HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Donoso, P Articles by Eisner, D A Search for Related Content PubMed PubMed Citation Articles by Donoso, P Articles by Eisner, D A

Department of Veterinary Preclinical Sciences, University of Liverpool.

1. The fluorescent Na+ indicator SBFI was incorporated into isolated ventricular myocytes using the acetoxymethyl (AM) ester. 2. The excitation spectrum was found to be shifted about 20 nm in the cell compared to in vitro. In the cell, an increase of [Na+] decreased fluorescence at 380 nm (F380) and had no effect at 340 nm (F340). The ratio (R = F340/F380) was used as a measure of [Na+]i. 3. In vivo calibration of SBFI for [Na+]i was obtained by equilibrating [Na+] across the plasma membrane with a divalent-free solution in the presence of gramicidin D. 4. Selective removal of the surface membrane with saponin or digitonin released only about 50% of the indicator. Following saponin treatment, cyanide or carbonylcyanide m-chlorphenylhydrazone (CCCP) increased the apparent [Na+] measured by the remaining (presumably mitochondrial) SBFI. It is suggested that mitochondrial [Na+] is normally less than cytoplasmic. 5. Attempts to examine the effects of metabolic inhibition on [Na+]i were hampered by changes of autofluorescence due to changes of [NADH]. It is shown that this effect can be corrected for using the isosbestic signal (excited at 340 nm). 6. Inhibition of both aerobic metabolism (with CN-) and glycolysis (glucose removal or iodoacetate) produced a gradual increase of [Na+]i. This began before the resting contracture developed and may (via Na(+)-Ca2+ exchange) account for some of the rise of diastolic [Ca2+]i seen in previous work. The rise of [Na+]i began at about the same time as the decrease of systolic contraction and therefore at a time when [ATP]i had begun to fall.

This article has been cited by other articles:

				Z. Cao, J. George, W. H. Gerwick, D. G. Baden, J. D. Rainier, and T. F. Murray Influence of Lipid-Soluble Gating Modifier Toxins on Sodium Influx in Neocortical Neurons J. Pharmacol. Exp. Ther., August 1, 2008; 326(2): 604 - 613. [Abstract] [Full Text] [PDF]

				E. Murphy and C. Steenbergen Ion Transport and Energetics During Cell Death and Protection Physiology, April 1, 2008; 23(2): 115 - 123. [Abstract] [Full Text] [PDF]

				E. Murphy and C. Steenbergen Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury Physiol Rev, April 1, 2008; 88(2): 581 - 609. [Abstract] [Full Text] [PDF]

				R. Birkedal and H. A. Shiels High [Na+]i in cardiomyocytes from rainbow trout Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2007; 293(2): R861 - R866. [Abstract] [Full Text] [PDF]

				M.-H. T. Nguyen, S. J. Dudycha, and M. S. Jafri Effect of Ca2+ on cardiac mitochondrial energy production is modulated by Na+ and H+ dynamics Am J Physiol Cell Physiol, June 1, 2007; 292(6): C2004 - C2020. [Abstract] [Full Text] [PDF]

				S. Baron, A. Caplanusi, M. van de Ven, M. Radu, S. Despa, I. Lambrichts, M. Ameloot, P. Steels, and I. Smets Role of Mitochondrial Na+ Concentration, Measured by CoroNa Red, in the Protection of Metabolically Inhibited MDCK Cells J. Am. Soc. Nephrol., December 1, 2005; 16(12): 3490 - 3497. [Abstract] [Full Text] [PDF]

				T. Yamamoto, P. Swietach, A. Rossini, S.-H. Loh, R. D. Vaughan-Jones, and K. W. Spitzer Functional diversity of electrogenic Na+-HCO3- cotransport in ventricular myocytes from rat, rabbit and guinea pig J. Physiol., January 15, 2005; 562(2): 455 - 475. [Abstract] [Full Text] [PDF]

				S. Despa, J. Kockskamper, L. A. Blatter, and D. M. Bers Na/K Pump-Induced [Na]i Gradients in Rat Ventricular Myocytes Measured with Two-Photon Microscopy Biophys. J., August 1, 2004; 87(2): 1360 - 1368. [Abstract] [Full Text] [PDF]

