Skip to main content

Electrophysiological responses to ischemia and reperfusion

  • Chapter
Myocardial Ischemia: Mechanisms, Reperfusion, Protection

Part of the book series: EXS ((EXS,volume 76))

Abstract

Myocardial ischemia, defined as an imbalance between energetic demands of the heart and supply of metabolic substrates (inclusive of O2), produces profound changes in cardiac electrical activity which can eventually lead to the development of severe arrhythmias and sudden death. While reperfusion of ischemic myocardium reduces or prevents myocardial necrosis, this procedure may also lead to arrhythmia development, contractile failure and the precipitation of cell death. Although both processes, ischemic and reperfusion injury may share the end point of inducing acute cardiac failure, the cellular events and the mechanisms involved may differ considerably.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 39.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 54.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Reimer KA, Jennings RB. Myocardial ischemia, hypoxia and infarction. In: Fozzard HA et al, editors: The Heart and Cardiovascular System: Scientific Foundations, 2nd edition. New York: Raven Press, 1992; 2: 1875–1973.

    Google Scholar 

  2. Gettes LS, Cascio WE, Effect of acute ischemia on cardiac electrophysiology. In: Fozzard HA et al, editors: The heart and Cardiovascular System: Scientific Foundations, 2nd edition. New York: Raven Press, 1992; 2: 2021–2054.

    Google Scholar 

  3. Karmazyn M, Moffat MP. Role of Na+/H+ exchange in cardiac physiology and pathophysiology: mediation of myocardial reperfusion injury by the pH paradox. Cardiovas Res 1993; 27: 915 – 924.

    Article  CAS  Google Scholar 

  4. Goerke J, Page E. Cat heart musclein vitro. VII. Potassium exchange in papillary muscles. J Gen Physiol 1965; 48: 933 – 948.

    Article  PubMed  CAS  Google Scholar 

  5. Rau EE, Shine KI, Langer GA. Potassium exchange and mechanical performance in anoxic mammalian myocardium. Am J Physiol 1977; 232: H85 – 94.

    PubMed  CAS  Google Scholar 

  6. Leblanc N, Ruiz-Petrich E, Chartier D. Potassium loss from hypoxic myocardium: influence of external K concentration. Can J Physiol Pharmacol 1987; 65: 861 – 866.

    Article  PubMed  CAS  Google Scholar 

  7. Rau EE, Langer GA. Dissociation of energetic state and potassium loss from anoxic myocardium. Am J Physiol 1978; 235: H537 – 543.

    PubMed  CAS  Google Scholar 

  8. Nakaya H, Kimura S, Kanno M. Intracellular K+ and Na+ activities under hypoxia, acidosis and no glucose in dog hearts. Am J Physiol 1985; 249: H1078 – 1085.

    PubMed  CAS  Google Scholar 

  9. Weiss J, Shine KI. Extracellular K+ accumulation during myocardial ischemia in isolated rabbit heart. Am J Physiol 1982; 242: H619 – 628.

    PubMed  CAS  Google Scholar 

  10. Kléber AG, Fleischhauer J, Cascio WE. Ischemia-induced propagation failure in the heart, In: Zipes DP & Jalife J editors. Cardiac Electrophysiology: From Cell to Bedside, 2nd edition. Philadelphia: Saunders, 1995; 174 – 182.

    Google Scholar 

  11. Vleugels A, Carmeliet E, Bosteels S, Zaman M. Differential effects of hypoxia with age on the chick embryonic heart. Changes in membrane potential, intracellular K and Na, K efflux and glycogen. Pflügers Arch 1976; 365: 159 – 166.

    Article  PubMed  CAS  Google Scholar 

  12. Weiss JN, Lamp ST, Shine KI. Cellular K+ loss and anion efflux during myocardial ischemia and metabolic inhibition. Am J Physiol 1989; 256: H1165 – 1175.

    PubMed  CAS  Google Scholar 

  13. Ruiz Petrich E, deLorenzi F, Chartier D. Role of the inward rectifier IK1 in the myocardial response to hypoxia. Cardiovasc Res 1991; 25: 17 – 26.

    Article  PubMed  CAS  Google Scholar 

  14. Noma A. ATP-regulated K+ channels in cardiac muscle. Nature 1983; 305: 147 – 148.

    Article  PubMed  CAS  Google Scholar 

  15. Gasser RNA, Vaughan-Jones RD. Mechanism of potassium efflux and action potential shortening during ischemia in isolated mammalian cardiac muscle. J Physiol (Lond) 1990; 431: 713 – 741.

