Ca2+ Sparks and Ca2+ waves are the subcellular events underlying Ca2+ overload during ischemia and reperfusion in perfused intact hearts

Journal of Molecular and Cellular Cardiology

Volumn 79, Issue , 2015, Pages 69-78

  Mattiazzi, Alicia ^a   Argenziano, Mariana ^b,c   Aguilar Sanchez, Yuriana ^c   Mazzocchi, Gabriela ^a   Escobar, Ariel L ^c  

^a UNIVERSIDAD NACIONAL DE LA PLATA   (Argentina)

^b UNIVERSIDAD NACIONAL DE SAN MARTÍN   (Argentina)

^c University of California   (United States)

Author keywords

Ca2+ sparks; Intact heart; Ischemia reperfusion

Indexed keywords

CALCIUM ION; CALCIUM; MESSENGER RNA;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM CELL LEVEL; CALCIUM CONDUCTANCE; CONFOCAL MICROSCOPY; CONTROLLED STUDY; CYTOSOL; DIASTOLE; HEART CONDUCTION; HEART INFARCTION; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; HEART PERFUSION; MALE; MOUSE; NONHUMAN; REPERFUSION INJURY; ANIMAL; C57BL MOUSE; CALCIUM SIGNALING; CARDIAC MUSCLE CELL; CELL FRACTIONATION; CELL SEPARATION; GENETICS; HEART; HEART VENTRICLE; IN VITRO STUDY; KINETICS; METABOLISM; MYOCARDIAL ISCHEMIA REPERFUSION INJURY; PATHOLOGY; PATHOPHYSIOLOGY; PERFUSION;

ANIMALS; CALCIUM; CALCIUM SIGNALING; CELL SEPARATION; HEART; HEART VENTRICLES; IN VITRO TECHNIQUES; KINETICS; MALE; MICE, INBRED C57BL; MYOCARDIAL REPERFUSION INJURY; MYOCYTES, CARDIAC; PERFUSION; RNA, MESSENGER; SUBCELLULAR FRACTIONS;

EID: 84910669192     PISSN: 00222828     EISSN: 10958584     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2014.10.011     Document Type: Article

References (44)

