Lethal Reperfusion Injury: Fact or Fancy?

  • Robert B. Jennings
  • Keith A. Reimer


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).


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© Macmillan Publishers Limited 1992

Authors and Affiliations

  • Robert B. Jennings
  • Keith A. Reimer

There are no affiliations available

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