AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Myocardial Reperfusion InjuryMyocardial IschemiaReperfusion InjuryMyocardial ReperfusionMyocardiumIschemiaCardiotonic AgentsIschemic Preconditioning, MyocardialIschemic PostconditioningReperfusionMyocardial InfarctionMyocytes, CardiacRats, Sprague-DawleyBrain IschemiaDisease Models, AnimalHeartCreatine KinaseRats, WistarL-Lactate DehydrogenaseHemodynamicsVentricular Function, LeftPeroxidaseHeart Function TestsApoptosisCoronary CirculationMitochondria, HeartTime FactorsMice, Inbred C57BLCyclic S-OxidesIschemic PreconditioningOxidative StressMyocardial ContractionReceptor, Adenosine A3Mice, KnockoutPeroxynitrous AcidDogsNitric OxideCoronary VesselsTroponin IRabbitsArrhythmias, CardiacKATP ChannelsSignal TransductionElectrocardiographyNeutrophilsCoronary DiseaseProto-Oncogene Proteins c-aktHeart RateSwineReactive Oxygen SpeciesNitric Oxide Synthase Type IIINitric Oxide Synthase Type IIAntioxidantsHeart VentriclesCaspase 3Blood PressureWarm IschemiaIn Situ Nick-End LabelingEnzyme InhibitorsPerfusionBlotting, WesternExercise TestMalondialdehydeTumor Necrosis Factor-alphaSuperoxidesProtective AgentsCold IschemiaAngina PectorisNecrosisMyocardial StunningDose-Response Relationship, DrugCells, CulturedIschemic Attack, TransientRandom AllocationEndothelium, VascularInfarction, Middle Cerebral ArteryConstrictionNeuroprotective AgentsPhosphorylationPhosphatidylinositol 3-KinasesMice, TransgenicNF-kappa BKidneyEnzyme ActivationAdenosineSpinal Cord IschemiaCytoprotectionElectrocardiography, AmbulatoryNeutrophil InfiltrationSuperoxide DismutaseCoronary AngiographyHydroxy AcidsTioproninDecanoic AcidsModels, AnimalMicrocirculationLiverTomography, Emission-Computed, Single-PhotonVasodilator AgentsGerbillinae
InfarctionAcuteDysfunctionIschemicVascular endothelial cellsInfarctCardioprotectionVitroInjuryCoronaryVivoImproved endothelial functionOxidativeCardiomyocyteMinutes of ischemiaInduceApoptosisProgenitor cellsAbstractMiceInflammatoryMyocardiumENOSAngiogenesisVentricularInnateNitric oxideCardiac functionCellsFunctionCardiovascularEndogenousTissuesEnzymesRatsStrokeProcessesCell
Infarction26
Acute6
  • 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)
  • Cardiac surgery-associated multiorgan dysfunction (CSA-MOD) is well recognized and includes acute kidney injury (AKI), hepatic impairment, myocardial damage, and postoperative neurologic deficit. (silverchair.com)
  • Before ischemia, acute troglitazone treatment had no effect on LV function, electrocardiogram, or substrate utilization. (diabetesjournals.org)
  • Acute treatment with troglitazone increases susceptibility to ventricular fibrillation during myocardial ischemia and reperfusion. (diabetesjournals.org)
  • Therefore, we studied whether an acute bout of endurance or interval exercise is able to protect against endothelial I/R injury. (artinis.com)
  • Therefore, the aim of this study was to investigate apoptosis in various cardiac diseases: in hyperlipidemia induced atherosclerosis, in acute rejected heart transplants, in ischemia and reperfusion as well as in chronic hypoxia. (uni-frankfurt.de)
Dysfunction8
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
  • Picking up on the original 1998 Nobel-winning work of Drs. Louis Ignarro and Ferid Murad, Dr. Bryan has focused on identifying specific changes in NO-related signaling pathways associated with endothelial dysfunction, ischemia and other disease states, and testing botanical interventions that improve NO signaling and vascular function. (holisticprimarycare.net)
  • In many people with endothelial dysfunction and NO deficiency, the arginine pathway itself is dysfunctional. (holisticprimarycare.net)
  • 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)
  • In addition to protective "immune response", sepsis is characterized by destructive "endothelial response" of the host, leading to endotheliopathy and its molecular dysfunction. (biomedcentral.com)
  • There is substantial evidence that endothelial injury during organ procurement and preservation, caused by ischemia and subsequent reperfusion, results in endothelial dysfunction. (frontierspartnerships.org)
  • Besides endothelial dysfunction, the progression of interstitial and perivascular fibrosis consecutively leads to impaired diastolic and systolic graft function, thus preservation of endothelial and vascular function is certainly a clinically desirable goal. (frontierspartnerships.org)
  • Apoptosis of endothelial cells could be an initial manifestation leading to endothelial dysfunction and subsequent plaque development. (uni-frankfurt.de)
Ischemic9
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • 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)
  • Reperfusion injury refers to the tissue damage inflicted when blood flow is restored after an ischemic period of more than about ten minutes. (benbest.com)
