Reperfusion injury after temporary coronary occlusion

Vinten-Johansen, J.; We, Johnston; Sa, Mills; Kb, Faust; Kr, Geisinger; Rj, DeMasi; Ar, Cordell

doi:10.1016/s0022-5223(19)35661-2

Cited by 25 publications

(5 citation statements)

References 25 publications

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“…Although there is no question that reperfusion is essential to salvage ischemic myocardium, it has been postulated that restoration of flow per se may have potentially deleterious consequences (2,3,31). Multiple adverse effects have been attributed to reperfusion including exacerbation of microvascular injury, myocardial stunning, reperfusion arrhythmias, and perhaps most notably, irreversible myocyte death (37).…”

Section: Reperfusion Injury Modified Reperfusion and The Concept Ofmentioning

confidence: 99%

Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2

Darling

Jiang

Maynard

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

182

149

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Emerging evidence suggests that restoration of blood flow in a stuttering manner may limit lethal myocardial ischemia-reperfusion injury. However, the mechanisms contributing to this phenomenon, termed postconditioning (post-C), remain poorly defined. Our aim was to test the hypothesis that activation of classic "survival kinases," phosphatidylinositol 3-kinase (PI3-kinase) and/or extracellular signal-regulated kinase (ERK)1/2, may play a role in post-C-induced cardioprotection. In protocol 1, isolated buffer-perfused rabbit hearts underwent 30 min of sustained coronary artery occlusion and were randomized to receive abrupt reperfusion (controls) or four cycles of 30 s of reperfusion and 30 s of reocclusion before full restoration of flow (post-C). Protocol 2 was identical except control and postconditioned hearts received the PI3-kinase inhibitor LY-294002 (protocol 2A) or the ERK1/2 antagonist PD-98059 (protocol 2B) throughout the first 25 min of reperfusion, whereas in protocol 3, myocardial samples were obtained during the early minutes of reflow from additional control, postconditioned, and nonischemic sham hearts for the assessment, by standard immunoblotting, of phospho-Akt (downstream target of PI3-kinase) and phospho-ERK. Protocols 1 and 2 corroborated that infarct size (delineated by tetrazolium staining and expressed as a percent of risk region) was reduced in postconditioned hearts vs. control hearts and also revealed that post-C-induced cardioprotection was maintained despite LY-294002 treatment but was abrogated by PD-98059. These pharmacological data were supported by protocol 3, which showed increased immunoreactivity of phospho-ERK but not phospho-Akt with post-C. Thus our results implicate the involvement of ERK1/2 rather than PI3-kinase/Akt in the reduction of infarct size achieved with post-C.

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Section: Reperfusion Injury Modified Reperfusion and The Concept Ofmentioning

confidence: 99%

Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2

Darling

Jiang

Maynard

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

182

149

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“…The latter point was expanded to include modifying the conditions and composition of the reperfusate, including the inclusion of drugs during early reperfusion. Despite considerable controversy over the very existence and clinical importance of myocardial reperfusion injury, there is now compelling evidence that reperfusion contributes to the extent of transient as well as permanent (lethal) post-ischaemic injury to the myocardium [ 27 , 65 , 73 , 251 , 274 ], and that this injury was initiated within moments after onset of reflow [ 246 ]. Early reports of the protective effects of gradual or gentle reperfusion (modified conditions of reperfusion) in the early moments of reperfusion [ 22 , 115 , 216 ] did not capture the attention of the scientific or clinical communities.…”

Section: Ischaemic Postconditioningmentioning

confidence: 99%

Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery

Barrabés²,

et al. 2016

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To commemorate the auspicious occasion of the 30th anniversary of IPC, leading pioneers in the field of cardioprotection gathered in Barcelona in May 2016 to review and discuss the history of IPC, its evolution to IPost and RIC, myocardial reperfusion injury as a therapeutic target, and future targets and strategies for cardioprotection. This article provides an overview of the major topics discussed at this special meeting and underscores the huge importance and impact, the discovery of IPC has made in the field of cardiovascular research.

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“…Myocardial edema formation is thought to be due to an in vivo "reperfusion injury" (19) that occurs after regional and global ischemia and subsequent restoration of oxygenated blood flow. Because metabolically active cells continue to use up vital metabolic precursors (i.e., ATP, creatine phosphate) during the ischemic period, demand for energy can not be matched by the lack of continuous supply of nutrients.…”

Section: Myocardial Edemamentioning

confidence: 99%

The Basic Science Aspect of Donor Heart Preservation: A Review

Rivard

Gallegos

Bianco

et al. 2004

J Extra Corpor Technol

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In cardiac transplantation, the transport time between harvest and recipient is limited by the viability of the donor heart. The problem of viability is a consistent limitation in cardiac transplantation. Since the 1960s, techniques, including hypothermia, perfusion, oxygenation, and hyperbaria, have been used to prolong the preservation of the transplantable heart. Continuing development of cardioplegic solutions has minimized edema and oxygen radical formation, which have resulted in extension of the donor heart viability. New research into the events leading to necrosis, oncosis, and apoptosis may allow further advancement of protective cardioplegic solutions in combination with technology of transporting the heart. With a prolonged preservation time there is potential to increase the donor pool and ultimately improve post-operative outcomes.

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Reperfusion injury after temporary coronary occlusion

Cited by 25 publications

References 25 publications

Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2

Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2

Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery

The Basic Science Aspect of Donor Heart Preservation: A Review

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