1. Marban E., Kitakaze M., Kusuoka H., Porterfield J.K., Yue D.T., Chacko V.P. Intracellular free calcium concentration measured with 19F NMR spectroscopy in intact ferret hearts. Proc Natl Acad Sci U S A 1987, 84:6005-6009.
2. 2+ ]m overload in rat hearts. Am J Physiol 1996, 271:H2145-H2153.
3. + exchange, against the development of rigor contracture in rat ventricular myocytes. Exp Physiol 2000, 85:17-25.
4. 2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion. Cardiovasc Res 2010, 85:671-680.
5. Pike M.M., Kitakaze M., Marban E. 23Na-NMR measurements of intracellular sodium in intact perfused ferret hearts during ischemia and reperfusion. Am J Physiol 1990, 259:H1767-H1773.
6. Inserte J., Barba I., Hernando V., Garcia-Dorado D. Delayed recovery of intracellular acidosis during reperfusion prevents calpain activation and determines protection in postconditioned myocardium. Cardiovasc Res 2009, 81:116-122.
7. Murphy E., Perlman M., London R.E., Steenbergen C. Amiloride delays the ischemia-induced rise in cytosolic free calcium. Circ Res 1991, 68:1250-1258.
8. + overload in isolated rat hearts. Am J Physiol Heart Circ Physiol 2005, 288:H287-H292.
9. + overload in rat hearts. Mol Cell Biochem 2007, 297:101-110.
10. 2+ channel alpha1 subunit and reduced ischemia/reperfusion injury. Circ Res 2006, 98:403-411.
11. Neely J.R., Rovetto M.J., Whitmer J.T., Morgan H.E. Effects of ischemia on function and metabolism of the isolated working rat heart. Am J Physiol 1973, 225:651-658.
12. Steenbergen C., Perlman M.E., London R.E., Murphy E. Mechanism of preconditioning. Ionic alterations. Circ Res 1993, 72:112-125.
13. Kass R.S., Tsien R.W. Fluctuations in membrane current driven by intracellular calcium in cardiac purkinje fibers. Biophys J 1982, 38:259-269.
14. Marban E., Robinson S.W., Wier W.G. Mechanisms of arrhythmogenic delayed and early afterdepolarizations in ferret ventricular muscle. J Clin Invest 1986, 78:1185-1192.
15. 2+ activation of contractionas a consequence of reperfusion-induced cellular calcium overload inferret hearts. J Clin Invest 1987, 79:950-961.
16. Piper H.M., Abdallah Y., Schafer C. The first minutes of reperfusion: a window of opportunity for cardioprotection. Cardiovasc Res 2004, 61:365-371.
17. Dou Y., Arlock P., Arner A. Blebbistatin specifically inhibits actin-myosin interaction in mouse cardiac muscle. Am J Cell Physiol 2007, 293:C1148-C1153.
18. 2+ release underlies the development of phase 2 in mouse ventricular action potentials. Am J Physiol Heart Circ Physiol 2012, 302(5):H1160-H1172.
19. 2+ after perfusion arrest in isolated, perfused mouse heart. Cardiovasc Res 2006, 70:335-345.
20. Mejía-Alvarez R., Manno C., Villalba-Galea C.A., Fernández L.D.V., Ribeiro Costa R., Fill M., et al. Pulsed local-field fluorescence microscopy: a new approach for measuring cellular signals in the beating heart. Pflugers Arch 2002, 445(6):747-758.
21. McManus O.B., Blatz A.L., Magleby K.L. Sampling, log binning, fitting, and plotting durations of open and shut intervals from single channels and the effects of noise. Pflugers Arch 1987, 410:530-553.
22. Sigworth F.J., Sine S.M. Data transformations for improved display and fitting of single- channel dwell time histograms. Biophys J 1987, 52:1047-1054.
23. 2+ 'sparks' and waves in intact ventricular muscle resolved by confocal imaging. Circ Res 1997, 81:462-469.
24. Boyett M.R. Effect of rate-dependent changes in the transient outward current on the action potential in sheep Purkinje fibres. J Physiol 1981, 319:23-41.
25. Litovsky S.H., Antzelevitch C. Transient outward current prominent in canine ventricular epicardium but not endocardium. Circ Res 1988, 62(1):116-126.
26. Cheng H., Lederer W.J., Cannell M.B. Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle. Science 1993, 262:740-744.
27. Kockskämper J., Sheehan K.A., Bare D.J., Lipsius S.L., Mignery G.A., Blatter L.A. Activation and propagation of Ca(2+) release during excitation-contraction coupling in atrial myocytes. Biophys J 2001, 81:2590-2605.
28. 2+ Signaling in Intact Mouse Heart. J Mol Cell Cardiol 2012, 3(6):768-779.
29. 2+ spark mass. J Mol Cell Cardiol 2010, 48:293-301.
30. 2+ waves in permeabilized myocytes lacking calsequestrin. J Mol Cell Cardiol 2011, 51:760-768.
31. 2+ /calmodulin-dependent protein kinase II. Am J Physiol Heart Circ Physiol 2008, 295:H1669-H1683.
32. Said M., Becerra R., Valverde C.A., et al. Calcium-calmodulin dependent protein kinase II (CaMKII): a main signal responsible for early reperfusion arrhythmias. J Mol Cell Cardiol 2011, 51:936-944.
33. Takamatsu T., Wier W.G. Calcium waves in mammalian heart: quantification of origin, magnitude, waveform, and velocity. FASEB J 1990, 4:1519-1525.
34. i waves in cardiac myocytes. Am J Physiol 1996, 270:C148-C159.
35. Kubalova Z., Gyorke I., Terentyeva R., et al. Modulation of cytosolic and intra-sarcoplasmic reticulum calcium waves by calsequestrin in rat cardiac myocytes. J Physiol 2004, 561:515-524.
36. Lloyd-Jones D., Adams R., Carnethon M., et al. Heart disease and stroke statistics-2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2009, 119:e181.
37. Gomez A.M., Guatimosim S., Dilly K.W., Vassort G., Lederer W.J. Heart failure after myocardial infarction: altered excitation-contraction coupling. Circulation 2001, 104:688-693.
38. Di Virgilio F., Steinberg T.H., Swanson J.A., Silverstein S.C. Fura-2 secretion and sequestration in macrophages. A blocker of organic anion transport reveals that these processes occur via a membrane transport system for organic anions. J Immunol 1988, 140:915-920.
39. 2+-ATPase of cardiac sarcoplasmic reticulum. A comparison with skeletal sarcoplasmic reticulum. Circ Res 1982, 50:310-317.
40. Salerno J.A., Previtali M., Chimienti M., Klersy C., Bobba P. Vasospasm and ventricular arrhythmias. Ann N Y Acad Sci 1984, 427:222-233.
41. Lakireddy V., Bub G., Baweja P., Syed A., Boutjdir M., El-Sherif N. The kinetics of spontaneous calcium oscillations and arrhythmogenesis in the in vivo heart during ischemia/reperfusion. Heart Rhythm 2006, 3:58-66.
42. Pogwizd S.M., Corr P.B. Electrophysiologic mechanisms underlying arrhythmias due to reperfusion of ischemic myocardium. Circulation 1987, 72:404-426.
43. Saint D.A. The role of the persistent Na(+) current during cardiac ischemia and hypoxia. J Cardiovasc Electrophysiol 2006, 17(Suppl. 1):S96-S103.
44. Pentecost B.L., Bennett M.A., George C.F. Bradyarrhythmia complicating myocardial infarction. Lancet 1968, 2:1300-1301.