  • Cryonics patients frequently experience ischemic & reperfusion injury between the time when the heart stops and cryostorage begins. (benbest.com)
  • In this article I attempt to evaluate the nature & extent of ischemic & reperfusion injury -- primarily focused on the impact for cryonics (although certainly relevant to stroke and cardiac arrest). (benbest.com)
  • I focus my attention on ischemic/reperfusion injury to the brain. (benbest.com)
  • Endothelial ischemia-reperfusion (I/R) injury importantly contributes to the poor prognosis during ischemic (myocardial) events. (artinis.com)
  • Remote ischemic conditioning (RIC) protects against sustained myocardial ischemia. (ox.ac.uk)
  • NEW & NOTEWORTHY Remote ischemic conditioning (RIC) and long-term glyceryl trinitrate (GTN) treatment protect against ischemia-reperfusion injury in both human endothelium and rat myocardium. (ox.ac.uk)
Vascular endothelial cells2
  • Evidence has been provided that activation of the vascular endothelial cells in the presence of the risk factors promotes oxidative stress and vascular inflammatory responses, leading to acceleration of atherosclerotic vascular disease. (frontiersin.org)
  • Tissue plasminogen activator (tPA) is a naturally occurring fibrinolytic agent found in vascular endothelial cells and is involved in the balance between thrombolysis and thrombogenesis. (medscape.com)
Infarct7
  • 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)
  • 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)
  • 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)
  • Reduction of myocardial infarct size by human mesenchymal stem cell conditioned medium. (nature.com)
  • We studied infarct size (IS) in rat hearts subjected to global ischemia-reperfusion (I/R) in vitro and endothelial function in healthy volunteers subjected to I/R of the upper arm. (ox.ac.uk)
  • However, focal accumulation in the infarct area started at day 3 (uptake ratio = 1.91 ± 0.22 vs. remote myocardium), peaked between 1 (3.43 ± 0.57) and 3 weeks (3.43 ± 0.95), and decreased to 1.96 ± 0.40 at 6 months after reperfusion. (elsevierpure.com)
Cardioprotection1
Vitro5
  • 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)
  • In project no. 81-02 a novel in vitro approach was established by replacing flatbed cultures through cultivation of endothelial cells on microcarrier beads. (forschung3r.ch)
  • This allows the interaction between blood cells and derived natural factors and interactions with endothelial cells to be studied in vitro . (forschung3r.ch)
  • The system is based on endothelial cells (as an example, porcine aortic endothelial cells, PAEC) which are previously expanded in vitro in conventional flatbed culture systems. (forschung3r.ch)
  • My overall research aim is (1) to describe innate immunity mechanisms in ischemia/reperfusion injury and (2) to attenuate the reperfusion injury both in vitro and in vivo with high potential for transfer to clinical studies. (ncrg.no)
Injury36
  • 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)
  • Haematoxylin and eosin staining was performed to observe the injury of myocardial tissues. (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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Recently, miRNAs were also found to be associated with myocardial I/R injury ( 6 , 7 ). (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)
  • It has been reported that SIRT1/peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/nuclear factor erythroid-2-related factor 2 (Nrf2) signalling can mediate oxidative stress, which plays an important role in myocardial I/R injury ( 14 , 15 ). (spandidos-publications.com)
  • 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)
  • ischemia/reperfusion injury (I/R injury). (nih.gov)
  • 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)
  • 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)
  • 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)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (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)
  • Although the role of the endothelium in the pathogenesis of sepsis is not clearly established yet, coagulopathy has been proposed to play a key role through crosstalk mechanism between inflammation and coagulation as a result of systemic endothelial injury [ 11 , 12 , 13 ]. (biomedcentral.com)
  • We have reported that retrograde application of embryonic endothelial progenitor cells (eEPCs) provides rapid paracrine protection against ischemia-reperfusion injury. (elsevierpure.com)
  • Cardiac ischemia/reperfusion (I/R) injury is a serious disease and threatens human health [ 1 ]. (hindawi.com)
  • The myocardial apoptosis and inflammation have been recognized as features of I/R injury. (hindawi.com)
  • Cold ischemia and subsequent reperfusion injury are non-immunologic cornerstones in the development of graft injury after heart transplantation. (frontierspartnerships.org)
