的减弱与IPC诱导的心脏保护作用有关，这不是通过mitoK（ATP）通道开放或ROS产生介导的。

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