Calcium Fluxes and Reperfusion Damage: The Role of Mitochondria
- 5 Downloads
Myocardial ischaemia in the absence of reperfusion ultimately leads to cell necrosis and the development of infarction (Mergner and Schaper, 1982; Lucchesi and Mullane, 1986; Smith et al., 1988). While restoration of flow is clearly a prerequisite for tissue recovery, the process of reperfusion itself results in the development of metabolic and functional abnormalities that were not apparent during the ischaemic period and can be regarded as the response of the myocardium to reperfusion. This response encompasses a variety of phenomena, including reperfusion arrhythmias (Woodward and Zakaria, 1985; Manning et al., 1985; Sugiyama and Ozawa, 1987), myocardial stunning (Gross et al., 1986; Bolli et al., 1989), cell lysis (Shen and Jennings, 1972a,b) and an inflammatory component characterized by neutrophil infiltration (Mullane et al., 1984; Lucchesi and Mullane, 1986; Smith et al., 1988). One of the key responses that occur as part of this continuum is the acute cell damage that occurs at the point of reperfusion. A component of this damage has been shown to be dependent on the reintroduction of oxygen to the tissue and on this basis it is frequently referred to as the ‘oxygen paradox’. Perturbations of cell calcium homoeostasis have been implicated in most aspects of reperfusion damage (Shen and Jennings, 1972a,b; Mergner and Schaper, 1982; Sugiyama and Ozawa, 1987), but in this present chapter we shall concentrate on the oxygen paradox and examine the role that calcium plays in this phenomenon.
Unable to display preview. Download preview PDF.
- Halestrap, A. P. and Davidsoh, A. M. (1990). Inhibition of calcium ion-induced large-amplitude swelling of liver and heart mitochondria by cyclosporin is probably caused by the inhibitory binding to mitochondrial-matrix peptidyl-prolyl cis-trans isomerase and preventing it interacting with the adenine nucleotide translocase. Biochem. J., 268, 153–160PubMedPubMedCentralCrossRefGoogle Scholar
- Kehrer, J. P., Park, Y. and Sies, H. (1988). Energy dependence of enzyme release from hypoxic isolated perfused rat heart tissue. Pfiiigers Arch., 61, 291–332Google Scholar
- Mergner, W. J. and Schaper, J. (1982). Cellular and subcellular changes in myocardial infarction. In Cowley, R. A. and Trump, B. F. (Eds), Pathophysiology of Shock, Anoxia and Ischaemia. Williams and Wilkins, London, pp. 658–680Google Scholar
- Nayler, W. G., Sturrock, W. J. and Panagiotopoulos, S. (1985). Calcium and myocardial ischaemia. In Parratt, J. R. (Ed.), Control and Manipulation of Calcium Movement. Raven Press, New York, pp. 303–324Google Scholar
- Poole-Wilson, P. A. (1985). The nature of myocardial damage following reoxygenation. In Parratt, J. R. (Ed.), Control and Manipulation of Calcium Movement. Raven Press, New York, pp. 325–340Google Scholar
- Reeves, J. P. (1984). Na-Ca exchange, [Cali and myocardial contraction. In Stone, L. and Weglicki, W. B. (Eds), Pathobiology of Cardiovascular Injury. Martinus Nijhoff, Boston, pp. 232–244Google Scholar