  • The nitric oxide donor S-nitroso-human-serum-albumin (S-NO-HSA) is known to attenuate myocardial ischemia-reperfusion (I/R)-injury. (frontierspartnerships.org)
  • We assessed whether donor preservation with S-NO-HSA affects isograft injury and myocardial expression of GATA2 as well as miR-126-3p, which are considered protective against vascular and endothelial injury. (frontierspartnerships.org)
  • Recent studies have demonstrated that supplementation of nitric oxide (NO), or increased expression of endothelial NO-synthase (eNOS) protects against both IR-injury and fibrosis ( 5 , 6 ). (frontierspartnerships.org)
  • Abstract ： OBJECTIVE To explore the similarities and differences of material basis, action, and mechanism of Puerariae Lobatae Radix(PLR) and Puerariae Thomsonii Radix(PTR) against myocardial cell injury, and compare the differences of relative amount of active ingredients and the effect against H9c2 cells OGD/R injury in different medicated systems. (magtechjournal.com)
  • Donepezil attenuated cardiac ischemia/reperfusion injury through balancing mitochondrial dynamics, mitophagy, and autophagy[J]. Transl Res, 2021,230:82-97. (magtechjournal.com)
  • Focus: Innate immunity in ischemia/reperfusion injury - transfer to the clinic. (ncrg.no)
  • Preconditioning, i.e., repeated exposure to short periods of ischemia, effectively reduces endothelial I/R injury. (artinis.com)
  • In the present study, we examined the hypothesis that exercise has preconditioning effects on endothelial I/R injury. (artinis.com)
  • Subsequently, I/R injury was induced by inflation of a blood pressure cuff around the upper arm to 220 mmHg for 20 min and 20 min of reperfusion followed by another FMD measurement. (artinis.com)
  • In conclusion, a single bout of lower limb interval exercise, but not moderate-intensity endurance exercise, effectively prevents brachial artery endothelial I/R injury. (artinis.com)
  • RIC and long-term GTN treatment both protect against rat myocardial and human endothelial I/R injury through ROS and NO-dependent mechanisms. (ox.ac.uk)
  • However, combined application of RIC and long-term GTN treatment abolishes the individual protective effects of RIC and GTN treatment on ischemia-reperfusion injury, suggesting an interaction of clinical importance. (ox.ac.uk)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
Coronary2
  • 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)
  • Methods and results: Male Wister rats were subjected to 20 min transient left coronary artery occlusion followed by reperfusion. (elsevierpure.com)
Vivo5
  • 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)
  • My group has developed unique models of hypoxia/reoxygenation of cultured endothelial cells in combination with a full blood model and the use of ex vivo machine perfusion to simulate reperfusion in porcine kidneys, porcine and human livers. (ncrg.no)
  • Autoradiographic analysis and in vivo PET imaging were used to determine myocardial 18 F-Galacto-RGD uptake at different time points following reperfusion. (elsevierpure.com)
  • Autoradiographic analysis and in vivo PET imaging were used to determine myocardial 18F-Galacto-RGD uptake at different time points following reperfusion. (elsevierpure.com)
  • Da in der Zellkultur protektive Effekte von NO gezeigt werden konnten, wurde deren physiologische Relevanz in der durch Ischämie/Reperfusion induzierten Apoptose ex vivo im Langendorff-Rattenherzen untersucht. (uni-frankfurt.de)
Improved endothelial function1
  • these socalled pleiotropic properties include anti-inflammatory effects, plaque stabilization, improved endothelial function and inhibition of vascular smooth muscle cell proliferation. (ac.ir)
Oxidative2
  • In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway. (spandidos-publications.com)
  • This may be mechanistically explained by attenuated endothelial oxidative damage and VCAM-1 expression in IL-36Ra-treated mice. (jci.org)
Cardiomyocyte2
  • 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)
  • Background-Prolonged myocardial ischemia results in cardiomyocyte loss despite successful revascularization. (elsevierpure.com)
Minutes of ischemia2
  • After 55 minutes of ischemia, control eEPCs (5×10 6 cells) or cells transfected with Tβ4 shRNA when indicated or 15 mg Tβ4 alone were retroinfused into the anterior interventricular vein. (elsevierpure.com)
  • Within two minutes of ischemia, extracellular pH can drop from about 7.3 to about 6.7. (benbest.com)
Induce1
  • In the host, MAC also may induce channel formation to innocent bystander endothelial cells (ECs) and ECs cannot be protected. (biomedcentral.com)
Apoptosis2
  • Wogonin could suppress apoptosis in rats experienced myocardial I/R [ 25 ]. (hindawi.com)
  • A doubling of Bax expression was observed in endothelial cells, indicating the induction of apoptosis in this cell type. (uni-frankfurt.de)
Progenitor cells2
