Hayashi H
Department of Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University, Japan.
Nagoya J Med Sci. 2000 Nov;63(3-4):91-8.
To study the regulation of [Na+]i and [Ca2+]i during myocardial ischemia/reperfusion, [Na+]i and [Ca2+]i were measured simultaneously using guinea pig ventricular myocytes which were dual-loaded with SBFI/AM and fluo-3/AM. It was suggested that: (1) [Na+]i increased during metabolic inhibition (MI: 3.3 mM amytal and 5 microM CCCP) by both the activated Na+ influx via Na+/H+ exchange and the suppressed Na+ extrusion via the Na+/K+ pump; (2) Na+/Ca2+ exchange was inhibited during MI, causing the dissociation between [Na+]i and [Ca2+]i; (3) Na+/Ca2+ exchange could be reactivated by energy repletion, resulting in a significant increase in [Ca2+], Furthermore, a Ca2+ influx via the reverse-mode of Na+/Ca2+ exchange may play a key role in the mechanism of Ca2+ overload on reoxygenation; and (4) cell contracture during MI was related to rigor due to energy depletion, while cell contracture after energy repletion was likely to be related to Ca2+ overload.
为研究心肌缺血/再灌注过程中胞内钠离子浓度（[Na⁺]i）和钙离子浓度（[Ca²⁺]i）的调节机制，采用同时装载了SBFI/AM和fluo-3/AM的豚鼠心室肌细胞同步测量[Na⁺]i和[Ca²⁺]i。结果表明：（1）在代谢抑制（MI：3.3 mM戊巴比妥和5 μM CCCP）期间，[Na⁺]i升高，其机制为通过Na⁺/H⁺交换激活Na⁺内流以及通过Na⁺/K⁺泵抑制Na⁺外流；（2）MI期间Na⁺/Ca²⁺交换被抑制，导致[Na⁺]i与[Ca²⁺]i解离；（3）能量补充可使Na⁺/Ca²⁺交换重新激活，导致[Ca²⁺]显著升高。此外，通过Na⁺/Ca²⁺交换反向模式的Ca²⁺内流可能在复氧时Ca²⁺超载机制中起关键作用；（4）MI期间的细胞挛缩与能量耗竭导致的强直收缩有关，而能量补充后的细胞挛缩可能与Ca²⁺超载有关。
