Ischaemic preconditioning alters the energy metabolism and protects the ischaemic myocardium in a stepwise fashion

Kavianipour, Mohammad; Ronquist, Gunnar; Wikström, Gerhard; Waldenström, Anders

doi:10.1046/j.1365-201x.2003.01108.x

Cited by 14 publications

(17 citation statements)

References 38 publications

(54 reference statements)

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“…This would be consistent with graded responses to Precon stimuli (107,187) and could explain variable data regarding age and Precon: studies of more profound Precon stimuli may detect efficacy in older hearts, while those using lower subthreshold stimuli may not. However, other investigations (86) identifying age-related abnormalities in cardioprotection have found that an enhanced stimulus is unable to overcome these changes.…”

Section: Age and Disease Dependence Of Cardioprotectionsupporting

confidence: 54%

Clinical cardioprotection and the value of conditioning responses

Peart

Headrick²

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Adjunctive cardioprotective strategies for ameliorating the reversible and irreversible injuries with ischemia-reperfusion (I/R) are highly desirable. However, after decades of research, the promise of clinical cardioprotection from I/R injury remains poorly realized. This may arise from the challenges of trialing and effectively translating experimental findings from laboratory models to patients. One can additionally consider whether features of the more heavily focused upon candidates could limit or preclude therapeutic utility and thus whether we might shift attention to alternate strategies. The phenomena of preconditioning and postconditioning have proven fertile in identification of experimental means of cardioprotection and are the most intensely interrogated responses in the field. However, there is evidence these processes, which share common molecular signaling elements and end effectors, may be poor choices for clinical exploitation. This includes evidence of age dependence, limiting efficacy in target aged or senescent hearts; refractoriness to conditioning stimuli in diseased myocardium; interference from a variety of relevant pharmaceuticals; inadvertent induction of these responses by prior ischemia or commonly used drugs, precluding further benefit; and sex dependence of protective signaling. This review focuses on these features, raising questions about current research strategies, and the suitability of these widely studied phenomena as rational candidates for clinical translation.

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Section: Age and Disease Dependence Of Cardioprotectionsupporting

confidence: 54%

Clinical cardioprotection and the value of conditioning responses

Peart

Headrick²

2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Our presumption is that lower levels of interstitial lactate during coronary ligation reflect events in the myocardium local to the catheter membrane, which is managing a longer period of ischemia with lower levels of lactate production. Earlier observations 20 in pig coronary occlusion models where injury/infarct and pre‐conditioning with myocardial protection have been validated have shown similar patterns of decrease in lactate production in a ‘protected’ myocardium during a 40‐min coronary occlusion.…”

Section: Discussionsupporting

confidence: 52%

Metabolic responses in ischemic myocardium after inhalation of carbon monoxide

Ahlström

Biber

Åberg

et al. 2009

Acta Anaesthesiol Scand

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“…Myocardial IPC was created by temporary snare-occlusion for 10 min followed by reperfusion during 20 min, repeated four times [20]. Coronary venous samples (10 mL each) were collected every second minute during a 20 min period, starting 20 min after last LAD snare release.…”

Section: Methodsmentioning

confidence: 99%

Myocardial ischemic preconditioning in a porcine model leads to rapid changes in cardiac extracellular vesicle messenger RNA content

Svennerholm

Rodsand

Hellman

et al. 2015

IJC Heart & Vasculature

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BackgroundExtracellular vesicles (EVs) are thought to exert protective effects after ischemic and remote ischemic preconditioning. It is not well understood which EV content factors are most relevant for protective effects. We hypothesize that ischemic preconditioning leads to qualitative changes in EV mRNA content and quantitative changes in EV size and number.MethodsUsing an in vivo porcine ischemic preconditioning model, EVs were collected from coronary venous blood, and isolated by differential ultracentrifugations. The presence and purity of EV were verified by electron microscopy and Western blot, and EV number was assessed by nanoparticle tracking analysis. The mRNA EV was identified by microarray.ResultsGene ontology analysis showed enrichment of EV mRNA coding for proteins associated with regulation of transcription, translation, extracellular matrix, morphogenic development and feeding behavior. There were 11,678 different mRNA transcripts detected in EV, where a total of 1103 was significantly increased or decreased after preconditioning, of which 638 mRNA sequences were up-regulated and/or emerged due to preconditioning. Several of them have known association with ischemic preconditioning. There was no significant difference in EV quantity or size before and after preconditioning.ConclusionsThese findings demonstrate in an in vivo model that myocardial ischemic preconditioning influences the composition of mRNA in EV, including gene transcripts for proteins associated with the protective effect of ischemic preconditioning. The finding that preconditioned parental cells release EV containing mRNA that is qualitatively different from those released by non-preconditioned cells shows the importance of the external milieu on parental cell EV production.

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Ischaemic preconditioning alters the energy metabolism and protects the ischaemic myocardium in a stepwise fashion

Cited by 14 publications

References 38 publications

Clinical cardioprotection and the value of conditioning responses

Clinical cardioprotection and the value of conditioning responses

Metabolic responses in ischemic myocardium after inhalation of carbon monoxide

Myocardial ischemic preconditioning in a porcine model leads to rapid changes in cardiac extracellular vesicle messenger RNA content

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