Copyright © 1993 by the European Society of Cardiology.
© 1993 The European Society of Cardiology
The mechanism of myocyte death in ischaemia
Ischaemic Heart Disease Research Unit of the Medical Research Council and University of Cape Town Medical School Observatory 7925, Cape Town, South Africa Cardiovascular Research, The Rayne Institute, St Thomas's Hospital London SE1 7EH, U.K.
Correspondence: Professor L. H. Opie, Heart Research Unit, University of Cape Town Medical School, Observatory 7925, Cape Town, South Africa
Mechanisms of myocyte cell death in severe ischaemia may include: (1) accumulated metabolic products; (2) activation of membrane phospholipases; (3) formation of oxygen-derived free-radicals; (4) infiltration by activated neutrophils; (5) increased circulating catecholamines; (6) cytosolic calcium overload; (7) an inadequate supply of glycolytically produced ATP. The hypothesis is proposed that failure of glycolysis leads to inadequate control of intracellular calcium, which is a lethal event. This hypothesis would explain the concept that in the hibernating myocardium, viable zones can be detected by positron emission tomography of fluoro-deoxygluco
Key Words: Myocyte death calcium overload glycolytic ATP catecholamines neutrophils free radicals glucose
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
S. Tsang, S. S. C. Wong, S. Wu, G. M. Kravtsov, and T.-M. Wong Testosterone-augmented contractile responses to {alpha}1- and {beta}1-adrenoceptor stimulation are associated with increased activities of RyR, SERCA, and NCX in the heart Am J Physiol Cell Physiol, April 1, 2009; 296(4): C766 - C782. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Baumann, S. Poitry, A. Roatti, and A. J. Baertschi Plasmalemmal KATP channels shape triggered calcium transients in metabolically impaired rat atrial myocytes Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2296 - H2305. [Abstract] [Full Text] [PDF] |
||||