    CAS  Google Scholar 

  16. Wilde AAM, Escande D, Schumacker CA, Thuringer D, Mestre M, Fiolet JWT, Janse MJ. Potassium accumulation in the globally ischemic mammalian heart: A role for the ATP-sensitive K+ channel. Circ Res 1990; 67: 835 – 843.

    PubMed  CAS  Google Scholar 

  17. Venkatesh N, Lamp ST, Weiss JN. Sylfonylureas. ATP-sensitive K+ channels and cellular K+ loss during hypoxia, ischemia, and metabolic inhibition in mammalian ventricle. Circ Res 1991; 69: 623 – 637.

    PubMed  CAS  Google Scholar 

  18. Vanheel B, de Hemptinne A. Influence of KATP channel modulation on net potassium efflux from ischemic mammalian cardiac tissue. Cardiovasc Res 1992; 26: 1030 – 1039.

    Article  PubMed  CAS  Google Scholar 

  19. Yan G-X, Yamada KA, Kléber AG, McHowat J, Corr PB. Dissociation between cellular K+ loss, reduction in repolarization time, and tissue ATP levels during myocardial hypoxia and ischemia. Circ Res 1993; 72: 560 – 570.

    PubMed  CAS  Google Scholar 

  20. Jiang C, Crake T, Poole Wilson PA. Inhibition by barium and glibenclamide of the net loss of 86Rb+ from rabbit myocardium during hypoxia. Cardiovasc Res 1991; 25: 414 – 420.

    Article  PubMed  CAS  Google Scholar 

  21. Mitani A, Shattock MJ. Role of Na-activated K channel, Na-K-Cl cotransport, and Na-K pump in [K]e changes during ischemia in rat heart. Am J Physiol 1992; 263: H333 – 340.

    PubMed  CAS  Google Scholar 

  22. Luk HN, Carmeliet E. Na+-activated K+ current in cardiac cells: rectification, open probability, block and role in digitalis toxicity. Pflügers Arch 1990; 416: 766 – 768.

    Article  PubMed  CAS  Google Scholar 

  23. Lederer WJ, Niggly E, Hadley RW. Sodium-Calcium exchange in excitable cells: fuzzy space. Science Wash DC 1990; 248: 283.

    Article  CAS  Google Scholar 

  24. Ruiz-Ceretti E, Ragault P, Leblanc N, Ponce Zumino AZ. Effects of hypoxia and altered K0 on the membrane potential of rabbit ventricle. J Mol Cell Cardiol 1983; 15: 845 – 854.

    Article  PubMed  CAS  Google Scholar 

  25. MacLeod KT. Effects of hypoxia and metabolic inhibition on the intracellular sodium activity of mammalian ventricular muscle. J Physiol (Lond) 1989; 416: 455 – 468.

    CAS  Google Scholar 

  26. Vanheel B, de Hemptinne A, Leusen I. Acidification and intracellular sodium ion activity during simulated myocardial ischemia. Am J Physiol 1990; 259: C169 – 179.

    PubMed  CAS  Google Scholar 

  27. Pike MM, Luo CS, Clark MD, Kirk KA, Kitakaze M, Madden MC et al. NMR measurements of Na+ and cellular energy in ischemic rat heart: role of Na+-H+ exchange. Am J Physiol 1993; 265: H2017 – 2026.

    PubMed  CAS  Google Scholar 

  28. Bielen FV, Bosteels S, Verdonck F. Consequences of CO2 acidosis for transmembrane Na+ transport and membrane current in rabbit cardiac Purkinje fibres. J Physiol (Lond) 1990; 427: 325 – 345.

    CAS  Google Scholar 

  29. Wallert MA, Fröhlich O. Na+-H+ exchange in isolated myocytes from adult rat heart. Am J Physiol 1989; 257: C207 – 213.

    PubMed  CAS  Google Scholar 

  30. Grace AA, Kirschenlohr HL, Metcalfe JC, Smith GA, Weissberg PL, Cragoe EJ Jr et al. Regulation of intracellular pH in the perfused heart by external HCO3- and Na+-H+ exchange. Am J Physiol 1993; 265: H289 – 298.

