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Myocardial IschemiaReperfusion InjuryIschemiaMyocardial Reperfusion InjuryBrain IschemiaReperfusionMyocardial ReperfusionMyocardiumMyocardial InfarctionIschemic Preconditioning, MyocardialIschemic PreconditioningDisease Models, AnimalCardiotonic AgentsRats, Sprague-DawleyCoronary CirculationRats, WistarTime FactorsHeartIschemic PostconditioningCerebral InfarctionWarm IschemiaHemodynamicsElectrocardiographyIschemic Attack, TransientCoronary DiseaseDogsInfarction, Middle Cerebral ArteryCreatine KinaseMyocytes, CardiacPeroxidaseMyocardial ContractionPerfusionCold IschemiaNeuroprotective AgentsVentricular Function, LeftCoronary VesselsMitochondria, HeartMice, Inbred C57BLExercise TestNecrosisApoptosisMyocardial StunningMalondialdehydeSpinal Cord IschemiaRandom AllocationL-Lactate DehydrogenaseAngina PectorisProtective AgentsOxidative StressHeart RateConstrictionRabbitsBrain InfarctionGerbillinaeArrhythmias, CardiacBlood PressureHydroxy AcidsCerebrovascular CirculationAdenosineDecanoic AcidsBrainSwineNitric OxideMice, KnockoutCytoprotectionKidneyElectrocardiography, AmbulatoryCoronary AngiographyTomography, Emission-Computed, Single-PhotonHeart VentriclesMicrocirculationNeutrophil InfiltrationSuperoxide DismutaseReactive Oxygen SpeciesAntioxidantsModels, AnimalHeart Function TestsTioproninHindlimbAcute DiseaseVentricular PressureIn Situ Nick-End LabelingVasodilator AgentsEnzyme InhibitorsCell DeathBrain EdemaSignal TransductionLiverAdenosine TriphosphateBlotting, WesternMyocardial Perfusion ImagingOxygenImmunohistochemistryCollateral CirculationCaspase 3NeutrophilsCardioplegic SolutionsEchocardiographyLactic AcidFree Radical Scavengers
InfarctionReduced infarct sizeMyocardiumInjuryIschemicInhibitionApoptosisPercutaneous coronary intMiceAcute myocardialOxidative stressRatsVentricular fibrillationInfarctionsReflowVivoOcclusionElectrocardiogramTriphenyltetrazoliumCardioprotectionSignificantlyArrhythmiasHypoxiaIncreasesMetabolismApoptoticPathwayRefractoryCardiac arrestInfusionDesflurane-inducedTissueReductionHemodynamicExperimentalAntibodyInflammationModelMortality
Infarction42
Reduced infarct size5
  • We show that Bbeta(15-42) robustly and reproducibly reduced infarct size in all models of ischemia-reperfusion. (bris.ac.uk)
  • In adult mouse hearts, post-conditioning significantly reduced infarct size via up-regulation of ERK (but not Akt) signaling. (nih.gov)
  • An IL-36R antagonist (IL-36Ra) decreased neutrophil recruitment, improved blood flow, and reduced infarct size in both adult and aged mice. (jci.org)
  • Similarly, cardiomyocyte-specific Txnip deletion reduced infarct size after reversible coronary ligation. (jci.org)
  • Esmolol given during the initial 30 min of reperfusion had no effect on infarct size (54 +/- 4%) but blocked desflurane-induced postconditioning (58 +/- 5%), whereas esmolol administered throughout reperfusion reduced infarct size in the absence or presence of desflurane to 42 +/- 6% and 41 +/- 7%, respectively. (silverchair.com)
Myocardium8
Injury53
  • Rotigaptide (ZP123) Prevents Spontaneous Ventricular Arrhythmias and Reduces Infarct Size During Myocardial Ischemia/Reperfusion Injury in Open-Chest Dogs. (wikipedia.org)
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • Many compounds have been shown to prevent reperfusion injury in various animal models, although to date, translation into clinic has revealed several obstacles. (bris.ac.uk)
  • In rodents, Bbeta(15-42) inhibits proinflammatory cytokine release and is cardioprotective during ischemia-reperfusion injury. (bris.ac.uk)
  • Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)
  • has been demonstrated to attenuate renal ischemia‑reperfusion (I/R) injury. (spandidos-publications.com)
  • However, the role of SA in myocardial I/R injury is unclear. (spandidos-publications.com)
  • The present study aimed to clarify the cardioprotective effect of SA in myocardial I/R injury in vitro and explore the potential molecular mechanisms. (spandidos-publications.com)
  • However, reperfusion following a period of prolonged ischemia can often cause myocardial ischemia-reperfusion (I/R) injury, leading to damage of cardiac tissues ( 5 ). (spandidos-publications.com)
  • The underlying mechanisms behind myocardial I/R injury are associated with a number of factors, including substantial free radical production, intracellular calcium overload, increased inflammation, myocardial necrosis and apoptosis ( 6 ). (spandidos-publications.com)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.com)
  • However, the role of SA in myocardial I/R injury remains to be elucidated. (spandidos-publications.com)
  • Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
  • These data indicate that elevated levels of the MPO substrate SCN-, which can be readily modulated by dietary means, can protect against acute ischemia-reperfusion injury. (ku.dk)
  • Time to rethink comorbidities in the reperfusion-injury phenomenon? (escardio.org)
  • Ischemic preconditioning and anesthetic preconditioning (APC) are reported to decrease myocardial infarct size during ischemia-reperfusion injury. (asahq.org)
  • Wild‐type C57BL/6J mice (male, 8-10 weeks old) were used and murine myocardial ischemia and reperfusion injury (IRI) model was conducted, cardiac function was evaluated by echocardiography. (edu.iq)
  • 2 Paradoxically, reperfusion itself can enlarge the infarct size, by complex mechanisms collectively termed ischemia/reperfusion injury. (dovepress.com)
  • 3 In a previous study, different pharmacological principles that aimed to reduce ischemia/reperfusion injury failed to show effect. (dovepress.com)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • and the underlying mechanism of CLU4A in myocardial ischemia/reperfusion injury needs to be investigated. (engreen.com.cn)
  • myocardial ischemia/reperfusion injury. (engreen.com.cn)
  • When subjected to myocardial ischemia-reperfusion injury, Caspase3 transgenic mice showed increased infarct size and a pronounced susceptibility to die. (uniroma5.it)
  • We also implicate Caspase3 in determining myocardial infarct size after ischemia-reperfusion injury, because its cardiomyocyte-specific overexpression increases infarct size. (uniroma5.it)
  • Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. (elifesciences.org)
  • Specific absence of homeostatic, monocyte-independent macrophages altered the immune cell crosstalk in response to injury and induced proinflammatory neutrophil polarization, resulting in impaired cardiac remodelling without influencing infarct size. (elifesciences.org)
  • In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. (elifesciences.org)
  • Using state-of-the-art fate-mapping models and genetic and pharmacological targeting approaches, the authors provide solid evidence that the absence of resident macrophages do not influence infarct size but instead alter the immune cell crosstalk in response to injury. (elifesciences.org)
  • Large infarct size and coronary microvascular injury, as the consequence of ischaemia-reperfusion injury and distal embolization of atherothrombotic debris, account for suboptimal long-term prognosis of STEMI patients. (ox.ac.uk)
  • These device-based therapies can be categorized according to the pathophysiological pathways they target: (i) techniques to prevent distal atherothrombotic embolization, (ii) techniques to prevent or mitigate ischaemia/reperfusion injury, and (iii) techniques to enhance coronary microvascular function/integrity. (ox.ac.uk)
  • The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Aromatase metabolizes testosterone to 17b- estradiol (E2) and thereby significantly contributes The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model. (ox.ac.uk)
  • In vivo, administration of the melanocortin agonist MTII (10 microg per mouse equivalent to 9.3 nmol) 30 min prior to ischemia (25 min) attenuated mouse heart 2 h reperfusion injury by approximately 40%, an effect prevented by the mixed MC3/4-R antagonist SHU9119 but not by the selective MC4-R antagonist HS204. (ox.ac.uk)
  • In conclusion, this study has highlighted a previously unrecognized protective role for MC3-R activation on acute and delayed heart reperfusion injury. (ox.ac.uk)
  • These data may open new avenues for therapeutic intervention against heart and possibly other organ ischemia-reperfusion injury. (ox.ac.uk)
  • Effect of magnesium infusion on myocardial reperfusion injury in swine. (doximity.com)
  • This results in a considerable improvement in injury caused by oxidative stress produced by different ischemia of cerebral areas of brain. (healthandhydrogen.com)
  • Whereas mitochondrial ATP synthesis was minimally decreased by Txnip deletion, cellular ATP content and lactate formation were higher in Txnip-KO hearts after ischemia-reperfusion injury. (jci.org)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
  • Current methods of cold static storage have reached their limits in storage time due to the extent of ischemia-reperfusion (I/R) injury induced during static cold storage. (gotomydoctor.com)
  • The extent of reperfusion injury is directly proportional to preservation time in cold storage, and research has shown that with static storage methods, heart storage time will not exceed six hours. (gotomydoctor.com)
