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Myocardial Reperfusion InjuryReperfusion InjuryMyocardial IschemiaMyocardial ReperfusionReperfusionMyocardiumIschemiaIschemic Preconditioning, MyocardialCardiotonic AgentsIschemic PostconditioningMyocardial InfarctionMyocytes, CardiacRats, Sprague-DawleyDisease Models, AnimalBrain IschemiaRats, WistarIschemic PreconditioningHeartCreatine KinasePeroxidaseL-Lactate DehydrogenaseTime FactorsApoptosisCoronary CirculationHemodynamicsMitochondria, HeartMice, Inbred C57BLVentricular Function, LeftHeart Function TestsOxidative StressMyocardial ContractionMice, KnockoutDogsCyclic S-OxidesWounds and InjuriesNitric OxideReceptor, Adenosine A3Peroxynitrous AcidWarm IschemiaRabbitsNeutrophilsCoronary VesselsMalondialdehydeSignal TransductionPerfusionTroponin IAntioxidantsProtective AgentsReactive Oxygen SpeciesNecrosisSwineKATP ChannelsNitric Oxide Synthase Type IIProto-Oncogene Proteins c-aktNitric Oxide Synthase Type IIICaspase 3ElectrocardiographyArrhythmias, CardiacCold IschemiaHeart RateCoronary DiseaseEnzyme InhibitorsIn Situ Nick-End LabelingBlood PressureBlotting, WesternRandom AllocationHeart VentriclesMyocardial StunningBrain InjuriesNeutrophil InfiltrationAcute Kidney InjuryKidneyTumor Necrosis Factor-alphaCytoprotectionInfarction, Middle Cerebral ArteryConstrictionNeuroprotective AgentsSuperoxidesCells, CulturedSuperoxide DismutaseLiverIschemic Attack, TransientCardioplegic SolutionsDose-Response Relationship, DrugOrgan PreservationEndothelium, VascularModels, AnimalAdenosineTioproninHeart Arrest, InducedOrgan Preservation SolutionsAspartate AminotransferasesHydroxy AcidsDecanoic AcidsMicrocirculationAlanine TransaminaseSpinal Cord IschemiaMice, TransgenicFree Radical ScavengersPhosphorylation
InfarctionMyocardiumApoptosisInhibitionCardiomyocyteAggravatesDysfunctionCardioprotectiveHypoxiaNrf2CardiomyocytesInfarctIschemic InjuryLigationMiceTissueInflammatoryRatsDiabetic complicationsCardioprotectionHypercholesterolemiaCoronary arteryProsurvival signalinApoptoticNeutrophilProteinsOxygenMechanismsModelAttenuatesVivoOcclusionHeartEnzymesNecrosisSystemicSignificantly lowerExpressionEffectsEosinConclusionRole
Infarction20
Myocardium10
  • The most effective early treatment for reducing AMI injury and limiting the infarcted myocardium is timely coronary revascularization using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) [ 2 - 4 ]. (hindawi.com)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. (hindawi.com)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • In rats and pigs, BSPC@HM NCs remarkably downregulates Sav1 in IR-injured myocardium, promotes myocardium regeneration, suppresses myocardial apoptosis, and recovers cardiac functions. (scimage.cn)
  • CABG may be performed as an emergency procedure in the context of an ST-segment elevation MI (STEMI) in cases where it has not been possible to perform percutaneous coronary intervention (PCI) or where PCI has failed and there is persistent pain and ischemia threatening a significant area of myocardium despite medical therapy. (medscape.com)
  • Last year, Dharmakumar and Kumar observed that damage to the heart from MI was not only a result of ischemia caused by a blocked artery, but also a result of bleeding in the myocardium after the artery had been opened. (medscape.com)
Apoptosis6
  • 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)
  • Myocardial I/R injury may induce cell apoptosis and autophagy by activating oxidative stress and upregulating inflammatory mediators, ultimately resulting in irreversible fibrotic damage ( 3 ). (spandidos-publications.com)
  • In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis. (aku.edu)
  • 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)
  • Dexmedetomidine pretreatment can obviously relieve myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis in rats probably by activating the Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway. (ijpsonline.com)
Inhibition3
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • Rationale: Both cardiomyocyte-restricted proteasome functional enhancement and pharmacological proteasome inhibition (PSMI) were shown to attenuate myocardial ischemia/reperfusion (I/R) injury. (elsevierpure.com)
Cardiomyocyte5
Aggravates1
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
Dysfunction2
  • 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)
