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胞内高钙诱发豚鼠心室肌细胞电紊乱

, PP. 38-45

Keywords: 细胞内钙,心律失常,动作电位,离子流,心肌细胞

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Abstract:

众多研究表明,各种心肌病理状态及心律失常的发生都与细胞内钙离子([Ca2+]i)调控失衡及钙超载有着十分密切的关系.为了进一步揭示细胞内急性钙超载对心室肌细胞电生理特性的影响,通过调节[Ca2+]i(对照组为65~100nmol/L,胞内高钙组为1μmol/L)模拟胞内钙超载状态,应用全细胞膜片钳技术记录细胞跨膜动作电位及各种离子电流变化,探讨胞内高钙引发心肌细胞电活动紊乱机制.结果表明,胞内高钙显著缩短动作电位时程(APD),减小动作电位幅值(APA)和最大除极速率(vmax),降低静息膜电位(RMP),并可引发迟发后除极(DADs)和触发激动;胞内高钙呈时间依赖性地增大晚钠电流(INaL)及快速延迟整流钾电流(IKr),减小L型钙电流和内向整流钾电流(IK1),但对缓慢延迟整流钾电流(IKs)无明显影响.本研究表明,胞内高钙可调节上述诸离子流活动导致细胞跨膜电位异常进而引发心室肌细胞电紊乱,为钙超载所致室性心律失常的机制提供了理论依据.

