AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Myocardial Reperfusion InjuryMyocardial ReperfusionReperfusion InjuryMyocardial InfarctionReperfusionIschemic PostconditioningCoronary CirculationMyocardiumThrombectomySuctionCreatine KinaseMyocardial IschemiaAngioplasty, Balloon, CoronaryCardioplegic SolutionsIschemic Preconditioning, MyocardialElectrocardiographyCoronary AngiographyThrombolytic TherapyTime FactorsCardiotonic AgentsDisease Models, AnimalCoronary VesselsVentricular Function, LeftAnterior Wall Myocardial InfarctionCoronary ThrombosisPeroxidaseCreatine Kinase, MB FormPercutaneous Coronary InterventionHeart Arrest, InducedPerfusionHeartDogsHemodynamicsRats, Sprague-DawleyRats, WistarTreatment OutcomeMyocardial ContractionMitochondrial Membrane Transport ProteinsP-SelectinMitochondria, HeartNecrosisMicrocirculationRandom AllocationImmunoglobulin Fab FragmentsPlatelet Glycoprotein GPIIb-IIIa ComplexMyocytes, CardiacNeutrophilsEchocardiographyRabbitsIschemic PreconditioningSwineIschemiaEndothelium, VascularCoronary DiseaseStentsProspective StudiesPredictive Value of TestsAntibodies, MonoclonalBrain IschemiaMice, Inbred C57BLMyocardial StunningMalondialdehydeOxidative StressApoptosisInfarction, Middle Cerebral ArteryIschemic Attack, TransientMice, KnockoutImmunohistochemistryWarm IschemiaSignal TransductionSuperoxide DismutaseKidneyLiverL-Lactate DehydrogenaseCells, CulturedBrainReactive Oxygen SpeciesConstrictionOrgan PreservationRNA, MessengerDecanoic AcidsHydroxy AcidsNitric OxideBlotting, WesternProtective AgentsAntioxidantsTioproninModels, AnimalFree RadicalsNeuroprotective AgentsEnzyme InhibitorsInflammationFibrinolytic AgentsNeutrophil InfiltrationFree Radical ScavengersOrgan Preservation SolutionsVentricular PressureTumor Necrosis Factor-alphaCytoprotectionCytokines
InfarctionAcuteInjuryNecrosisContribute to the pathogenesis of myocardialApoptosisMyocardiumCardiacSubjected to ischemia followed by reperfusionOxidative stress in the pathogenesisMechanismsSubsequent reperfusionCardiovascularPerfusionCardiomyocyte deathDysfunctionEndothelialVivoApoptoticContributesClinicalOnsetTissueOrgansInflammationAutophagyCellularLipidEvidence suggestsMitochondrialFree radical generationOxygenContractionRoleSignificantly higherTreatment
Infarction33
Acute3
  • 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)
  • Our study found that fibrinogen-like protein 2 (Fgl2) gene silencing activates angiopoietin/Tie system and induces myocardial microvascular endothelial Cells proliferation and cell migration, we also found that serum Fgl2 levels elevated in patients with acute coronary syndrome (ACS), these results are preliminary, but very meaningful [ 1 , 2 ]. (silverchair.com)
  • Although chronic hyperlipidemia contributes to the pathogenesis of obesity/diabetes-related cardiomyopathy, it unclear how these hearts are affected by an acute high FA-load. (bioblast.at)
Injury49
  • Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR‑133b‑5p in myocardium was measured. (spandidos-publications.com)
  • Following myocardial I/R injury, the expression of miR‑133b‑5p was decreased in myocardium, while this decrease was restored by IPC. (spandidos-publications.com)
  • 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)
  • 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)
  • 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)
  • 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)
  • The invention pertains to a polypeptide for the protection against heart ischemia-reperfusion injury. (justia.com)
  • This is called reperfusion injury. (justia.com)
  • Ischemia-reperfusion injury (IRI) is a syndrome affecting the myocardium upon blood flow restoration following a sufficiently long interruption, such as encountered in a coronary thrombosis or heart surgery [1,2]. (justia.com)
  • One object of the present invention is to provide a therapy of heart ischemia-reperfusion injury by applying GLP-1 analogues which can be administered as single component and avoiding administration of the drug with a second compound. (justia.com)
  • The present invention is based on the surprising finding that the peptides of the invention have protective cardiovascular effects without simultaneous administration of other compounds, specifically they have protective effects on the heart against ischemia-reperfusion injury. (justia.com)
  • Postconditioning using N-Ac-GLP-1(7-34)amide N-terminally blocked and C-terminally truncated results in a limitation of ischemia-reperfusion injury in an isolated rat heart. (justia.com)
  • Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • Dive into the research topics of 'Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • This has included extensive work on the pathogenesis of myocardial ischemic and hypoxic injury. (lmbujamd.org)
  • 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)
  • 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)
  • There is substantial evidence that endothelial injury during organ procurement and preservation, caused by ischemia and subsequent reperfusion, results in endothelial dysfunction. (frontierspartnerships.org)
  • 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)
  • In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. (molcells.org)