    PubMed  CAS  Google Scholar 

  31. Mohabir R, Lee H-C, Kurz RW, Clusin WT. Effects of ischemia and hypercarbic acidosis on myocyte calcium transients, contraction, and pH¡ in perfused rabbit hearts. Circ Res 1991; 69: 1525 – 15

    PubMed  CAS  Google Scholar 

  32. Murphy E, Perlman M, London RE, Steenbergen C. Amiloride delays the ischemia-induced rise in cytosolic free calcium. Circ Res 1991; 68: 1250 – 1258.

    PubMed  CAS  Google Scholar 

  33. Sperelakis N. Regulation of calcium slow channels of cardiac muscle by cyclic nucleotides and phosphorylation. J Mol Cell Cardiol (Suppl II ) 1988; 20: 75 – 105.

    Article  Google Scholar 

  34. Vleugels A, Vereecke J, Carmeliet E. Ionic currents during hypoxia in voltage clamped cat ventricular muscle. Circ Res 1980; 47: 501 – 508.

    PubMed  CAS  Google Scholar 

  35. Isenberg G, Vereecke J, Van Der Heyden G, Carmeliet E. The shortening of the action potential by DNP in guinea pig ventricular myocytes is mediated by an increase of a time-independent K conductance. Pflägers Arch 397: 251–259.

    Google Scholar 

  36. Irisawa, H, Sato R. Intra- and extracellular actions of proton on the calcium current of isolated guinea pig ventricular cells. Circ Res 1986; 59: 348 – 355.

    PubMed  CAS  Google Scholar 

  37. Leblanc N, Ruiz-Ceretti E. The diffusion and electrogenic components of the membrane potential of hypoxic myocardium. Can J Physiol 1987; 65: 246 – 251.

    Article  CAS  Google Scholar 

  38. Ruiz-Ceretti E, Nguyen-Thi A, Schanne OF, Caille J-P. An electrogenic component of resting potential in rabbit ventricular muscle? Am J Physiol 1981; 240: C28 – 34.

    PubMed  CAS  Google Scholar 

  39. Ruiz Petrich E, de Lorenzi F, Cai S, Schanne OF. Ionic channels involved in the myocardial response to metabolic stress. In: Bkaily G, editor: Membrane Physiopathyology. Boston: Kluwer Academic Publishers, 1994; 71 – 100.

    Chapter  Google Scholar 

  40. de Lorenzi F, Cai S, Schanne OF, Ruiz Petrich E. Partial contribution of the ATP-sensi-tive K+ current to the effects of mild metabolic depression in rabbit myocardium. Mol Cell Biochem 1994; 132: 133 – 143.

    Article  PubMed  Google Scholar 

  41. Friedrich M, Benndorf K, Schwalb M, Hirche Hj. Effects of anoxia on K and Ca currents in isolated guinea pig cardiocytes. Pflügers Arch 1990; 416: 207 – 209.

    Article  PubMed  CAS  Google Scholar 

  42. Nakaya H, Takeda Y, Tohse N, Kanno M. Effects of ATP-sensitive K+ channel blockers on the action potential shortening in hypoxic and ischemic myocardium. Br J Pharmacol 1991; 103: 1019 – 1026.

    PubMed  CAS  Google Scholar 

  43. Ruiz-Petrich E, Leblanc N, de Lorenzi F, Allard Y, Schanne OF. Effects of K+ channel blockers on the action potential of hypoxic rabbit myocardium. Br J Pharmacol 1992; 106: 924 – 930.

    PubMed  CAS  Google Scholar 

  44. Elliot AC, Smith GL, Allen DG. Simultaneous measurement of action potential duration and intracellular ATP in isolated ferret hearts exposed to cyanide. Circ Res 1989; 64: 583 – 591.

    Google Scholar 

  45. Weiss JN, Venkatesh N, Lamp ST. ATP-sensitive K+ channels and cellular K+ loss in hypoxic and ischemic mammalian ventricle. J Physiol (Lond) 1992; 447: 649 – 673.

    CAS  Google Scholar 

  46. Ackerman JM, Clapham DE. Cardiac Chloride channels. Cardiovasc Med 1993; 3: 23 – 28.

    Article  CAS  Google Scholar 

  47. Hume JR, Harvey RD. Chloride conductance pathways in heart. Am J Physiol 1991; 261: C399 – 412.

    PubMed  CAS  Google Scholar 

  48. Zygmunt AC, Gibbons WR. Calcium-activated chloride current in rabbit ventricular myocytes. Circ Res 1991; 68: 424 – 437.

