Myocardial Protection by Brief Ischemia in Noncardiac Tissue

Gho, B. C. G.; Schoemaker, Regien G.; Doel, M. A. van den; Duncker, Dirk J.; Verdouw, Pieter D.

doi:10.1161/01.cir.94.9.2193

Cited by 554 publications

(497 citation statements)

References 21 publications

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“…18 Neuronal and Humoral Pathways Involvement of neuronal pathways is mostly based on the finding that blockade of the autonomic ganglion reversed the cardioprotective effects of rIPC when the preconditioning ischemic insult is performed via mesenteric artery occlusion. 19 This concept appears to also apply to the rIPC-associated neuroprotection in cerebral tissue, as was recently demonstrated. 20 In addition, adenosine receptors, particularly the subtype A1, have been implicated as the mediators of neuroprotection in rIPC, likely through increased production of specific antioxidants and NO.…”

Section: Signal Transduction Pathwaysmentioning

confidence: 75%

Remote Ischemic Preconditioning and Renoprotection

Gassanov¹,

Nia

Caglayan³

et al. 2014

Journal of the American Society of Nephrology

123

106

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There is currently no effective prophylactic regimen available to prevent contrastinduced AKI (CI-AKI), a frequent and life-threatening complication after cardiac catheterization. Therefore, novel treatment strategies are required to decrease CI-AKI incidence and to improve clinical outcomes in these patients. Remote ischemic preconditioning (rIPC), defined as transient brief episodes of ischemia at a remote site before a subsequent prolonged ischemia/reperfusion injury of the target organ, is an adaptational response that protects against ischemic and reperfusion insult. Indeed, several studies demonstrated the tissue-protective effects of rIPC in various target organs, including the kidneys. In this regard, rIPC may offer a novel noninvasive and virtually cost-free treatment strategy for decreasing CI-AKI incidence. This review evaluates the current experimental and clinical evidence for rIPC as a potential renoprotective strategy, and discusses the underlying mechanisms and key areas for future research.

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Section: Signal Transduction Pathwaysmentioning

confidence: 75%

Remote Ischemic Preconditioning and Renoprotection

Gassanov¹,

Nia

Caglayan³

et al. 2014

Journal of the American Society of Nephrology

123

106

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“…However, the discovery that an IPC stimulus applied to the circumflex coronary artery reduced the size of an MI arising from sustained occlusion of the left anterior descending artery (6) was subsequently extended by the demonstration that the heart could be protected by subjecting a remote organ or tissue, such as kidney, small intestine, liver, or limb, to short episodes of IR, a phenomenon known as remote IPC (7)(8)(9)(10). Application of a tourniquet to the hind limb before prolonged cardiac IR reduced arrhythmias in rats and IS in pigs (9,11).…”

mentioning

confidence: 99%

Hypoxia-inducible factor 1 is required for remote ischemic preconditioning of the heart

