Heterogeneous changes in action potential and intracellular Ca2+ in left ventricular myocyte sub-types from rabbits with heart failure.
暂无分享,去创建一个
[1] F. Charpentier,et al. Electrophysiologic characteristics of cells spanning the left ventricular wall of human heart: evidence for presence of M cells. , 1995, Journal of the American College of Cardiology.
[2] S. Pogwizd,et al. Biochemical and electrophysiological alterations underlying ventricular arrhythmias in the failing heart. , 1994, European heart journal.
[3] G. Gintant,et al. Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells. , 1991, Circulation research.
[4] W Grossman,et al. Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure. , 1987, Circulation research.
[5] R. Tsien,et al. A new generation of Ca2+ indicators with greatly improved fluorescence properties. , 1985, The Journal of biological chemistry.
[6] A. Varró,et al. Estimate of net calcium fluxes and sarcoplasmic reticulum calcium content during systole in rat ventricular myocytes. , 1995, The Journal of physiology.
[7] A. Levi,et al. Effect on the fura‐2 transient of rapidly blocking the Ca2+ channel in electrically stimulated rabbit heart cells. , 1996, The Journal of physiology.
[8] A. Gerdes,et al. Differences in regional capillary distribution and myocyte sizes in normal and hypertrophic rat hearts. , 1979, The American journal of anatomy.
[9] R A Bassani,et al. Calibration of indo-1 and resting intracellular [Ca]i in intact rabbit cardiac myocytes. , 1995, Biophysical journal.
[10] Sarcoplasmic reticulum Ca2+ loading in rabbits 8 and 15 weeks after coronary artery ligation , 1998, Pflügers Archiv.
[11] J. Chamunorwa,et al. Regional differences in the regulation of intracellular sodium and in action potential configuration in rabbit left ventricle , 1997, Pflügers Archiv.
[12] Action potential prolongation and potassium currents in left-ventricular myocytes isolated from hypertrophied rabbit hearts. , 1998, Journal of molecular and cellular cardiology.
[13] S. Houser,et al. Calcium currents in normal and hypertrophied isolated feline ventricular myocytes. , 1988, The American journal of physiology.
[14] E. Sonnenblick,et al. The cellular basis of dilated cardiomyopathy in humans. , 1995, Journal of molecular and cellular cardiology.
[15] S. Oparil,et al. Regional Myocyte Size in Normotensive and Spontaneously Hypertensive Rats , 1979, Hypertension.
[16] A comparative study of four methods for analysing repeated measures data. , 1996, Statistics in medicine.
[17] S. Cobbe,et al. Arrhythmogenesis in experimental models of heart failure: the role of increased load. , 1996, Cardiovascular research.
[18] W. Giles,et al. Regional variations in action potentials and transient outward current in myocytes isolated from rabbit left ventricle. , 1991, The Journal of physiology.
[19] C. Gibbs,et al. Effect of Changes in Frequency of Stimulation Upon Rabbit Ventricular Action Potential , 1961, Circulation research.
[20] G. Steinbeck,et al. Regional differences in current density and rate-dependent properties of the transient outward current in subepicardial and subendocardial myocytes of human left ventricle. , 1996, Circulation.
[21] Godfrey L. Smith,et al. Non-uniform prolongation of intracellular Ca2+ transients recorded from the epicardial surface of isolated hearts from rabbits with heart failure. , 1998, Cardiovascular research.
[22] S. Chugh,et al. Isolated myocyte contractile function is normal in postinfarct remodeled rat heart with systolic dysfunction. , 1997, Circulation.
[23] C Antzelevitch,et al. Distribution of M Cells in the Canine Ventricle , 1994, Journal of cardiovascular electrophysiology.
[24] F. Takatsu,et al. Cigarette Smoking Is a Major Risk Factor for Coronary Spasm , 1993, Circulation.
[25] R. Aronson,et al. Cellular mechanisms of arrhythmias in hypertrophied and failing myocardium , 1993 .
[26] G Olivetti,et al. Cellular basis of ventricular remodeling after myocardial infarction. , 1991, The American journal of cardiology.
[27] C. H. Conrad,et al. Intracellular calcium transients in myocardium from spontaneously hypertensive rats during the transition to heart failure. , 1991, Circulation research.
[28] C. Vahl,et al. Intracellular calcium transient of working human myocardium of seven patients transplanted for congestive heart failure. , 1994, Circulation research.
[29] S. Bryant,et al. Effects of hypertrophy on regional action potential characteristics in the rat left ventricle: a cellular basis for T-wave inversion? , 1997, Circulation.
[30] P. Poole‐Wilson,et al. Cellular mechanisms of contractile dysfunction in human heart failure. , 1996, European heart journal.