  • Human endothelial progenitor cells (hEPCs) are adult stem cells, located in the bone marrow and peripheral blood. (intechopen.com)
  • Different phenotypes and subtypes of endothelial progenitor cells (EPCs), such as early and late EPCs, have been described according to their functionality. (intechopen.com)
Abstract1
  • Klier M, Ayhan A, Dannenberg L, Gorressen S, Polzin A, Elvers M. Role of Platelets in Processes of Myocardial Healing After Myocardial Ischemia and Reperfusion in Mice [abstract]. (isth.org)
Mice1
Inflammatory2
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.com)
Myocardium1
ENOS2
  • Another mechanism by which β3-AR agonists exert their relaxative effects on vasculature is by promoting endothelial nitric oxide synthase (eNOS) activity and NO bioavailability. (wikipedia.org)
  • is the parent ROS molecule produced by the one electron reduction of oxygen catabolized by various enzymes including NADPH oxidase, cyclooxygenase, lipoxygenases, cytochrome P450 enzymes, enzymes in the mitochondrial electron transport chain ( Yang and Lüscher, 2002 ), and also endothelial NO ⋅ Synthase (eNOS, see below). (frontiersin.org)
Angiogenesis1
  • These cells can be differentiated into mature endothelial cells, which are involved in processes of angiogenesis and vessel regeneration. (intechopen.com)
Ventricular1
  • 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)
Innate2
  • Until today the activity of such substances had to be tested in animal models because of complex interactions between endothelial cells, coagulation and innate immunity. (forschung3r.ch)
  • Now, we know that complement system, protecting the host through innate immune system, could trigger harmful endothelial pathogenesis. (biomedcentral.com)
Nitric oxide2
Cardiac function1
  • Reperfusion treatment has a potential risk of worsening tissue damage after ischemia, which can accelerate the deterioration of cardiac function [ 2 ]. (hindawi.com)
Cells6
  • Thus, it has been shown that early EPCs release cytokines that promote tissue regeneration and neovasculogenesis, whereas late EPC and endothelial colony forming cells (ECFCs) contribute to the formation of blood vessels and stimulate tube formation. (intechopen.com)
  • Accordingly, the interaction between blood cells and derived natural factors and interactions with endothelial cells cannot be studied in conventional cell culture systems. (forschung3r.ch)
  • However, replacing flatbed cultures through cultivation of endothelial cells on microcarrier beads increases the surface-to-blood volume ratio twenty-fold to reach that of small arteries and veins (16 cm 2 endothelial cell surface per ml of blood). (forschung3r.ch)
  • In this system potential "endothelial cell protectants", i.e. substances which preserve endothelial integrity and prevent activation of the endothelial cells, can be pre-incubated with the cells in the flask or co-incubated with the whole blood, and their effects assessed. (forschung3r.ch)
  • Porcine aortic endothelial cells (PAEC, used here as an example of endothelial cells in general) are expanded in conventional flatbed cell culture and then grown to confluence on microcarriers. (forschung3r.ch)
  • Protein localization studies revealed that aromatase was abundant in the murine cardiovascular system with the highest expression levels in endothelial and smooth muscle cells. (uni-wuerzburg.de)
Function2
  • In 17 healthy young subjects, we examined changes in brachial artery endothelial function using flow-mediated dilation (FMD) before and after a bout of high-intensity interval exercise, moderate-intensity endurance exercise, or a control intervention. (artinis.com)
  • In humans, I/R reduced endothelial function ( P = 0.01 vs. baseline). (ox.ac.uk)
Cardiovascular1
  • As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)
Endogenous1
  • In conventional flatbed culture systems, work with whole, non-anticoagulated blood leads to coagulation as the endothelial surface per blood volume does not suffice to ensure that the endogenous anticoagulant state can be maintained. (forschung3r.ch)
Tissues2
  • miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)
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)
Rats1
  • Results: PET imaging and autoradiography demonstrated no significant focal myocardial 18 F-Galacto-RGD uptake in non-operated control rats and at day 1 after reperfusion. (elsevierpure.com)
Stroke1
Processes1
  • This new PET tracer is promising for the monitoring of myocardial repair processes. (elsevierpure.com)
Cell2
  • Robert Rieben's research group has been investigating the potential of endothelial cell protectants for the last 10 years. (forschung3r.ch)
  • These conditions have different etiologies, but the underlying mechanism is the same, i.e. cell death due to the stop of blood supply during ischemia and aggravation of organ damage after the restoration of blood supply during reperfusion. (ncrg.no)