  • Additionally, machine reperfusion induces the production of ROS, which results in I/R injury to the heart. (gotomydoctor.com)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • Above all, PGRN also provides protection in the initial phase following myocardial ischemia-reperfusion injury. (biomedcentral.com)
  • Intracellular mechanisms underlying this so-called reperfusion injury presumably include increased levels of reactive oxygen species, Ca 2+ overload, rapid restoration of physiologic pH, and inflammatory processes resulting in opening of the mitochondrial permeability transition pore (mPTP). (silverchair.com)
Ischemic6
  • Inhibition of neutrophil sequestration with CLB54 administered before reperfusion reduces infarct size, preserves ischemic zone microvascular perfusion and minimizes the decline of regional wall motion. (johnshopkins.edu)
  • Hypoxia/reoxygenation (H/R) as well as hypoxic preconditioning (HPC) is widely used for simulating in vivo myocardial I/R and ischemic preconditioning (IPC) in a cell culture model. (spandidos-publications.com)
  • 3 In 2003, Zhao and et all published experimental data demonstrating a considerable reduction of infarct size by a reperfusion procedure termed ischemic postconditioning (IPost), consisting of brief, repetitive cycles of reperfusion and reocclusion, followed by sustained reperfusion. (dovepress.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Several studies have been conducted on rodents to gain morphological, functional and molecular insights into sex-related differences in response to myocardial ischemic insults. (biomedcentral.com)
  • The production of antioxidant enzymes that scavenge free radicals in ischemic tissue is then impaired, thereby exacerbating the damage caused by these free radicals in the post ischemic reperfusion tissue. (frontiersin.org)
Inhibition1
  • The cardioprotective effect of CLU4A inhibition was detected by monitoring the cell viability, cell apoptosis, and LDH activity in vitro and in vivo , and examining the infarct size and cardiac function in vivo . (engreen.com.cn)
Apoptosis3
  • Also, curcumin reduces cell apoptosis induced by myocardial IRI, curcumin reduces cell apoptosis induced by myocardial IRI and activates the Nrf-2/HO-1 signaling pathway during myocardial. (edu.iq)
  • Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
  • Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
Percutaneous coronary int2
  • Primary percutaneous coronary intervention (PCI) is the preferred method of reperfusion if this can be performed within recommended time frames. (dovepress.com)
  • An IABP may be placed in the emergency department (ED) as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), to decrease myocardial workload, and to improve end-organ perfusion. (medscape.com)
Mice2
  • Isolated buffer-perfused hearts were obtained from 3- to 4-month-old (adult) and 20- to 24-month-old C57BL/6J mice and subjected to 30 min of ischemia. (nih.gov)
  • CLU4A expression was measured after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment by q-PCR and western blotting. (engreen.com.cn)
Acute myocardial2
  • Acute myocardial infarctions (MIs) are common. (medscape.com)
  • MC-3 receptor and the inflammatory mechanisms activated in acute myocardial infarct. (ox.ac.uk)
Oxidative stress2
  • Infarct size measurement, cardiac troponin-I assays, oxidative stress analysis and histopathological analyzed. (edu.iq)
  • The resulted data showed that curcumin alleviates myocardial inflammatory responses and oxidative stress during myocardial IRI. (edu.iq)
Rats3
  • Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
  • Pretreating the rats with simvastatin 18 hour prior to the induction of ischemiareperfusion has been shown to reduce cardiac dysfunction and improve coronary flow [ 7 ]. (ac.ir)
  • Ischemia was induced in male (M-Isch) and female (F-Isch) rats with sc. (biomedcentral.com)
Ventricular fibrillation2
Infarctions1
  • In the US, about 1.0 million myocardial infarctions occur annually. (msdmanuals.com)
Reflow2
  • For each cohort, hearts were randomized to receive standard, abrupt (control) reperfusion, or were post-conditioned with 3 or 6 10-s cycles of stuttered reflow. (nih.gov)
  • 12. Galiuto L. Optimal therapeutic strategies in the setting of post-infarct no reflow: the need for a pathogenetic classification. (razavihospital.ir)
Vivo2
  • It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
  • Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo . (engreen.com.cn)
Occlusion2
