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Ischemic preconditioning: protection against myocardial necrosis and apoptosis.

Iliodromitis EK, Lazou A, Kremastinos DT - Vasc Health Risk Manag (2007)

Bottom Line: Apoptosis, a genetically programmed form of cell death, has been associated with cardiomyocyte cell loss in a variety of cardiac pathologies, including cardiac failure and those related to ischemia/reperfusion injury.While ischemic preconditioning significantly reduces DNA fragmentation and apoptotic myocyte death associated with ischemia-reperfusion, the potential mechanisms underlying this effect have not been fully clarified.A comprehensive understanding of these mechanisms and application to clinical scenarios will provide new directions in research and translate this information into new treatment approaches for reducing the extent of ischemia/reperfusion injury.

View Article: PubMed Central - PubMed

Affiliation: 2nd University Department of Cardiology, Medical School, University of Athens, Greece.

ABSTRACT
The phenomenon of ischemic preconditioning has been recognized as one of the most potent mechanisms to protect against myocardial ischemic injury. In experimental animals and humans, a brief period of ischemia has been shown to protect the heart from more prolonged episodes of ischemia, reducing infarct size, attenuating the incidence, and severity of reperfusion-induced arrhythmias, and preventing endothelial cell dysfunction. Although the exact mechanism of ischemic preconditioning remains obscure, several reports indicate that this phenomenon may be a form of receptor-mediated cardiac protection and that the underlying intracellular signal transduction pathways involve activation of a number of protein kinases, including protein kinase C, and mitochondrial K(ATP) channels. Apoptosis, a genetically programmed form of cell death, has been associated with cardiomyocyte cell loss in a variety of cardiac pathologies, including cardiac failure and those related to ischemia/reperfusion injury. While ischemic preconditioning significantly reduces DNA fragmentation and apoptotic myocyte death associated with ischemia-reperfusion, the potential mechanisms underlying this effect have not been fully clarified. A comprehensive understanding of these mechanisms and application to clinical scenarios will provide new directions in research and translate this information into new treatment approaches for reducing the extent of ischemia/reperfusion injury.

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Effect of ischemic preconditioning on DNA fragmentation in rabbit hearts subjected to ischemia/reperfusion Lane 1 represents control non-ischemic tissue; lane 2 represents ischemic tissue after ischemia without reperfusion; lanes 3 and 4 represent ischemic tissue after ischemia/reperfusion in nonpreconditioned and preconditioned hearts, respectively. M, marker lane (from Lazou et al 2006).
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fig4: Effect of ischemic preconditioning on DNA fragmentation in rabbit hearts subjected to ischemia/reperfusion Lane 1 represents control non-ischemic tissue; lane 2 represents ischemic tissue after ischemia without reperfusion; lanes 3 and 4 represent ischemic tissue after ischemia/reperfusion in nonpreconditioned and preconditioned hearts, respectively. M, marker lane (from Lazou et al 2006).

Mentions: Accumulating evidence from in vivo and in vitro studies suggests that ischemic preconditioning significantly reduces DNA fragmentation (Figure 4) and apoptotic myocyte death that is associated with ischemia/reperfusion in isolated rabbit and rat heart (Gottlieb et al 1996; Maulik et al 1999; Nakamura et al 2000; Zhao and Vinten-Johansen 2002; Lazou et al 2006). In addition, activation of receptors that are involved in the initiation of the mechanism of preconditioning, such as δ-opioid and bradykinin, also results in reduced apoptosis after ischemia/reperfusion (Okubo et al 2004; Feng et al 2005). It is clear from these studies that attenuation of apoptosis by ischemic preconditioning is associated with a reduction in infarct size analysed early at reperfusion. It is not known, however, whether a reduction in infarct size measured days after reperfusion is achieved by inhibiting apoptosis since apoptosis progresses after reperfusion over a number of days. The potential mechanisms underlying preconditioning attenuated myocardial apoptosis have not been fully clarified and they are under intense investigation. However, a number of mediators have been implicated.