[31] E. Kranias,et al. Phospholamban: a prominent regulator of myocardial contractility. , 1996, Circulation research.
[32] M. Weiner,et al. Endocardial versus epicardial differences of intracellular free calcium under normal and ischemic conditions in perfused rat hearts. , 1993, Circulation research.
[33] R. Robinson,et al. Frequency dependent effects on Cai transients and cell shortening in myocytes that survive in the infarcted heart. , 1997, Cardiovascular research.
[34] R A Bassani,et al. Temperature and relative contributions of Ca transport systems in cardiac myocyte relaxation. , 1996, The American journal of physiology.
[35] E. Sonnenblick,et al. Myocyte cellular hypertrophy is responsible for ventricular remodelling in the hypertrophied heart of middle aged individuals in the absence of cardiac failure. , 1994, Cardiovascular research.
[36] S. Cobbe,et al. Ventricular fibrillation threshold and local dispersion of refractoriness in isolated rabbit hearts with left ventricular dysfunction , 2000, Basic Research in Cardiology.
[37] A. Gerdes,et al. Regional changes in myocyte size during the reversal of thyroid-induced cardiac hypertrophy. , 1988, Journal of molecular and cellular cardiology.
[38] M. Boyett,et al. Diastolic, systolic and sarcoplasmic reticulum [Ca2+] during inotropic interventions in isolated rat myocytes. , 1991, The Journal of physiology.
[39] E. Sonnenblick,et al. Relation of Ultrastructure to Function in the Intact Heart: Sarcomere Structure Relative to Pressure Volume Curves of Intact Left Ventricles of Dog and Cat , 1966, Circulation research.
[40] G. Hart. Cellular electrophysiology in cardiac hypertrophy and failure. , 1994, Cardiovascular research.
[41] D. Bers,et al. Kinetics of [Ca]i decline in cardiac myocytes depend on peak [Ca]i. , 1995, The American journal of physiology.
[42] D. Garcia-Dorado,et al. Cardiovascular Research , 1966 .
[43] J M de Bakker,et al. Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts. , 1994, Cardiovascular research.
[44] S. Pogwizd,et al. Nonreentrant mechanisms underlying spontaneous ventricular arrhythmias in a model of nonischemic heart failure in rabbits. , 1995, Circulation.
[45] S. Cobbe,et al. Comparison of in vivo and in vitro haemodynamic function in experimental heart failure: use of echocardiography. , 1996, Cardiovascular research.
[46] S. Litwin,et al. Enhanced Na(+)-Ca2+ exchange in the infarcted heart. Implications for excitation-contraction coupling. , 1997, Circulation Research.
[47] M. Mitchell,et al. RABBITS , 2009, Lancet.
[48] C. Antzelevitch,et al. Transient Outward Current Prominent in Canine Ventricular Epicardium but Not Endocardium , 1988, Circulation research.
[49] E Erdmann,et al. Intracellular Calcium Handling in Isolated Ventricular Myocytes From Patients With Terminal Heart Failure , 1992, Circulation.
[50] G. Vassort,et al. Regional alteration of the transient outward current in human left ventricular septum during compensated hypertrophy. , 1997, Circulation.
[51] W. Parmley,et al. Intracellular Ca2+ handling and vulnerability to ventricular fibrillation in spontaneously hypertensive rats. , 1997, Hypertension.
[52] Godfrey L. Smith,et al. The effects of metabolic inhibition on intracellular calcium and pH in isolated rat ventricular cells. , 1989, The Journal of physiology.
[53] K. Mahaffey,et al. Left ventricular performance and remodeling in rabbits after myocardial infarction. Effects of a thyroid hormone analogue. , 1995, Circulation.
[54] W. Wier,et al. Mechanism of release of calcium from sarcoplasmic reticulum of guinea‐pig cardiac cells. , 1988, The Journal of physiology.
[55] S. Bishop,et al. Regional myocyte size in two-kidney, one clip renal hypertension. , 1988, Journal of molecular and cellular cardiology.
[56] S. Bryant,et al. Regional differences in electrical and mechanical properties of myocytes from guinea-pig hearts with mild left ventricular hypertrophy. , 1997, Cardiovascular research.
[57] S. Lehnart,et al. Relationship between Na+-Ca2+-exchanger protein levels and diastolic function of failing human myocardium. , 1999, Circulation.
[58] F. Siri,et al. Depressed intracellular calcium transients and contraction in myocytes from hypertrophied and failing guinea pig hearts. , 1991, The American journal of physiology.
[59] Shinfuku Nomura,et al. Effects of changes in frequency of ultrasonic vibrations on heat transfer , 2000 .