  • Preclinical studies have identified autophagy as a process that can be activated during vascular disorders, including ischemia - reperfusion injury of the heart and other organs, cardiomyopathy, myocardial injury, and atherosclerosis. (houstonmethodist.org)
  • We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.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)
  • The phenomenon has a multifactorial pathogenesis including: distal embolization, ischemia-reperfusion injury, and individual predisposition of coronary microcirculation to injury. (unipr.it)
  • The preclinical work focuses on animal models of myocardial ischemia-reperfusion injury, which is an experimental model for STEMI, as well as ex-vivo models of myocardial ischemia. (gu.se)
  • A highly toxic aldehyde formed by reactive oxygen species (ROS) is 4-hydroxy-2-nonenal (HNE) through lipid peroxidation following myocardial ischemia/reperfusion (I/R) injury. (lsuhs.edu)
  • Therefore, we hypothesize that HNE adduction to AIFm2 mediates mitochondrial stress signaling through translocation of AIFm2 from mitochondria to the nucleus and contributes to the pathogenesis of heart failure following I/R injury. (lsuhs.edu)
  • Supplemental oxygen therapy has been used in clinical settings based on the rationale that this might enhance delivery of oxygen to the ischemic myocardium and thereby alleviating the myocardial injury. (totalassignmenthelp.com)
  • In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
  • Bone marrow mesenchymal stem cells (BMSCs) have been reported to attenuate myocardial I/R injury via their paracrine effects, which can be enhanced by hypoxic preconditioning. (researchsquare.com)
  • Previous studies have shown that ischemia/reperfusion (I/R) injury acts as a significant role in PGD(4), contributing to adverse short- and long-term clinical outcomes in the recipients. (researchsquare.com)
  • The key mechanisms underlying myocardial I/R injury include increased intracellular calcium concentration, sudden generation of reactive oxygen species (ROS) and inflammatory cytokines, adenosine triphosphate (ATP) depletion, and development of metabolic acidosis. (researchsquare.com)
  • Therefore, attenuating myocardial I/R injury during the heart transplant procedure would have a favorable impact on improving short- and long-term graft function and recipient's survival(6). (researchsquare.com)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
Necrosis4
  • Myocardial stunning or transient post-ischemic myocardial dysfunction is a state of mechanical cardiac dysfunction that can occur in a portion of myocardium without necrosis after a brief interruption in perfusion, despite the timely restoration of normal coronary blood flow. (wikipedia.org)
  • Studies have elucidated that cardiac troponin (cTn) acts as a reliable biomarker for myocardial necrosis. (totalassignmenthelp.com)
  • Following onset of myocardial necrosis as in STEMI, the values often remain elevated for 2 weeks and beyond (Badimon, 2018). (totalassignmenthelp.com)
  • A common diagnostic strategy involves ED cardiac monitoring while excluding myocardial necrosis, followed by stress testing. (westjem.com)
Contribute to the pathogenesis of myocardial1
Apoptosis7
  • Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax. (karger.com)
  • In summary, Res treatment effectively suppressed myocardial hypertrophy and apoptosis at least partially via inhibiting ER stress. (karger.com)
  • 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)
  • 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)
  • Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. (molcells.org)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
Myocardium4
Cardiac3
  • Munagala M, Phancao A. Cardiac Allograft Vasculopathy: A Review of Risk Factors and Pathogenesis. (lidsen.com)
  • Donor pre-treatment with S-NO-HSA lead to reduced fibrosis and preservation of myocardial miR-126-3p and GATA2 levels in murine cardiac isografts 60 days after transplantation. (frontierspartnerships.org)
  • 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)
Subjected to ischemia followed by reperfusion1
  • In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia followed by reperfusion with intralipid (0.5%, 1% and 2% ex-vivo, and 20% in vivo), cyclosporine-A (0.2 μM, 0.8 μM, and 1.5 μM ex- vivo and 10 mg/kg in vivo), or vehicle. (silverchair.com)
Oxidative stress in the pathogenesis1
  • OBJECTIVES: Our goal was to evaluate the role of myocardial nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and plasma markers of oxidative stress in the pathogenesis of post-operative atrial fibrillation (AF). (ox.ac.uk)
Mechanisms4
  • The underlying mechanisms of myocardial stunning have remained the subject of debate for several decades. (wikipedia.org)
  • Investigating the underlying mechanisms and understanding TIPARP for GETV will be essential to fully understanding viral pathogenesis and developing novel broad-spectrum therapeutic strategies against alphavirus infection. (bvsalud.org)
  • Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs. (google.ca)
  • Cellular mechanisms of myocardial infarct expansion. (google.ca)
Subsequent reperfusion1
  • Myocardial stunning was first described in laboratory canine experiments in the 1970s where LV wall abnormalities were observed following coronary artery occlusion and subsequent reperfusion. (wikipedia.org)