Cai

Luo

Zhan

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

157

146

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Both preclinical and clinical studies suggest that brief cycles of ischemia and reperfusion in the arm or leg may protect the heart against injury following prolonged coronary artery occlusion and reperfusion, a phenomenon known as remote ischemic preconditioning. Recent studies in mice indicate that increased plasma interleukin-10 (IL-10) levels play an important role in remote ischemic preconditioning induced by clamping the femoral artery for 5 min followed by 5 min of reperfusion for a total of three cycles. In this study, we demonstrate that remote ischemic preconditioning increases plasma IL-10 levels and decreases myocardial infarct size in wild-type mice but not in littermates that are heterozygous for a knockout allele at the locus encoding hypoxia-inducible factor (HIF) 1α. Injection of a recombinant adenovirus encoding a constitutively active form of HIF-1α into mouse hind limb muscle was sufficient to increase plasma IL-10 levels and decrease myocardial infarct size. Exposure of C2C12 mouse myocytes to cyclic hypoxia and reoxygenation rapidly increased levels of IL-10 mRNA, which was blocked by administration of the HIF-1 inhibitor acriflavine or by expression of short hairpin RNA targeting HIF-1α or HIF-1β. Chromatin immunoprecipitation assays demonstrated that binding of HIF-1 to the Il10 gene was induced when myocytes were subjected to cyclic hypoxia and reoxygenation. Taken together, these data indicate that HIF-1 activates Il10 gene transcription and is required for remote ischemic preconditioning.cardiac surgery | cardioprotection | coronary heart disease | myocardial infarction C oronary heart disease (CHD) is the leading cause of mortality in the US population, accounting for one in every six deaths, at a rate of one death from CHD every minute (1). Coronary artery stenosis due to atherosclerotic plaques results in reduced perfusion and myocardial ischemia. Plaque rupture results in complete arterial occlusion and the death of cardiac cells (myocardial infarction; MI) due to oxygen deprivation (2). Rapid reperfusion by thrombolytic therapy or percutaneous coronary intervention is the most important clinical factor to limit infarct size (IS), while at the same time reperfusion contributes to tissue injury by increasing intracellular reactive oxygen species and Ca 2+ levels (3, 4). Exposure of the heart to short (5-min) episodes of ischemia (I 5 ) and reperfusion (R 5 ) protects the heart against injury caused by a subsequent prolonged episode of ischemia and reperfusion (IR), a phenomenon known as ischemic preconditioning (IPC) (5).Although IPC was shown to have a powerful protective effect in animal models, the obvious difficulties involved in subjecting the heart to direct IPC restrict its potential clinical applications. However, the discovery that an IPC stimulus applied to the circumflex coronary artery reduced the size of an MI arising from sustained occlusion of the left anterior descending artery (6) was subsequently extended by the demonstration that the heart could be protected by su...

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“…1 Apart from the local effects, the protection of remote tissues can also be achieved through brief periods of arterial occlusions of the intestine, kidneys, and many other organs. 2,3 Although the remote effects of intraabdominal IPC may be notable, the extremities provide better opportunities for clinical purposes. IPC of the limbs in humans can be easily performed, the risk of surgical complications is low, and moreover, the large tissue mass may theoretically provide strong defense-triggering IPC signals.…”

mentioning

confidence: 99%

Ischemic limb preconditioning downregulates systemic inflammatory activation

Szabó

Varga

Keresztes

et al. 2008

Journal Orthopaedic Research

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We examined local and systemic antiinflammatory consequences of ischemic preconditioning (IPC) in a rat model of limb ischemia-reperfusion (I-R) by characterizing the leukocyte-endothelial interactions in the periosteum and the expression of adhesion molecules playing a role in leukocyte-mediated inflammatory processes. IPC induction (2 cycles of 10 min of complete limb ischemia and 10 min of reperfusion) was followed by 60 min of ischemia/180 min of reperfusion or sham-operation. Data were compared with those on animals subjected to I-R and sham-operation. Neutrophil leukocyte-endothelial cell interactions (intravital videomicroscopy), intravascular neutrophil activation (CD11b expression changes by flow cytometry), and soluble and tissue intercellular adhesion molecule-1 (ICAM-1; ELISA and immunohistochemistry, respectively) expressions were assessed. I-R induced enhanced leukocyte rolling and adherence in the periosteal postcapillary venules after 120 and 180 min of reperfusion. This was associated with a significantly enhanced CD11b expression (by $80% and 72%, respectively) and moderately increased soluble and periosteal ICAM-1 expressions. IPC prevented the I-R-induced increases in leukocyte adherence and CD11b expression without influencing the soluble and tissue ICAM-1 levels. The results show that limb IPC exerts not only local, but distant antiinflammatory effects through significant modulation of neutrophil recruitment. ß

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Myocardial Protection by Brief Ischemia in Noncardiac Tissue

Cited by 554 publications

References 21 publications

Remote Ischemic Preconditioning and Renoprotection

Remote Ischemic Preconditioning and Renoprotection

Hypoxia-inducible factor 1 is required for remote ischemic preconditioning of the heart

Ischemic limb preconditioning downregulates systemic inflammatory activation

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