Adenosine slows the rate of K+-induced membrane depolarization in ventricular cardiomyocytes: Possible implication in hyperkalemic cardioplegia

被引:26
作者
Alekseev, AE
Jovanovic, A
Lopez, JR
Terzic, A
机构
[1] MAYO CLIN & MAYO FDN, DEPT MED, DIV CARDIOVASC DIS, ROCHESTER, MN 55905 USA
[2] MAYO CLIN & MAYO FDN, DEPT PHARMACOL, ROCHESTER, MN 55905 USA
关键词
adenosine; K+; Ca2+; depolarization; cardioplegia; cardiomyocyte;
D O I
10.1006/jmcc.1996.0110
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Hyperkalemic cardioplegic solutions produce cardiac arrest during open heart surgery by depolarizing the sarcolemma, A recognized adverse effect of hyperkalemic cardioplegia is the possible development of ventricular dysfunction believed to be related to intracellular Ca2+ loading, a consequence of K+-induced membrane depolarization. Adenosine has been proposed as an adjunct to hyperkalemic cardioplegic solutions. However, it is not known whether adenosine can affect K+-induced membrane depolarization, and associated intracellular Ca2+ loading. Perforated patch-clamp method, applied to isolated single guinea-pig ventricular myocytes, revealed that adenosine (1 mM) did not significantly reduce the magnitude of K+-induced membrane depolarization (35.7 +/- 1.7 v 31.0 +/- 1.1 mV in the absence v presence of adenosine), Yet, adenosine significantly slowed the rate of K+-induced membrane depolarization (167 +/- 32.8 v 67.9 +/- 12.9 mV/min in the absence v presence of adenosine) without directly affecting Ca2+, Na+, and K+ currents. Imposed ramp-pulses, with different rates (ranging from 0.33 to 0.05 V/s), but same magnitude of depolarization (100 mV), demonstrated that reduction in the rate of membrane depolarization decreases net inward Ca2+ current. Indeed, in Fluo-3 loaded ventricular myocytes, imaged by laser confocal microscopy, adenosine (1 mM) prevented K+- induced intracellular Ca2+ loading. The present findings indicate that adenosine slows the rate of K+-induced membrane depolarization, and reduces K+-induced intracellular Ca2+ loading in ventricular myocytes. Such findings support the notion that adenosine may play a cardioprotective role in hyperkalemic cardioplegia. (C) 1996 Academic Press Limited
引用
收藏
页码:1193 / 1202
页数:10
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