Lethal Reperfusion Injury: Fact or Fancy?
- 5 Downloads
The sudden onset of severe ischaemia in previously healthy myocytes sets into motion a series of events that continue until the myocytes die. These changes begin seconds after the vessel is occluded and occur because the supply of 02 is insufficient to support oxidative phosphorylation. Within 8–10 s, the myocardium converts to anaerobic glycolysis (AG) as its only source of new high-energy phosphate (˜P). Because the demand of the ischaemic tissue for ˜P exceeds the supply provided by the reserve supplies of ˜P, and by anaerobic glycolysis, net myocardial adenosine triphosphate (ATP) decreases rapidly (Figure 2.1). Simultaneously, as a result of the marked reduction in arterial flow, tissue pH decreases as large quantities of lactate and other glycolytic intermediates accumulate in the tissue. By the time 40 min of severe ischaemia has passed, little ATP remains (Figure 2.1), and the tissue contains a large osmotic load of lactate, alpha glycerol phosphate (aGP), creatine, phosphate (Pi), H+, etc. (Figure 2.2).
Unable to display preview. Download preview PDF.
- Jennings, R. B. and Ganote, C. E. (1976). Mitochondrial structure and function in acute myocardial ischemic injury. Circ. Res., 38 (Suppl.), I-80-I-91Google Scholar
- Jennings, R. B. and Hawkins, H. K. (1980). Ultrastructural changes of acute myocardial ischemia. In Wildenthal, K. (Ed.), Degradative Processes in Heart and Skeletal Muscle. Elsevier, Amsterdam/New York, pp. 295–344Google Scholar
- Jennings, R. B., Murry, C. E., Steenbergen, C., Jr., and Reimer, K. A. (1989). The acute phase of regional ischemia. In Cox, R. H. (Ed.), Acute Myocardial Infarction: Emerging Concepts of Pathogenesis and Treatment. Praeger Scientific, New York, pp. 67–84Google Scholar
- Jennings, R. B., Murry, C. E., Steenbergen, C., Jr., and Reimer, K. A. (1990). Development of cell injury in sustained acute ischemia. Circulation, 82 (Suppl.), II-2-II-12Google Scholar
- Jennings, R. B. and Reimer, K. A. (1983). Factors involved in salvaging ischemic myocardium: effect of reperfusion of arterial blood. Circ. Res., 68 (Suppl.), 1-25-1-36Google Scholar
- Jennings, R. B., Reimer, K. A. and Steenbergen, C., Jr. (1985a). Myocardial ischemia and reperfusion: Role of calcium. In Parratt, J. R. (Ed.), Control and Manipulation of Calcium Movement. Raven Press, New York, pp. 273–302Google Scholar
- Jennings, R. B., Sommers, H., Smyth, G. A., Flack, H. A. and Linn, H. (1960). Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch. Pathol. Lab. Med., 70, 68–78Google Scholar
- Reimer, K. A., Tanaka, M., Murry, C. E., Richard, V. J. and Jennings, R. B. (1991). Evaluation of free radical injury in myocardium. Toxicol. Pathol. (in press)Google Scholar
- Schaper, W. (1984). Experimental infarcts and the microcirculation. In Hearse, D. and Yellon, D. (Eds), Therapeutic Approaches to Myocardial Infarct Size Limitation, Raven Press, New York, pp. 79–90Google Scholar
- Tanaka, M., Stoler, R. B., FitzHarris, G. P., Jennings, R. B. and Reimer, K. A. (1990). Evidence against the ‘early protection-delayed death’ hypothesis of superoxide dismutase (SOD) therapy in experimental myocardial infarction: PEG-SOD plus catalase do not limit myocardial infarct size in dog. Circ. Res., 67, 636–644PubMedCrossRefGoogle Scholar