Cardiology of Xijing hospital, Fourth Military Medical University, 710032, Xi'an, China.
Int J Cardiol. 2010 Apr 15;140(2):161-8. doi: 10.1016/j.ijcard.2008.11.037. Epub 2008 Dec 6.
The effects of low K(+) on post-ischemic reperfused heart cells are not clearly understood. Calcium overload is one of the major causes for myocardial reperfusion injury, the present study was to investigate the role of intracellular calcium oscillations in the effects of reperfusion with low K(+) on rat myocytes.
Ischemic myocytes were reperfused with Tyrode solution containing K(+) at 5.4 (control) or 3.0 mM (low K(+)) for 10 min. the changes of intracellular calcium was recorded by spectrofluorometry. The exclusion of trypan blue by myocytes served as indices of viability. Measurements of cell length, reverse-mode Na(+)-Ca(2+) exchanger (NCX) and Na(+), K(+) ATPase activity were performed.
Compared to control, myocytes reperfused with low K(+) had greater number of calcium oscillations and reverse-mode NCX activity, which were accompanied with decreased cell length recovery and cell viability. Reperfusion with KB-R7943, an inhibitor of reverse-mode NCX, attenuated the effects of low K(+) on all the parameters. Inhibition of Na(+), K(+) ATPase with Ouabain increased the susceptibility to calcium oscillations in myocytes reperfused with low K(+), which was accompanied with cell length shortening and decreased cell viability. Reperfusion with K(+) at 9.0 mM, which activated Na(+), K(+) ATPase, attenuated calcium oscillations, protected cell length recovery, and increased cell viability.
These results suggest that increased calcium oscillations mediate the exacerbating reperfusion injury with low K(+) on myocytes, and inhibition of Na(+), K(+) ATPase activity and increase of reverse-mode NCX activity contribute to these effects.
低 K(+)对缺血后再灌注心脏细胞的影响尚不清楚。钙超载是心肌再灌注损伤的主要原因之一，本研究旨在探讨细胞内钙振荡在低 K(+)再灌注对大鼠心肌细胞的影响中的作用。
用含 5.4（对照）或 3.0 mM（低 K(+)）K(+)的 Tyrode 溶液对缺血心肌细胞进行 10 分钟再灌注。通过荧光分光光度法记录细胞内钙的变化。用台盼蓝排斥法测定心肌细胞活力。测量细胞长度、反向模式钠钙交换体（NCX）和钠钾 ATP 酶活性。
与对照相比，用低 K(+)再灌注的心肌细胞钙振荡次数更多，反向模式 NCX 活性更高，细胞长度恢复和细胞活力降低。用反向模式 NCX 抑制剂 KB-R7943 再灌注可减弱低 K(+)对所有参数的影响。用哇巴因抑制钠钾 ATP 酶增加了低 K(+)再灌注心肌细胞钙振荡的易感性，同时伴随着细胞长度缩短和细胞活力降低。用 9.0 mM 的 K(+)再灌注可激活钠钾 ATP 酶，减弱钙振荡，保护细胞长度恢复，增加细胞活力。
这些结果表明，增加的钙振荡介导了低 K(+)对心肌细胞再灌注损伤的加重作用，抑制钠钾 ATP 酶活性和增加反向模式 NCX 活性有助于这种作用。