  • Left main coronary artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. (medscape.com)
  • In hearts with a right coronary dominance (with the right artery supplying the posterior descending branch), a right coronary artery occlusion causes a posterior (inferior) infarct. (medscape.com)
Electrocardiogram1
  • Before ischemia, acute troglitazone treatment had no effect on LV function, electrocardiogram, or substrate utilization. (diabetesjournals.org)
Triphenyltetrazolium2
  • Coronary flow was determined using radiolabeled microspheres, infarct size by triphenyltetrazolium chloride staining, global and regional ventricular function by contrast ventriculography and neutrophil accumulation by a myeloperoxidase assay. (johnshopkins.edu)
  • Myocardial infarct size was assessed by triphenyltetrazolium staining. (silverchair.com)
Cardioprotection1
Significantly2
  • Creatine kinase and infarct sizes were significantly reduced and left ventricular developed pressure was improved with APC in the young adult and middle-aged groups but not the aged group. (asahq.org)
  • Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)
Arrhythmias1
  • We previously demonstrated that chronic pretreatment with a thiazolidinedione peroxisome proliferator-activated receptor (PPAR)-γ activator, troglitazone, improves recovery of left ventricular (LV) function and substrate metabolism after ischemia and reperfusion, without causing arrhythmias. (diabetesjournals.org)
Hypoxia1
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
Increases1
  • Ischemia decreases intracellular pH and increases intracellular Na and intracellular Ca in all age groups. (asahq.org)
Metabolism1
  • Thus, although Txnip deletion suppresses mitochondrial function, protection from myocardial ischemia is enhanced as a result of a coordinated shift to enhanced anaerobic metabolism, which provides an energy source outside of mitochondria. (jci.org)
Apoptotic1
  • It was discovered in 2007 that inhaled hydrogen had genuine protection against brain damage caused by ischemia and reperfusion because of its anti-inflammatory and anti-apoptotic properties (Fukuda et al. (healthandhydrogen.com)
Pathway2
  • The aim of the study is to investigate the effects of curcumin in attenuates myocardial ischemia and reperfusion-induced proinflammatory response through activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • Inconclusion, this study demonstrates that curcumin attenuates myocardial IRI by inhibiting proinflammatory cytokines through a mechanism that may be related to activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
Refractory1
  • Old mouse hearts are refractory to infarct size reduction with post-conditioning, possibly because of an age-associated increase in MKP-1 and resultant deficit in ERK phosphorylation. (nih.gov)
Cardiac arrest1
Infusion1
  • Fifteen pigs were treated with troglitazone (10 mg/kg load, 5 mg · kg −1 · h −1 infusion i.v.) beginning 1 h before ischemia. (diabetesjournals.org)
Desflurane-induced1
  • ICI 118,551 and KN-93 did not affect infarct size (62 +/- 4% and 62 +/- 6%, respectively) but abolished desflurane-induced postconditioning (57 +/- 5% and 64 +/- 3%, respectively). (silverchair.com)
Tissue2
  • FFPE tissue slides were scanned and analyzed digitally, while myocardial proteins were quantified by liquid chromatography-tandem mass spectrometry (LC-MS/MS) using isobaric labeling. (biomedcentral.com)
  • The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. (frontiersin.org)
Reduction1
  • 4 An infarct-reducing effect of IPost was confirmed in several animal models, 3 and subsequently, in small-sized "proof of concept" clinical studies, reduction of infarct size by IPost was reported. (dovepress.com)
Hemodynamic1
  • Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94615.5% vs. 17.163.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. (uni-wuerzburg.de)
Experimental1
  • Previous experimental/simulation study suggested a terminal T-wave inversion (TTWI) in ischemia-related ECG leads corresponding to anterior infarct localization as an independent predictor of reperfusion VF (rVF). (lu.se)
Antibody1
  • Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
Inflammation1
  • Myocardial protection was associated with reduced markers of systemic and local inflammation, including cytokine contents (interleukin-1 and KC) and myeloperoxidase activity. (ox.ac.uk)
Model1
  • The random effects model pooled estimate for the outcome infarct size assessed by cardiac magnetic resonance was estimated by the standardized mean difference (SMD) =−0.06, 95% confidence interval (CI): −0.34 to 0.21, ie, no effect of IPost. (dovepress.com)
Mortality1