Ischemic preconditioning: protection against myocardial necrosis and apoptosis.

Iliodromitis EK, Lazou A, Kremastinos DT - Vasc Health Risk Manag (2007)

Effect of ischemic preconditioning on DNA fragmentation in rabbit hearts subjected to ischemia/reperfusion Lane 1 represents control non-ischemic tissue; lane 2 represents ischemic tissue after ischemia without reperfusion; lanes 3 and 4 represent ischemic tissue after ischemia/reperfusion in nonpreconditioned and preconditioned hearts, respectively. M, marker lane (from Lazou et al 2006).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2291307&req=5

fig4: Effect of ischemic preconditioning on DNA fragmentation in rabbit hearts subjected to ischemia/reperfusion Lane 1 represents control non-ischemic tissue; lane 2 represents ischemic tissue after ischemia without reperfusion; lanes 3 and 4 represent ischemic tissue after ischemia/reperfusion in nonpreconditioned and preconditioned hearts, respectively. M, marker lane (from Lazou et al 2006).
Mentions: Accumulating evidence from in vivo and in vitro studies suggests that ischemic preconditioning significantly reduces DNA fragmentation (Figure 4) and apoptotic myocyte death that is associated with ischemia/reperfusion in isolated rabbit and rat heart (Gottlieb et al 1996; Maulik et al 1999; Nakamura et al 2000; Zhao and Vinten-Johansen 2002; Lazou et al 2006). In addition, activation of receptors that are involved in the initiation of the mechanism of preconditioning, such as δ-opioid and bradykinin, also results in reduced apoptosis after ischemia/reperfusion (Okubo et al 2004; Feng et al 2005). It is clear from these studies that attenuation of apoptosis by ischemic preconditioning is associated with a reduction in infarct size analysed early at reperfusion. It is not known, however, whether a reduction in infarct size measured days after reperfusion is achieved by inhibiting apoptosis since apoptosis progresses after reperfusion over a number of days. The potential mechanisms underlying preconditioning attenuated myocardial apoptosis have not been fully clarified and they are under intense investigation. However, a number of mediators have been implicated.

Bottom Line: Apoptosis, a genetically programmed form of cell death, has been associated with cardiomyocyte cell loss in a variety of cardiac pathologies, including cardiac failure and those related to ischemia/reperfusion injury.While ischemic preconditioning significantly reduces DNA fragmentation and apoptotic myocyte death associated with ischemia-reperfusion, the potential mechanisms underlying this effect have not been fully clarified.A comprehensive understanding of these mechanisms and application to clinical scenarios will provide new directions in research and translate this information into new treatment approaches for reducing the extent of ischemia/reperfusion injury.

View Article: PubMed Central - PubMed

Affiliation: 2nd University Department of Cardiology, Medical School, University of Athens, Greece.

ABSTRACT
The phenomenon of ischemic preconditioning has been recognized as one of the most potent mechanisms to protect against myocardial ischemic injury. In experimental animals and humans, a brief period of ischemia has been shown to protect the heart from more prolonged episodes of ischemia, reducing infarct size, attenuating the incidence, and severity of reperfusion-induced arrhythmias, and preventing endothelial cell dysfunction. Although the exact mechanism of ischemic preconditioning remains obscure, several reports indicate that this phenomenon may be a form of receptor-mediated cardiac protection and that the underlying intracellular signal transduction pathways involve activation of a number of protein kinases, including protein kinase C, and mitochondrial K(ATP) channels. Apoptosis, a genetically programmed form of cell death, has been associated with cardiomyocyte cell loss in a variety of cardiac pathologies, including cardiac failure and those related to ischemia/reperfusion injury. While ischemic preconditioning significantly reduces DNA fragmentation and apoptotic myocyte death associated with ischemia-reperfusion, the potential mechanisms underlying this effect have not been fully clarified. A comprehensive understanding of these mechanisms and application to clinical scenarios will provide new directions in research and translate this information into new treatment approaches for reducing the extent of ischemia/reperfusion injury.

Show MeSH
Related in: MedlinePlus