Energy and Cation Control in the Reoxygenated Myocardial Cell

  • H. Michael Piper
  • Yury V. Ladilov
  • Berthold Siegmund
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 181)

Abstract

The development of cell injury in ischemic tissue starts with a deficit in the cellular balance of energy. The energetic deficit leads to a slowdown or cessation of important metabolic functions, among these the cellular control of Na+ and Ca 2+ ions. When the cellular reserves of energy are depleted, cation pumps regulating the normal intracellular ionic milieu fail due to a lack of energy. A lone-lasting overload of the cytosolic space and intracellular organelles with excess Car 2+ can be deleterious for the cell, as a number of structure degrading processes may become activated. In muscle cells, the activation of the myofibrillar contractile apparatus by high levels of Ca 2+ may additionally cause mechanical cell damage. The loss of cellular Ca 2+ homeostasis is a sign of advanced, but not necessarily irreversibly cell injury. For a better understanding of the pathogenesis of progressive myocardial injury the energy and cation control in the oxygen deprived and reoxygenated cardiomyocyte must be analyzed. This article provides a brief review.

Keywords

Hydrolysis Depression Ischemia Respiration Adenosine 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Noll T, de Groot H, Wissemann P. A computer-supported oxystat system maintaining steady-state O2 partial pressures and simultaneously monitoring O2 uptake in biological systems. Biochem J 1986;236:765–9.PubMedGoogle Scholar
  2. 2.
    Zimmer HG, Trendelenburg C, Kammermeier H et al. De novo synthesis of myocardial adenine nucleotides in the rat. Circ Res 1973;32:635–42.PubMedGoogle Scholar
  3. 3.
    Siegmund B, Koop A, Klietz T et al. Sarcolemmal integrity and metabolic competence of cardiomyocytes under anoxia-reoxygenation. Am J Physiol 1990;258:H285–91.PubMedGoogle Scholar
  4. 4.
    Hearse DJ, Humphrey SM, Chain EB Abrupt reoxygenation of the anoxic potassium-arrested perfused rat heart: A study of myocardial enzyme release. J Mol Cell Cardiol 1973;5:395–407.PubMedCrossRefGoogle Scholar
  5. 5.
    Ganote CE. Contraction band necrosis and irreversible moycardial injury. J Mol Cell Cardiol 1983;15:67–73.PubMedCrossRefGoogle Scholar
  6. 6.
    Vander Heide RS, Angelo JP, Altschuld RA et al. Energy dependence of contraction band formation in perfused hearts and isolated adult cardiomyocytes. Am J Pathol 1986;125:55–68.Google Scholar
  7. 7.
    Allshire A, Piper HM, Cuthbertson KSR et al. Cytosolic free Ca2+ in single rat heart cells during anoxia and reoxygenation. Biochem J 1987;244:381–5.PubMedGoogle Scholar
  8. 8.
    Siegmund B, Klietz T, Schwartz P et al. Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes. Am J Physiol 1991;260:H426–35.PubMedGoogle Scholar
  9. 9.
    Siegmund B, Zude R, Piper HM. Recovery of anoxic-reoxygenated cardiomyocytes from severe Ca2+ overload. Am J Physiol 1992;263:H1262–9.PubMedGoogle Scholar
  10. 10.
    Siegmund B, Ladilov Y, Piper HM. Importance of sodium for the recovery of Ca2+ control in reoxygenated cardiomyocytes. Am J Physiol 1994;267:H506–13.PubMedGoogle Scholar
  11. 11.
    Schlüter KD, Weber M, Schraven E et al. No donor SINå_1 protects against reoxygenation-induced cardiomyocyte injury by a dual action. Am J Phyiol 1994;267:H1461–6.Google Scholar
  12. 12.
    Ladilov Y, Siegmund B, Piper HM. Protection of reoxygenated cardiomyocytes against hypercontracture by inhibtion of Na+/H+ exchange. Am J Physiol, in press.Google Scholar
  13. 13.
    Marban E, Kitakaze M, Kusuoka HJ et al. Intracellular free calcium concentration measured with 19F NMR spectroscopy in intact ferret hearts. Proc Natl Acad Sci USA 1987;84:6005–9.PubMedCrossRefGoogle Scholar
  14. 14.
    Steenbergen C, Murphy E, Levy L et al. Elevation in cytosolic free calcium concentration early in myocardial ischemia in perfused rat heart. Circ Res 1987;60:700–7.PubMedGoogle Scholar
  15. 15.
    Elz J, Nayler WG. Contractile activity and reperfusion-induced calcium gain after ischemia in the isolated rat heart. Lab Invest 1988;58:653–9.PubMedGoogle Scholar
  16. 16.
    Schlüter KD, Schwartz P, Siegmund B et al. Prevention of the oxygen paradox in anoxic-reoxygenated hearts. Am J Physiol 1991;261:H416–23.PubMedGoogle Scholar
  17. 17.
    Garc ía -Dorado D, Theroux P, Duran JM et al. Selective inhibition of the contractile apparatus. A new approach to modification of infarct size, infarct composition, and infarct geometry during coronary artery occlusion and reperfusion. Circulation 1992;85:1160–74.Google Scholar
  18. 18.
    Schlack W, Uebing A, Schäfer M et al. Regional contractile blockade at the outset of reperfusion reduces infarct size in the dog heart. Pflügers Arch 1994;428:134–41.PubMedCrossRefGoogle Scholar
  19. 19.
    Weissberg PL, Little PJ, Cragoe EJ et al. The pH of spontaneously beating cultured rat heart cells is regulated by an ATP-calmodulin-dependent Na+/H+ antiport. Circ Res 1989;64:676–85.PubMedGoogle Scholar
  20. 20.
    Ikeda U, Arisaka H, Takayasu T et al. Protein kinase C activation aggravates hypoxic myocardial injury by stimulating Na+/H+ exchange. J Mol Cell Cardiol 1988;20:493–500.PubMedCrossRefGoogle Scholar
  21. 21.
    Anderson SE, Murphy E, Steenbergen C et al. Na+/H+ exchange in myocardium: effects of hypoxia and acidification on Na+ and Ca2+. Am J Physiol 1990;259:C940–48.PubMedGoogle Scholar
  22. 22.
    Pike MM, Luo CS, Clark MD et al. NMR measurements of Na+ and cellular energy in ischemic rat heart: role of Na+/H+ exchange. Am J Physiol 1993;265:H2017–26.PubMedGoogle Scholar
  23. 23.
    Scheufler E, Henrichs M, Guttmann I et al. Effect of the Na+/H+exchange inhibitor Ethyl-Isopropyl-Amiloride (EIPA) during ischemia and reperfusion. Brit J Pharmacol 1993;108–118P.Google Scholar
  24. 24.
    Tani M, Neely JR. Role of intracellular Na+ in Ca2+ overload and depressed recovery of ventricular function of reperfused ischemic rat hearts. Circ Res 1989;65:1045–56.PubMedGoogle Scholar

Copyright information

© Kluwer Academic Publishers 1996

Authors and Affiliations

  • H. Michael Piper
    • 1
  • Yury V. Ladilov
    • 1
  • Berthold Siegmund
    • 1
  1. 1.Physiologisches InstitutJustus-Liebig-UniversitätGiessenGermany

Personalised recommendations