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Ischemia and Reperfusion

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Cardiomyocytes – Active Players in Cardiac Disease

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Abstract

Ischemia, the interruption of blood perfusion of the heart, and reperfusion, the revascularization after an ischemic event, are both events that trigger certain signaling mechanisms and cellular adaptation to cardiomyocytes. Ischemia itself induces metabolic and structural changes to cardiomyocytes that are prone to reperfusion-induced stress, i.e., by inducing plasmalemmal fragility. Reperfusion restores immediately energy resources, but due to ischemia-dependent calcium overload, it generates the risk of hypercontracture. At the same time, oxidative stress further stresses postischemic cardiomyocytes. The well-described cellular changes during ischemia and subsequent reperfusion allowed researchers in the past to develop distinct protocols that reduce infarct sizes and protect at least part of non-irreversible damaged cardiomyocytes. Signaling events specifically targeted by such protocols, however, also affect subsequent wound healing processes. An optimal reperfusion strategy must therefore be directed by three different aims: (i) the reduction of infarct size to protect as much as myocardial tissue as possible; (ii) the immediate recovery of full pump function to perfuse not only the heart properly but also all other organs, i.e., the kidney; and (iii) signaling pathways must be activated that direct post-infarct remodeling into a direction that stabilizes pump function for longer time periods. In this chapter, a detailed description of ischemia-dependent, reperfusion-dependent, and postischemic adaptations of cardiomyocytes is given.

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  1. Institute of Physiology, Justus-Liebig-Universität Gießen; Physiologisches Institut, Aulweg 129, Giessen, 35392, Germany

    Jacqueline Heger

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  1. Institute of Physiology, Justus-Liebig-Universität Giessen, Giessen, Hessen, Germany

    Klaus-Dieter Schlüter

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Heger, J. (2016). Ischemia and Reperfusion. In: Schlüter, KD. (eds) Cardiomyocytes – Active Players in Cardiac Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-31251-4_8

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