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 Ca2+ 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 Car2+ 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 Ca2+ may additionally cause mechanical cell damage. The loss of cellular Ca2+ 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.
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References
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.
Zimmer HG, Trendelenburg C, Kammermeier H et al. De novo synthesis of myocardial adenine nucleotides in the rat. Circ Res 1973;32:635–42.
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.
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.
Ganote CE. Contraction band necrosis and irreversible moycardial injury. J Mol Cell Cardiol 1983;15:67–73.
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.
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.
Siegmund B, Klietz T, Schwartz P et al. Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes. Am J Physiol 1991;260:H426–35.
Siegmund B, Zude R, Piper HM. Recovery of anoxic-reoxygenated cardiomyocytes from severe Ca2+ overload. Am J Physiol 1992;263:H1262–9.
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.
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.
Ladilov Y, Siegmund B, Piper HM. Protection of reoxygenated cardiomyocytes against hypercontracture by inhibtion of Na+/H+ exchange. Am J Physiol, in press.
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.
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.
Elz J, Nayler WG. Contractile activity and reperfusion-induced calcium gain after ischemia in the isolated rat heart. Lab Invest 1988;58:653–9.
Schlüter KD, Schwartz P, Siegmund B et al. Prevention of the oxygen paradox in anoxic-reoxygenated hearts. Am J Physiol 1991;261:H416–23.
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.
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.
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.
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.
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.
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.
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.
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.
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© 1996 Kluwer Academic Publishers
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Piper, H.M., Ladilov, Y.V., Siegmund, B. (1996). Energy and Cation Control in the Reoxygenated Myocardial Cell. In: Abd-Elfattah, AS.A., Wechsler, A.S. (eds) Purines and Myocardial Protection. Developments in Cardiovascular Medicine, vol 181. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0455-5_34
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DOI: https://doi.org/10.1007/978-1-4613-0455-5_34
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