Van Emous J G, Vleggeert-Lankamp C L, Nederhoff M G, Ruigrok T J, Van Echteld C J
Interuniversity Cardiology Institute of The Netherlands and Department of Cardiology, Heart Lung Institute, University Medical Center, 3508 GA Utrecht, The Netherlands.
Am J Physiol Heart Circ Physiol. 2001 May;280(5):H2189-95. doi: 10.1152/ajpheart.2001.280.5.H2189.
Normalization of intracellular sodium (Na) after postischemic reperfusion depends on reactivation of the sarcolemmal Na(+)-K(+)-ATPase. To evaluate the requirement of glycolytic ATP for Na(+)-K(+)-ATPase function during postischemic reperfusion, 5-s time-resolution 23Na NMR was performed in isolated perfused rat hearts. During 20 min of ischemia, Na increased approximately twofold. In glucose-reperfused hearts with or without prior preischemic glycogen depletion, Na decreased immediately upon postischemic reperfusion. In glycogen-depleted pyruvate-reperfused hearts, however, the decrease of Na was delayed by approximately 25 s, and application of the pyruvate dehydrogenase (PDH) activator dichloroacetate (DA) did not shorten this delay. After 30 min of reperfusion, Na had almost normalized in all groups and contractile recovery was highest in the DA-treated hearts. In conclusion, some degree of functional coupling of glycolytic ATP and Na(+)-K(+)-ATPase activity exists, but glycolysis is not essential for recovery of Na homeostasis and contractility after prolonged reperfusion. Furthermore, the delayed Na(+)-K(+)-ATPase reactivation observed in pyruvate-reperfused hearts is not due to inhibition of PDH.
缺血后再灌注期间细胞内钠（Na）的正常化取决于肌膜Na(+)-K(+)-ATP酶的重新激活。为了评估缺血后再灌注期间糖酵解ATP对Na(+)-K(+)-ATP酶功能的需求，在离体灌注大鼠心脏中进行了5秒时间分辨率的23Na核磁共振研究。在20分钟的缺血期间，Na增加了约两倍。在有或没有缺血前糖原耗竭的葡萄糖再灌注心脏中，缺血后再灌注时Na立即下降。然而，在糖原耗竭的丙酮酸再灌注心脏中，Na的下降延迟了约25秒，并且应用丙酮酸脱氢酶（PDH）激活剂二氯乙酸（DA）并没有缩短这种延迟。再灌注30分钟后，所有组中的Na几乎都恢复正常，并且在DA处理的心脏中收缩功能恢复最高。总之，糖酵解ATP与Na(+)-K(+)-ATP酶活性存在一定程度的功能偶联，但糖酵解对于长时间再灌注后Na稳态和收缩性的恢复并非必不可少。此外，在丙酮酸再灌注心脏中观察到的延迟的Na(+)-K(+)-ATP酶重新激活并非由于PDH的抑制。
