The role of ATP produced by glycolysis in the maintenance of intramyocardial ion homeostasis

据报道，在心肌中，用于机械功的能量由氧化磷酸化提供，而维持离子稳态的能量由糖酵解产生。在这项研究中，糖酵解抑制对心肌内钙稳态的影响进行了研究。我们的结果表明糖酵解ATP不是维持心肌钙稳态所必需的，糖酵解抑制导致的糖磷酸盐积累导致了心肌钙超载，但其机制尚不清楚。同时观察顿抑心肌对葡萄糖的摄取。短暂缺血后再灌注的心肌表现为收缩功能障碍，无坏死，称为“顿抑心肌”。“据报道，顿抑心肌的糖酵解和糖原生成增加，表明顿抑心肌对外源性葡萄糖的需求增加。本研究还试图量化心肌葡萄糖摄取的增加，并阐明顿抑心肌葡萄糖摄取增加的途径。用2-脱氧葡萄糖替代葡萄糖后，用P-31核磁共振从大鼠心肌磷酸糖共振的时间过程中定量葡萄糖摄取率。我们的研究结果表明，顿抑心肌中的葡萄糖摄取增加高达胰岛素刺激的心肌，并在顿抑心肌中增加的葡萄糖摄取是由葡萄糖转运蛋白维持。急性心肌梗死患者再灌注心肌葡萄糖摄取的增加也得到了F-18氟脱氧葡萄糖和正电子发射断层扫描的临床证实。

It has been reported in myocardium that energy for mechanical work is provided by oxidative phosphorylation whereas that to maintain ion homeostasis is generated by glycolysis. In this study, the effects of glycolytic inhibition on intramyocardial calcium homeostasis was investigated. Our results indicate that glycolytic ATP is not necessary to maintain calcium homeostasis in myocardium ; the sugar phosphates accumulated by glycolytic inhibition induce the calcium overload, but the further mechanism was not clarified. The glucose uptake in stunned myocardium was also investigated. The myocardium reperfused after a brief period of ischemia shows contractile dysfunction without necrosis, and is called as "stunned myocardium." Glycolysis and glycogenesis have been reported to be augmented in stunned myocardium, suggesting that the demand for exogenous glucose is increased in stunned myocardium. This study also seeks to quantify the increase in myocardial glucose uptake and to clarify the pathway of augmented glucose uptake in stunned myocardium. Glucose uptake rate was quantified from the time course of sugar phosphate resonance in rat myocardium using P-31 nuclear magnetic resonanceafter substitution of glucose by its analogue, 2-deoxyglucose. Our results indicate that the glucose uptake in stunned myocardium is augmented as high as in the myocardium stimulated by insulin, and that the augmented glucose uptake in stunned myocardium is maintained by glucose transporter. The increase of glucose uptake in reperfused myocardium was also confirmed clinically in patients with acute myocardial infarction using F-18 fluorodeoxyglucose and positron emmission tomography.