  • The role of cardiac proteasome dysfunction during I/R and the perspective to diminish I/R injury by manipulating proteasome function remain unclear. (elsevierpure.com)
Cardioprotective4
  • Our results indicate that estrogen plays a cardioprotective role in global myocardial ischemia-reperfusion injury in female rats. (illinois.edu)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • Cardioprotective effects of acidified sodium nitrite in myocardial ischemia with reperfusion. (aspetjournals.org)
  • Thus, acidified NaNO2 exerts a significant protective action during ischemia and reperfusion injury, which suggests that endothelium-derived relaxing factor has a cardioprotective effect in MI. (aspetjournals.org)
Hypoxia2
  • Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. (spandidos-publications.com)
  • 3. Agomir-503 treatment worsens hypoxia/reoxygenation-induced injuries, while antagomir-503 treatment attenuates them and increases phosphorylation of Stat3 (Y705) and Akt (T450). (fullpicture.app)
Nrf24
Cardiomyocytes1
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
Infarct3
  • 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)
  • 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)
  • We reported that there is infarct expansion after reperfusion, so once you open up the vessel, the heart attack actually gets larger. (medscape.com)
Ischemic Injury1
  • The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)
Ligation1
  • Methods and Results: Myocardial I/R were modeled by ligation (30 minutes) and subsequent release of the left anterior descending artery in mice overexpressing GFPdgn, a validated surrogate proteasome substrate. (elsevierpure.com)
Mice2
Tissue2
  • The objectives of this study were to 1) determine the extent to which ascorbate or catechin alone at levels which could be in blood after dietary supplementation, can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic protective effect of ascorbate and catechin when given together. (usask.ca)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
Inflammatory3
  • Abouzaki NA, Christopher S, Trankle C, Van Tassell BW, Carbone S, Mauro AG, Buckley L, Toldo S and Abbate A: Inhibiting the inflammatory injury after myocardial ischemia reperfusion with plasma-derived Alpha-1 Antitrypsin: A post hoc analysis of the VCU-α1RT study. (spandidos-publications.com)
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Apparent histologic injury and elevated levels of serum myocardial enzymes and inflammatory factors were observed in the myocardial I/R model. (spandidos-publications.com)
Rats3
  • We investigated the effects of estrogen on global myocardial ischemia-reperfusion injury in rats that were ovariectomized (Ovx), sham-operated, or ovariectomized and then given 17β-estradiol (E 2 β) supplementation (Ovx+E 2 β). (illinois.edu)
  • 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)
  • To evaluate the effects of dexmedetomidine on myocardial ischemia-reperfusion injury in rats and its anti-apoptotic role, as well as the mechanism by which it regulates Janus kinase 2/signal transducers and activators of transcription 3 signal. (ijpsonline.com)
Diabetic complications1
  • Here we review the current literature on scutellarin to provide a comprehensive understanding of the pharmacological activity, mechanism of action, toxicity, and therapeutic potential of scutellarin for the treatment of ischemia, diabetic complications, and other chronic diseases. (cdc.gov)
Cardioprotection2
  • 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)
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.com)
Hypercholesterolemia1
  • Therefore, our aim was to develop a medium throughput comorbidity cell-based test system of myocardial I/R injury, hypercholesterolemia and hyperglycemia that mimics comorbidity conditions. (nih.gov)
Coronary artery3
  • A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. (spandidos-publications.com)
  • The left anterior descending coronary artery was ligated to construct the model of myocardial ischemia-reperfusion. (ijpsonline.com)
  • Acidified NaNO2 (12.5-50 mmol/kg/hr) was infused i.v., starting 30 min postocclusion followed by reperfusion 1 hr later, in cats subjected to MI by occlusion of the left anterior descending coronary artery. (aspetjournals.org)
Prosurvival signalin1
  • 1. MicroRNA-503 (miR-503) exacerbates myocardial ischemia/reperfusion (I/R) injury by inhibiting prosurvival signaling pathways, including PI3K/Akt and STAT3. (fullpicture.app)
