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IschemiaCold IschemiaWarm IschemiaMyocardial IschemiaBrain IschemiaReperfusion InjuryOrgan PreservationDelayed Graft FunctionWounds and InjuriesMembrane FusionTissue DonorsGraft SurvivalTime FactorsNephrectomyCell FusionKidney TransplantationLiver TransplantationMyocardial Reperfusion InjuryTissue and Organ HarvestingBrain InjuriesDeathTissue and Organ ProcurementCadaverLiving DonorsRecombinant Fusion ProteinsOrgan Preservation SolutionsDisease Models, AnimalRaffinoseBiliary TractIschemic Attack, TransientRats, Sprague-DawleyReperfusionAthletic InjuriesSpinal Cord InjuriesRetrospective StudiesPancreas TransplantationIschemic PreconditioningLaparoscopyBrain DeathTransplantsSpinal FusionRoboticsTreatment OutcomeRats, WistarKidneySpinal Cord IschemiaViral Fusion ProteinsGerbillinaeGraft RejectionMyocardiumGene FusionAllopurinolPostoperative ComplicationsNeuroprotective AgentsIschemic Preconditioning, MyocardialKidney Tubular Necrosis, AcuteBile DuctsInjury Severity ScorePrimary Graft DysfunctionLung InjuryInfarction, Middle Cerebral ArteryLeg InjuriesMyocardial ReperfusionBiliary Tract DiseasesLiver FailureHepatic ArteryBrainAcute Kidney InjuryTissue PreservationOncogene Proteins, FusionCerebrovascular CirculationDonor SelectionRisk FactorsLiverHindlimbMice, Inbred C57BLCerebral InfarctionEye InjuriesCoronary CirculationTissue FixationTransplantation, HomologousAcute Lung InjuryHeartFollow-Up StudiesCreatinineNeck InjuriesMyocardial InfarctionPerfusionDogsArm InjuriesAbdominal InjuriesHemodynamicsRenal ArteryAnastomosis, SurgicalProspective StudiesCardiotonic AgentsNecrosisNeuronsConstrictionCoronary Disease
PathophysiologicalTherapeuticMechanismsPathwaysOxygenTreatmentFunctionDysfunctionModel
Pathophysiological3
  • 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)
  • 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)
  • Putative pathophysiological mechanisms linking I/R injury and liver cancer recurrence include an increased implantation of circulating cancer cells in the ischemic liver and the upregulation of proliferation and angiogenic factors following the ischemic insult. (123dok.net)
Therapeutic2
  • 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)
  • Therapeutic strategies tackling I/R injury could not only improve post-surgical organ function, but also allow a reduction in the risk of cancer recurrence. (123dok.net)
Mechanisms2
  • 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)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
Pathways1
  • I/R injury, through the liberation of radical oxygen species and the activation of inflammatory pathways, induces cellular injury and mi-crocirculatory damage, which translate to organ dysfunc-tion, morbidity, and increased health care costs [7, 8]. (123dok.net)
Oxygen1
Treatment2
  • 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)
  • Clinical studies have shown that pre-treatment and post-operative treatment with Coenzyme Q10 attenuates the extent of ischemia reperfusion injury. (q10facts.com)
Function3
  • 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)
  • In conclusion, on top of its harmful early impact on organ function, I/R injury is linked to increased tumor growth. (123dok.net)
  • In liver transplantation, tissue damage at reperfusion is mostly correlated with warm and cold ischemia times and leads in turn to poor graft function [13] and biliary complications [14,15]. (123dok.net)
Dysfunction2
  • Furthermore, the effects of IR-injured skeletal muscle in clinical conditions such as compartment syndrome or crush syndrome may induce rhabdomyolysis and are associated with so-called remote injuries as acute kidney dysfunction. (bvsalud.org)
  • An uncontrolled balance of mitochondrial dynamics has been shown to contribute to cardiac dysfunction during ischemia/reperfusion (I/R) injury. (silverchair.com)
Model1
  • This chapter will provide a detailed experimental setup and a step-by-step protocol for the dynamic imaging of leukocyte-endothelial-interaction in an ischemia/reperfusion injury model. (bvsalud.org)