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 Elliott, A C Articles by Allen, D G Search for Related Content PubMed PubMed Citation Articles by Elliott, A C Articles by Allen, D G

Department of Physiological Sciences, University of Manchester.

1. The metabolic consequences of an increase in the frequency of stimulation were examined in isolated ferret hearts. Intracellular pH (pHi) and the intracellular concentrations of phosphocreatine ([PCr]i), inorganic phosphate ([Pi]i) and ATP were measured by 31P nuclear magnetic resonance (NMR) spectroscopy. 2. Increasing the stimulus rate from 0.1-0.7 to 2 Hz caused an increase in [Pi]i and a decrease recovery of both [PCr]i and [Pi]i during continued stimulation. There was no change in [ATP]i during stimulation at 2 Hz. Increasing the stimulus rate caused an intracellular acidosis of around 0.1 pH units. 3. Increasing the stimulus rate generally caused an initial increase in developed pressure, followed by a decrease over 1-2 min to a steady level slightly lower than developed pressure at the low (control) stimulus rate. The increase in stimulus rate caused a 4- to 6-fold increase in time-averaged muscle activity. 4. Both oxygen uptake and production of lactate increased on 2 Hz stimulation. Lactate production accounted for less than 5% of ATP production at low or high stimulus rates, suggesting that significant anoxia was not occurring during stimulation. The observed lactate production was, however, sufficient to explain most of the intracellular acidosis observed when the stimulus rate was raised. When glycolysis was prevented by removal of glucose and depletion of glycogen stores, 2 Hz stimulation was accompanied by an intracellular alkalosis rather than an acidosis, suggesting that lactate production by glycolysis was the cause of the intracellular acidosis. 5. Reducing the rate of glycolysis increased the size of changes in [PCr]i and [Pi]i evoked by stimulation at 2 Hz. Furthermore, there was now no partial reversal of the changes in [PCr]i and [Pi]i during 2 Hz stimulation. 6. When oxidative phosphorylation was inhibited by replacing O2 with N2, increasing the rate of stimulation from 0.1-0.7 to 1-2 Hz caused an initial increase followed by a large fall in developed pressure, which declined to a level well below that at the control stimulus rate. The increase in stimulus rate was accompanied by a large fall in [PCr]i, an increase in [Pi]i, and an intracellular acidosis of 0.1-0.3 pH units. The fall in developed pressure was consistent with the known effects of the rise in [Pi]i and the fall in pHi on the contractile apparatus.

This article has been cited by other articles:

				P. Swietach, K. W. Spitzer, and R. D. Vaughan-Jones pH-Dependence of Extrinsic and Intrinsic H+-Ion Mobility in the Rat Ventricular Myocyte, Investigated Using Flash Photolysis of a Caged-H+ Compound Biophys. J., January 15, 2007; 92(2): 641 - 653. [Abstract] [Full Text] [PDF]

				S. Cortassa, M. A. Aon, B. O'Rourke, R. Jacques, H.-J. Tseng, E. Marban, and R. L. Winslow A Computational Model Integrating Electrophysiology, Contraction, and Mitochondrial Bioenergetics in the Ventricular Myocyte Biophys. J., August 15, 2006; 91(4): 1564 - 1589. [Abstract] [Full Text] [PDF]

				P. Swietach, C.-H. Leem, K. W. Spitzer, and R. D. Vaughan-Jones Experimental Generation and Computational Modeling of Intracellular pH Gradients in Cardiac Myocytes Biophys. J., April 1, 2005; 88(4): 3018 - 3037. [Abstract] [Full Text] [PDF]

				P. Swietach and R. D. Vaughan-Jones Novel method for measuring junctional proton permeation in isolated ventricular myocyte cell pairs Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H2352 - H2363. [Abstract] [Full Text] [PDF]

				D. G Allen and X.-H. Xiao Role of the cardiac Na+/H+ exchanger during ischemia and reperfusion Cardiovasc Res, March 15, 2003; 57(4): 934 - 941. [Abstract] [Full Text] [PDF]

				L. J. Mellors and C. J. Barclay The energetics of rat papillary muscles undergoing realistic strain patterns J. Exp. Biol., January 11, 2001; 204(21): 3765 - 3777. [Abstract] [Full Text] [PDF]

				T. Tatsumi, S. Matoba, A. Kawahara, N. Keira, J. Shiraishi, K. Akashi, M. Kobara, T. Tanaka, M. Katamura, C. Nakagawa, et al. Cytokine-induced nitric oxide production inhibits mitochondrial energy production and impairs contractile function in rat cardiac myocytes J. Am. Coll. Cardiol., April 1, 2000; 35(5): 1338 - 1346. [Abstract] [Full Text] [PDF]

				C.-O. Park, X.-H. Xiao, and D. G. Allen Changes in intracellular Na+ and pH in rat heart during ischemia: role of Na+/H+ exchanger Am J Physiol Heart Circ Physiol, May 1, 1999; 276(5): H1581 - H1590. [Abstract] [Full Text] [PDF]

				R. Brandes and D. M. Bers Intracellular Ca2+ Increases the Mitochondrial NADH Concentration During Elevated Work in Intact Cardiac Muscle Circ. Res., January 1, 1997; 80(1): 82 - 87. [Abstract] [Full Text]