Kuki S, Suzuki E, Watari H, Takami H, Matsuda H, Kawashima Y
Department of Molecular Physiology, National Institute for Physiological Sciences, Okazaki, Japan.
Circ Res. 1990 Aug;67(2):401-5. doi: 10.1161/01.res.67.2.401.
The intracellular potassium content of perfused rat heart was measured by potassium-39 nuclear magnetic resonance (NMR) spectroscopy at 33 degrees C with an inversion recovery technique based on the fact that the spin-lattice relaxation time (T1) of the intracellular potassium (8.3 msec at 8.45 T) is much faster than that of the extracellular potassium (68 msec). Intracellular potassium decreased to 60.2 +/- 4.3% of the control level (mean +/- SEM, n = 6) at 40 minutes from the start of metabolic inhibition (2 mM cyanide, 0 mM glucose). Removal of cyanide restored intracellular potassium to 94.2 +/- 3.9% at 30 minutes from the restart of oxidative metabolism. The cumulative potassium loss was determined from the flow rate and potassium concentration of the coronary effluent, which reached 139 +/- 12 mumol/g dry wt during 40 minutes of metabolic inhibition. This value was calculated as 41.8% of intracellular potassium in the control heart and agreed with the decrement of intracellular potassium measured by NMR. During the metabolic inhibition and recovery period, a linear correlation was observed between the changes in 39K NMR-observed intracellular potassium and the cumulative potassium loss. The present results evaluate the inversion recovery technique as a method to successfully monitor the myocardial intracellular potassium.
采用基于细胞内钾(在8.45T时自旋晶格弛豫时间(T1)为8.3毫秒)比细胞外钾(68毫秒)快得多这一事实的反转恢复技术,在33℃下通过钾-39核磁共振(NMR)光谱法测量灌注大鼠心脏的细胞内钾含量。从代谢抑制(2 mM氰化物,0 mM葡萄糖)开始40分钟时,细胞内钾降至对照水平的60.2±4.3%(平均值±标准误,n = 6)。去除氰化物后,从氧化代谢重新开始30分钟时,细胞内钾恢复至94.2±3.9%。根据冠状动脉流出液的流速和钾浓度确定累积钾损失,在代谢抑制的40分钟内累积钾损失达到139±12 μmol/g干重。该值计算为对照心脏中细胞内钾的41.8%,与通过NMR测量的细胞内钾减少量一致。在代谢抑制和恢复期间,观察到39K NMR观察到的细胞内钾变化与累积钾损失之间存在线性相关性。本研究结果评估了反转恢复技术作为一种成功监测心肌细胞内钾的方法。