References

[1]  1 Berridge M J. Elementary and global aspects of calcium signalling. J Physiol, 1997, 499(Pt 2): 291-306
[2]  2 de Diego C, Pai R K, Chen F, et al. Electrophysiological consequences of acute regional ischemia/reperfusion in neonatal rat ventricular myocyte monolayers. Circulation, 2008, 118: 2330-2337??
[3]  3 Casini S, Verkerk A O, van Borren M M, et al. Intracellular calcium modulation of voltage-gated sodium channels in ventricular myocytes. Cardiovasc Res, 2009, 81: 72-81??
[4]  4 Koster O F, Szigeti G P, Beuckelmann D J. Characterization of a
[5]  [Ca2+]i-dependent current in human atrial and ventricular cardiomyocytes in the absence of Na+ and K+. Cardiovasc Res, 1999, 41: 175-187??
[6]  5 Rocchetti M, Besana A, Mostacciuolo G, et al. Diverse toxicity associated with cardiac Na+/K+ pump inhibition: evaluation of electrophysiological mechanisms. J Pharmacol Exp Ther, 2003, 305: 765-771??
[7]  6 Shutt R H, Ferrier G R, Howlett S E. Increases in diastolic
[8]  [Ca2+] can contribute to positive inotropy in guinea pig ventricular myocytes in the absence of changes in amplitudes of Ca2+ transients. Am J Physiol Heart Circ Physiol, 2006, 291: H1623-1634??
[9]  7 Kihara Y, Morgan J P. Intracellular calcium and ventricular fibrillation. Studies in the aequorin-loaded isovolumic ferret heart. Circ Res, 1991, 68: 1378-1389
[10]  8 Zaugg C E, Wu S T, Lee R J, et al. Importance of calcium for the vulnerability to ventricular fibrillation detected by premature ventricular stimulation: single pulse versus sequential pulse methods. J Mol Cell Cardiol, 1996, 28: 1059-1072??
[11]  9 Lakatta E G, Capogrossi M C, Kort A A, et al. Spontaneous myocardial calcium oscillations: overview with emphasis on ryanodine and caffeine. Fed Proc, 1985, 44: 2977-2983
[12]  10 Song Y, Shryock J C, Wagner S, et al. Blocking late sodium current reduces hydrogen peroxide-induced arrhythmogenic activity and contractile dysfunction. J Pharmacol Exp Ther, 2006, 318: 214-222??
[13]  11 Xie L H, Chen F, Karagueuzian H S, et al. Oxidative-stress-induced afterdepolarizations and calmodulin kinase II signaling. Circ Res, 2009, 104: 79-86??
[14]  12 Karin R. S. Calcium overload, spontaneous calcium release, and ventricular arrhythmias. Heart Rhythm, 2006, 3: 977-979??
[15]  13 Clusin W T. Calcium and cardiac arrhythmias: DADs, EADs, and alternans. Crit Rev Clin Lab Sci, 2003, 40: 337-375??
[16]  14 Nakajima I, Watanabe H, Iino K, et al. Ca2+ overload evokes a transient outward current in guinea-pig ventricular myocytes. Circ J, 2002, 66: 87-92??
[17]  15 Wang Y, Tandan S, Cheng J, et al. Ca2+/calmodulin-dependent protein kinase II-dependent remodeling of Ca2+ current in pressure overload heart failure. J Biol Chem, 2008, 283: 25524-25532??
[18]  16 Livshitz L M, Rudy Y. Regulation of Ca2+ and electrical alternans in cardiac myocytes: role of CAMKII and repolarizing currents. Am J Physiol Heart Circ Physiol, 2007, 292: H2854-2866??
[19]  17 Ho P D, Fan J S, Hayes N L, et al. Ras reduces L-type calcium channel current in cardiac myocytes. Corrective effects of L-channels and SERCA2 on
[20]  [Ca(2+)](i) regulation and cell morphology. Circ Res, 2001, 88: 63-69
[21]  18 Heath B M, Terrar D A. Protein kinase C enhances the rapidly activating delayed rectifier potassium current, IKr, through a reduction in C-type inactivation in guinea-pig ventricular myocytes. J Physiol, 2000, 522(Pt 3): 391-402??
[22]  19 Walsh K B, Zhang J. Neonatal rat cardiac fibroblasts express three types of voltage-gated K+ channels: regulation of a transient outward current by protein kinase C. Am J Physiol Heart Circ Physiol, 2008, 294: H1010-1017??
[23]  20 McGuigan J A, Luthi D, Buri A. Calcium buffer solutions and how to make them: a do it yourself guide. Can J Physiol Pharmacol, 1991, 69: 1733-1749
[24]  21 Maltsev V A, Reznikov V, Undrovinas N A, et al. Modulation of late sodium current by Ca2+, calmodulin, and CaMKII in normal and failing dog cardiomyocytes: similarities and differences. Am J Physiol Heart Circ Physiol, 2008, 294: H1597-1608??
[25]  22 Richard S, Perrier E, Fauconnier J, et al. ''Ca(2+)-induced Ca(2+) entry'' or how the L-type Ca(2+) channel remodels its own signalling pathway in cardiac cells. Prog Biophys Mol Biol, 2006, 90: 118-135??
[26]  23 Tsuji Y, Opthof T, Kamiya K, et al. Pacing-induced heart failure causes a reduction of delayed rectifier potassium currents along with decreases in calcium and transient outward currents in rabbit ventricle. Cardiovasc Res, 2000, 48: 300-309??
[27]  24 Mukherjee R, Hewett K W, Spinale F G. Myocyte electrophysiological properties following the development of supraventricular tachycardia-induced cardiomyopathy. J Mol Cell Cardiol, 1995, 27: 1333-1348??
[28]  25 Fauconnier J, Lacampagne A, Rauzier J M, et al. Ca2+-dependent reduction of IK1 in rat ventricular cells: a novel paradigm for arrhythmia in heart failure? Cardiovasc Res, 2005, 68: 204-212
[29]  26 Nitta J, Furukawa T, Marumo F, et al. Subcellular mechanism for Ca(2+)-dependent enhancement of delayed rectifier K+ current in isolated membrane patches of guinea pig ventricular myocytes. Circ Res, 1994, 74: 96-104
[30]  27 Klockner U, Isenberg G. Calmodulin antagonists depress calcium and potassium currents in ventricular and vascular myocytes. Am J Physiol, 1987, 253: H1601-1611
[31]  28 Cheng T O. Digitalis administration: an underappreciated but common cause of short QT interval. Circulation, 2004, 109: e152; author reply e152??
[32]  29 Schimpf R, Borggrefe M, Wolpert C. Clinical and molecular genetics of the short QT syndrome. Curr Opin Cardiol, 2008, 23: 192-198??
[33]  30 Vlasblom R, Muller A, Musters R J, et al. Contractile arrest reveals calcium-dependent stimulation of SERCA2a mRNA expression in cultured ventricular cardiomyocytes. Cardiovasc Res, 2004, 63: 537-544??
[34]  31 Tohse N, Kameyama M, Sekiguchi K, et al. Protein kinase C activation enhances the delayed rectifier potassium current in guinea-pig heart cells. J Mol Cell Cardiol, 1990, 22: 725-734??
[35]  32 O-Uchi J, Sasaki H, Morimoto S, et al. Interaction of alpha1-adrenoceptor subtypes with different G proteins induces opposite effects on cardiac L-type Ca2+ channel. Circ Res, 2008, 102: 1378-1388??
[36]  33 Zaza A, Belardinelli L, Shryock J C. Pathophysiology and pharmacology of the cardiac “late sodium current.” Pharmacol Ther, 2008, 119: 326-339??
[37]  34 Berlin J R, Cannell M B, Lederer W J. Cellular origins of the transient inward current in cardiac myocytes. Role of fluctuations and waves of elevated intracellular calcium. Circ Res, 1989, 65: 115-126
[38]  35 Goldhaber J I. Free radicals enhance Na+/Ca2+ exchange in ventricular myocytes. Am J Physiol, 1996, 271: H823-833
[39]  36 Zygmunt A C, Gibbons W R. Calcium-activated chloride current in rabbit ventricular myocytes. Circ Res, 1991, 68: 424-437
[40]  37 Noble D, Noble P J. Late sodium current in the pathophysiology of cardiovascular disease: consequences of sodium-calcium overload. Heart, 2006, 92: iv1-iv5??
[41]  38 Levi A J, Dalton G R, Hancox J C, et al. Role of intracellular sodium overload in the genesis of cardiac arrhythmias. J Cardiovasc Electrophysiol, 1997, 8: 700-721??
[42]  39 Belardinelli L, Shryock J C, Fraser H. Inhibition of the late sodium current as a potential cardioprotective principle: effects of the late sodium current inhibitor ranolazine. Heart, 2006, 92: iv6-iv14

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