				B. Pieske and S. R Houser [Na+]i handling in the failing human heart Cardiovasc Res, March 15, 2003; 57(4): 874 - 886. [Abstract] [Full Text] [PDF]

				D. M Bers, W. H Barry, and S. Despa Intracellular Na+ regulation in cardiac myocytes Cardiovasc Res, March 15, 2003; 57(4): 897 - 912. [Abstract] [Full Text] [PDF]

				B. Pieske, L. S. Maier, V. Piacentino III, J. Weisser, G. Hasenfuss, and S. Houser Rate Dependence of [Na+]i and Contractility in Nonfailing and Failing Human Myocardium Circulation, July 23, 2002; 106(4): 447 - 453. [Abstract] [Full Text] [PDF]

				J. An, S. G. Varadarajan, A. Camara, Q. Chen, E. Novalija, G. J. Gross, and D. F. Stowe Blocking Na+/H+ exchange reduces [Na+]i and [Ca2+]i load after ischemia and improves function in intact hearts Am J Physiol Heart Circ Physiol, December 1, 2001; 281(6): H2398 - H2409. [Abstract] [Full Text] [PDF]

				A. Diarra, C. Sheldon, and J. Church In situ calibration and [H+] sensitivity of the fluorescent Na+ indicator SBFI Am J Physiol Cell Physiol, June 1, 2001; 280(6): C1623 - C1633. [Abstract] [Full Text] [PDF]

				P. J. Cooper, M.-L. Ward, P. J. Hanley, G. R. Denyer, and D. S. Loiselle Metabolic consequences of a species difference in Gibbs free energy of Na+/Ca2+ exchange: rat versus guinea pig Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2001; 280(4): R1221 - R1229. [Abstract] [Full Text] [PDF]

				C. L. Overend, D. A. Eisner, and S. C. O'Neill Altered Cardiac Sarcoplasmic Reticulum Function of Intact Myocytes of Rat Ventricle During Metabolic Inhibition Circ. Res., February 2, 2001; 88(2): 181 - 187. [Abstract] [Full Text] [PDF]

				M.-L. Wu, C.-C. Chan, and M.-J. Su Possible Mechanism(s) of Arachidonic Acid-Induced Intracellular Acidosis in Rat Cardiac Myocytes Circ. Res., February 18, 2000; 86 (3): e55 - e62. [Abstract] [Full Text] [PDF]

				B. N. Eigel and R. W. Hadley Contribution of the Na+ channel and Na+/H+ exchanger to the anoxic rise of [Na+] in ventricular myocytes Am J Physiol Heart Circ Physiol, November 1, 1999; 277(5): H1817 - H1822. [Abstract] [Full Text] [PDF]

				E. Carmeliet Cardiac Ionic Currents and Acute Ischemia: From Channels to Arrhythmias Physiol Rev, July 1, 1999; 79(3): 917 - 1017. [Abstract] [Full Text] [PDF]

				H. S. Choi, D. Y. Wang, D. Noble, and C. O. Lee Effect of isoprenaline, carbachol, and Cs+ on Na+ activity and pacemaker potential in rabbit SA node cells Am J Physiol Heart Circ Physiol, January 1, 1999; 276(1): H205 - H214. [Abstract] [Full Text] [PDF]

				Z. Su, A. Zou, A. Nonaka, I. Zubair, M. C. Sanguinetti, and W. H. Barry Influence of prior Na+ pump activity on pump and Na+/Ca2+ exchange currents in mouse ventricular myocytes Am J Physiol Heart Circ Physiol, November 1, 1998; 275(5): H1808 - H1817. [Abstract] [Full Text] [PDF]

				M.E. Diaz, S.J. Cook, J.P. Chamunorwa, A.W. Trafford, M.K. Lancaster, S.C. O'Neill, and D.A. Eisner Variability of Spontaneous Ca2+ Release Between Different Rat Ventricular Myocytes Is Correlated With Na+-Ca2+ Exchange and [Na+]i Circ. Res., May 1, 1996; 78(5): 857 - 862. [Abstract] [Full Text]