Cardiovascular3
  • Mitochondrial dysfunction has been proven to play a critical role in the pathogenesis of cardiovascular diseases. (frontiersin.org)
  • Dr. Buja is a physician-scientist who is internationally recognized for his expertise cardiovascular pathology and his research work on the pathogenesis of cardiovascular diseases. (lmbujamd.org)
  • 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)
Perfusion3
Cardiomyocyte death1
Dysfunction2
  • Imaging techniques such as echocardiography, ventriculography, and nuclear imaging can be used to detect a contractile dysfunction following reperfusion after an episode of ischemia. (wikipedia.org)
  • Some evidence supports the use of inotropic drugs in the case of severe myocardial dysfunction. (wikipedia.org)
Endothelial2
  • Now, we know that complement system, protecting the host through innate immune system, could trigger harmful endothelial pathogenesis. (biomedcentral.com)
  • Polymorphonuclear neutrophils (PMNs) contribute to postischemic reperfusion damage in many organs and tissues, a prerequisite being adhesion of PMNs to vascular endothelial cells. (silverchair.com)
Vivo1
Apoptotic1
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
Contributes1
  • Lysosomes play a pivotal role in the inflammation process, and PGRN is one of the key regulators in their functioning, which contributes to the immunomodulatory mechanism in the pathogenesis of CVDs. (biomedcentral.com)
Clinical2
  • Treatment considerations for myocardial stunning should be determined based on the clinical judgment of the cardiologist or physician, the degree of LV impairment and symptoms, and the wishes of the person. (wikipedia.org)
  • cTn has been found to show high myocardial tissue specificity and even high myocardial clinical sensitivity (Jennings, 2016). (totalassignmenthelp.com)
Onset2
Tissue1
  • Excessive production of inflammatory mediators associated with excessive activation of inflammatory cells causes circulatory and hemodynamic changes related to the pathogenesis of sepsis, characterized by microcirculatory disturbances and cellular changes that cause an imbalance between blood flow and tissue metabolic requirements, resulting in failure of multiple organs. (fapesp.br)
Organs1
  • Several factors such as contact of blood with foreign surfaces, surgical trauma, ischemia reperfusion to the organs, and release of endotoxin have been widely documented to cause SIRS after CPB. (peertechzpublications.com)
Inflammation1
  • Recently, a growing body of evidence suggests that platelets have the pivotal role in the pathogenesis of several poor prognostic mediacal conditions like inflammation and cancer (10). (peertechzpublications.com)
Autophagy1
  • The functional significance of autophagy inhumancardiovascular disease pathogenesis remains incompletely understood, andpotentially involves both adaptiveandmaladaptive outcomes, depending on model system. (houstonmethodist.org)
Cellular2
  • Short periods of myocardial ischemia are often associated with incomplete recovery of contractile function during reperfusion, despite complete preservation of cellular integrity. (silverchair.com)
  • Depressed Ca2+ activation of contraction as a consequence of reperfusion-induced cellular calcium overload in ferret hearts. (google.ca)
Lipid1
  • Plasma markers of lipid and protein oxidation (thiorbabituric acid-reactive substances, 8-isoprostane, and protein carbonyls) were also measured in blood samples drawn from a central line before surgery and after reperfusion. (ox.ac.uk)
Evidence suggests1
Mitochondrial2
  • However, harmful stimuli (such as ischemia-reperfusion, oxidative stress, and toxic chemicals) can change the direction and efficiency of intercellular mitochondrial transfer. (frontiersin.org)
  • Left ventricular (LV) function, FA oxidation rate, myocardial oxygen consumption and mechanical efficiency were assessed, followed by analysis of myocardial oxidative stress, mitochondrial respiration, protein acetylation as well as gene expression. (bioblast.at)
Free radical generation1
  • Results from canine experimental trials investigating the oxygen free-radical hypothesis for myocardial stunning have shown a reduction in free radical generation and improvement in myocardial function following anti-oxidant infusion. (wikipedia.org)
Oxygen1
  • Two leading hypotheses implicate reperfusion-induced oxygen free-radical damage and altered calcium flux resulting in intracellular hypercalcemia and desensitization of myofilaments. (wikipedia.org)
Contraction1
  • Accurate detection of regional myocardial blood flow and contraction function abnormalities must be detected at levels of high sensitivity. (wikipedia.org)
Role1
  • While the bioactive glycerophospholipid lysophosphatidic acid (LPA) plays a well-known role in atherosclerotic disease, its role in myocardial function remains virtually unexplored. (lsuhs.edu)
Significantly higher1
  • 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)
Treatment2
  • Nevertheless, significant knowledge gaps persist in scientific understanding of risk factors, pathogenesis, prevention and treatment of CAV. (lidsen.com)
  • Focusing on OB-OC-MΦ Axis and miR-23a to Explore the Pathogenesis and Treatment Strategy of Osteoporosis. (nih.gov)