Yoshino H
Sigfied and Janet Weis Center for Research, Geisinger Clinic.
Kokyu To Junkan. 1991 Nov;39(11):1151-7.
Isolated working rat hearts were exposed to 25 min ischemia, and functional recovery was assessed by aortic flow (AoF) and rate-pressure product (RPP) to evaluate the beneficial effects of potassium (20 mM) induced arrest (K-arrest) prior to ischemia. K-arrest improved the recovery of function after 30 min of reperfusion compared with the control group (%AoF: 68 +/- 6 vs 0%, %RPP: 90 +/- 3% vs 60 +/- 3%, p less than 0.01). The accumulation of Ca++ at the end of reperfusion was less in hearts with K-arrest (2.2 +/- 0.1 vs 4.5 +/- 0.3 mumol/g dry, p less than 0.01). There was no difference between the two groups in high energy phosphate content at the end of ischemia. The increase in intracellular Na+ (Nai) during ischemia was reduced in hearts with K-arrest (delta: 19 vs 46 mumol/g dry), and the level of intracellular K+ (Ki) was higher at the end of ischemia in hearts with K-arrest (341 +/- 4 vs 318 +/- 2 mumol/g dry, p less than 0.01). During the first 5 min of reperfusion, the level of Ki in K-arrested hearts jumped to a higher level than in the control group (delta: 15 vs 2 mumol/g dry, p less than 0.01). The level of Nai was lower in hearts with K-arrest after 5 min of reperfusion. These data suggested that K-arrest might preserve the activity of Na+/K+ ATPase during ischemia and early reperfusion, and that it attenuated the increase in Nai during ischemia and reperfusion, which resulted in less Ca++ overload during reperfusion via the Na+/Ca++ exchange mechanism and led to improved recovery.
将离体工作的大鼠心脏暴露于25分钟的缺血状态，通过主动脉流量（AoF）和速率-压力乘积（RPP）评估功能恢复情况，以评价缺血前钾离子（20 mM）诱导停搏（钾停搏）的有益作用。与对照组相比，钾停搏改善了再灌注30分钟后的功能恢复（AoF%：68±6 vs 0%，RPP%：90±3% vs 60±3%，p<0.01）。再灌注结束时，钾停搏心脏中钙离子的蓄积较少（2.2±0.1 vs 4.5±0.3 μmol/g干重，p<0.01）。缺血结束时，两组的高能磷酸盐含量无差异。钾停搏心脏在缺血期间细胞内钠离子（Nai）的增加减少（差值：19 vs 46 μmol/g干重），钾停搏心脏在缺血结束时细胞内钾离子（Ki）水平较高（341±4 vs 318±2 μmol/g干重，p<0.01）。在再灌注的前5分钟，钾停搏心脏中的Ki水平跃升至高于对照组的水平（差值：15 vs 2 μmol/g干重，p<0.01）。再灌注5分钟后，钾停搏心脏中的Nai水平较低。这些数据表明，钾停搏可能在缺血和早期再灌注期间维持钠钾ATP酶的活性，并且它减弱了缺血和再灌注期间Nai的增加，这通过钠钙交换机制导致再灌注期间较少的钙离子超载并导致恢复改善。
