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Doketone Bodies Contribute to Protect Agaist Damage Caused by Both Myocardial Ischemia and Reperfusion Injury?

多酮体有助于保护心肌缺血和再灌注损伤引起的损伤？

基本信息

批准号：
09670747
负责人：
SATO Kiyotaka
金额：
$ 1.15万
依托单位：
Kitasato University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670747/
关键词：
reperfusion unjury ischemic heart ketone body mitochondria respiratory chain respiratoru chain

项目摘要

Effects of ketone bodies on cardiac performance and mitochondrial energetics were investigated in experimental myocardial ischemia with a special focus on the following reperfusion injury.Twenty-one isolated rat hearts were classified into three categories by perfusion mode after ischemia: 7 hearts were exposed to 10 min of myocardial ischemi a and followed by 30 min of coronary reperfusion with normal Krebs-Henseleit (K-H) buffer without using ketone bodies (K(-) group), and the other 7 hearts were exposed to the same ischemia and reperfused with K-H buffer containing 5 mM ketone bodies-(Ke group). These were compared with 7 normal hearts, that were exposed to neither ischemia nor reperfusion (control group). Cardiac performance was assessed by several indices: max dp/dt, cardiac output, cardiac work, and cardiac efficiency. Mitochondrial energetics were estimated by using mitochondrial redox state, its potentiality and cytosolic △GATP hydrolysis energy.As a result, the Ke group demonstrated a more rapid improvement of LV contractility than the K(-) group after reperfusion. From the standpoint of energetics, the ketone bodies seemed to economically augment the mitochondrial metabolism, because the mitochondrial redox state(Eh NAD/NADH: C=280.8 mV, Ke=297.1 mV, K(-)=291.1 mV), cytosolic △GATP hydrolysis energy (△GATP: C=56.4 KJ/mol, Ke=58.2 KJ/mol, K(-)=56.0 KJ/mol) and concentration of phosphocreatine were remarkably increased.Thus, it was concluded that, in myocardial ischemia, ketone bodies function as a substrate to produce mitochondrial energy, and through this function, work to protect the myocardium against both transient ischemia and the following reperfusion injury.

本实验研究了酮体对实验性心肌缺血及再灌注损伤的心功能和线粒体能量学的影响。7只心脏缺血10 min，再灌注30 min，用正常K-H曲线另7只心脏缺血后用含5 mM酮体的K-H缓冲液再灌注（Ke组）。将这些与7个正常心脏进行比较，这些心脏既不暴露于缺血也不暴露于再灌注（对照组）。通过几个指标评估心脏性能：最大dp/dt、心输出量、心脏作功和心脏效率。用线粒体氧化还原状态、氧化还原电位和胞浆△GATP水解能估算线粒体能量，结果表明，再灌注后Ke组左室收缩力的改善比K（-）组快。从能量学的观点来看，酮体似乎经济地增加了线粒体代谢，因为线粒体的氧化还原状态（Eh NAD/NADH：C=280.8 mV，Ke=297.1 mV，K（-）=291.1 mV），胞浆△GATP水解能（△GATP：C= 56.4KJ/mol，Ke= 58.2KJ/mol，K（-）= 56.0KJ/mol）和磷酸肌酸浓度均显著升高。酮体作为产生线粒体能量的底物发挥作用，并通过该功能保护心肌免受短暂缺血和随后的再灌注损伤。