    PubMed  CAS  Google Scholar 

  49. Hagiwara N, Masuda H, Shoda M, Irisawa H. Stretch activated anion currents of rabbit cardiac myocytes. J Physiol (Lond) 1992; 456: 285 – 302.

    CAS  Google Scholar 

  50. Yamawake N, Hirano Y, Sawanobori T, Hiraoka M. Arrhythmogenic effects of isoproterenol activated C1- current in guinea pig ventricular myocytes. J Mol Cell Cardiol 1992; 24: 1047 – 1058.

    Article  PubMed  CAS  Google Scholar 

  51. Antzelevitch C, Sicouri S, Lukas A, Nesterenko W, Liu D-W, Di Diego JM. Regional differences in the electrophysiology of ventricular cells: Physiological and clinical implications. In: Zipes DP & Jalife J, editors: Cardiac Electrophysiology: From Cell to Bedside, 2nd edition. Philadelphia: Saunders, 1995; 228 – 246.

    Google Scholar 

  52. Fermini B, Wang Z, Duan D, Nattel S. Differences in rate dependence of transient outward current in rabbit and human atrium. Am J Physiol 1992; 263: H1747 – 1754.

    PubMed  CAS  Google Scholar 

  53. Kimura S, Bassett AL, Furukawa T, Furukawa N, Meyerburg RJ. Differences in the effect of metabolic inhibition on action potentials and calcium currents in endocardial and epicardial cells. Circulation 1991; 84: 768 – 777.

    PubMed  CAS  Google Scholar 

  54. Furukawa T, Kimura S, Furukawa N, Bassett AL, Myerburg RJ. Role of cardiac ATP-regulated potassium channels in differential responses of endocardial and epicardial cells to ischemia. Circ Res 1991; 68: 1693 – 1702.

    PubMed  CAS  Google Scholar 

  55. Gilmour Jr RF, Evans JJ, Zipes DP. Purkinje-muscle coupling and endocardial response to hyperkalemia, hypoxia and acidosis. Am J Physiol 1984; 247: H303 – 311.

    PubMed  Google Scholar 

  56. Moffat MP, Duan J, Ward CA. Role of Na/H exchange and [Ca2+]¡ in electrophysiolog¬ical responses to acidosis and realkalization in isolated guinea pig ventricular myocytes. In: Bkaily G, editor: Membrane Physiopathology. Boston: Kluwer Academic Publishers, 1994; 101 – 114.

    Chapter  Google Scholar 

  57. Moffat MP, Karmazyn M. Protective effects of the potent Na/H exchange inhibitor methylisobutyl amiloride against post-ischemic contractile dysfunction in rat and guineapig hearts. J Mol Cell Cardiol 1993; 25: 959 – 971.

    Article  PubMed  CAS  Google Scholar 

  58. Pierce GN, Cole WC, Liu K, Massaeli H, Maddaford TG, Chen YJ et al. Modulation of cardiac performance by amiloride and several selected derivatives of amiloride. J Pharmacol Exper Ther 1993; 265: 1280 – 1291.

    CAS  Google Scholar 

  59. Han X, Ferrier GR. Ionic mechanisms of transient inward current in the absence of Na+-Ca2+ exchange in rabbit cardiac Purkinje fibres. J Physiol (Lond) 1992; 456: 19 – 38.

    CAS  Google Scholar 

  60. Curtis MJ, Garlick PB, Ridley PD. Anion manipulation, a novel antiarrhythmic approach: mechanism of action. J Mol Cell Cardiol 1993; 25; 417 – 436.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1996 Birkhäuser Verlag Basel/Switzerland

About this chapter

Cite this chapter

Ruiz Petrich, E., Schanne, O.F., Ponce Zumino, A. (1996). Electrophysiological responses to ischemia and reperfusion. In: Karmazyn, M. (eds) Myocardial Ischemia: Mechanisms, Reperfusion, Protection. EXS, vol 76. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-8988-9_8

Download citation

  • DOI: https://doi.org/10.1007/978-3-0348-8988-9_8

  • Publisher Name: Birkhäuser Basel

  • Print ISBN: 978-3-0348-9857-7

  • Online ISBN: 978-3-0348-8988-9

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics