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Myocardial Stress Response, Cytoprotective Proteins and the Second Window of Protection Against Infarction

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Myocardial Preconditioning

Part of the book series: Medical Intelligence Unit ((MIU.LANDES))

Abstract

The cellular stress response is a multifactorial process, the nature of which is dependent on the organism, the metabolic status of the cell involved and the nature of the stress imposed. It is known that many cells and tissues, ranging from prokaryotes to highly organized and complex tissues such as myocardium are able to respond to a variety of metabolic stresses so that they become better able to withstand a subsequent period of metabolic stress several hours later.1,2 The ischemic preconditioning phenomenon in myocardium is well recognized and could be regarded as a very particular form of acute stress response in myocytes (and possibly in other cellular components of heart tissue).3,4 However, the stress response to hyperthermia and hypoxia, originally described in lower organisms such as yeasts and bacteria, differs fundamentally from ischemic preconditioning of myocardium in timecourse and quite probably in the mechanism of cellular preservation. The presence of a rapid preconditioning mechanism in myocardium does not preclude the occurrence of other stress response mechanisms and there is now reason to believe that myocardium has the potential to respond to ischemic stress with at least two different adaptive routes to cytoprotection. The first of these is the preconditioning response that has been considered comprehensively in the preceding chapters of this volume, and which for the sake of clarity we will refer to as classic preconditioning. The other is analogous to the stress (or ‘heat-shock’) response, originally recognized in lower organisms. It is this latter form of adaptation that is thought to underlie the delayed phase of protection that develops following transient ischemic stress, many hours after classic preconditioning protection has disappeared.5,6 We have coined the term “second window of protection” for this delayed protection following transient ischemia.7 In this brief review, we will describe the background relevant to the discovery of the second window, review the evidence for its occurrence in myocardium and other tissues, discuss some of the cellular mechanisms that may be involved and speculate on its pathophysiological relevance.

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Authors
  1. Gary F. Baxter
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  2. Michael S. Marber
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  3. Derek M. Yellon
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© 1996 Springer-Verlag Berlin Heidelberg

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Baxter, G.F., Marber, M.S., Yellon, D.M. (1996). Myocardial Stress Response, Cytoprotective Proteins and the Second Window of Protection Against Infarction. In: Myocardial Preconditioning. Medical Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-22206-5_13

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  • DOI: https://doi.org/10.1007/978-3-662-22206-5_13

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-22208-9

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