Apoptotic1
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
Neutrophil1
  • An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. (jci.org)
Proteins1
  • Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
Oxygen1
  • The aims of premedication are to minimize myocardial oxygen demands by reducing heart rate and systemic arterial pressure and to improve myocardial blood flow with vasodilators. (medscape.com)
Mechanisms4
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. (spandidos-publications.com)
  • However, despite numerous studies on myocardial I/R injury, deeper insight into the underlying mechanisms of myocardial I/R injury is needed. (spandidos-publications.com)
  • However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)
Model3
  • A comparison of IR hearts with two controls, sham (perfused for a 15 min stabilization period) and continuous perfusion (perfused for 135 min), showed in most but not all measurements that this was a suitable model of IR injury. (usask.ca)
  • Although the mechanism remains elusive, the interest in exploring the therapeutic potential of MSC-Exo has greatly increased after the first report of MSC-Exo ameliorating myocardial ischemia/reperfusion injury in a mouse model 10 . (nature.com)
  • The effects of acidified sodium nitrite (NaNO2) which releases nitric oxide, a substance which is thought to be indistinguishable from endothelium-derived relaxing factor, were investigated in a 6-h model of myocardial ischemia (MI) with reperfusion in open-chest, anesthetized cats. (aspetjournals.org)
Attenuates1
Vivo1
  • 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)
Occlusion1
  • Myocardial reperfusion is the restoration of coronary blood flow after a period of coronary occlusion. (aku.edu)
Heart4
  • Ischaemia-reperfusion (I/R) injury is the most important and common cause of myocardial damage and subsequent heart failure worldwide ( 1 , 2 ). (spandidos-publications.com)
  • Interleukin-36 (IL-36), a newly discovered proinflammatory member of the IL-1 superfamily, may mediate this injury, but its role in the injured heart is currently not known. (jci.org)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • British Library EThOS: Aspects of ischaemia and reperfusion injury in the isolated rat heart. (bl.uk)
Enzymes1
  • The GRh2 pre‑treatment reduced the I/R‑ or H/R‑induced release of myocardial enzymes and the production of IL‑1β, IL‑18 and TNF‑α. (spandidos-publications.com)
Necrosis1
Systemic1
  • This study reports a bioinspired strategy to overcome the multiple systemic barriers against myocardial siRNA delivery, and holds profound potential for gene therapy against cardiac injuries. (scimage.cn)
Significantly lower2
  • At 24 hours of reperfusion, myocardial proteasome activities were significantly lower whereas total ubiquitin conjugates and GFPdgn protein levels were markedly higher in all regions of the I/R hearts than the sham controls, indicative of proteasome functional insufficiency. (elsevierpure.com)
  • However, the necrotic area expressed as a percentage of the myocardial area at risk was significantly lower in the 25 and 50 mmol/kg/hr NaNO2-treated cats. (aspetjournals.org)
Expression3
  • We first demonstrated the presence of IL-36(α/β) and its receptor (IL-36R) in ischemia/reperfusion-injured (IR-injured) mouse hearts and, interestingly, noted that expression of both increased with aging. (jci.org)
  • However, the influence of atorvastatin on Fas expression in I/R injury was not studied. (ac.ir)
  • 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)
Effects1
  • Effects of monophosphoryl lipid A on myocardial ischemia/reperfusion injury in dogs. (doximity.com)
Eosin1
Conclusion1
  • In conclusion, this study showed strong protection by ascorbate, which could be used in clinically relevant situations, and is the first to report the protection by catechin at this dose under conditions of myocardial ischemia-reperfusion injury. (usask.ca)
Role1
  • 2 ] hypothesised that the phosphatidylcholines are prime oxidising targets in the asthmatic airway based on their relative abundance, and that oxidised phosphatidylcholines (OxPC) are mechanistic effectors of oxidised stress in asthma, suggested by prior research demonstrating the ability of OxPC to perpetuate inflammation in ageing-related diseases, and their known causal role in both acute lung injury and acute respiratory distress syndrome [ 3 - 5 ]. (ersjournals.com)