Search results for "reperfusion injury"

showing 10 items of 140 documents

Carbon Monoxide Protects Against Ischemia-reperfusion Injury in Vitro via Antioxidant Properties

2012

Carbon monoxide (CO) is believed to mediate many of the cytoprotective effects attributed to the activation of heme oxygenase (HO-1), the enzyme responsible for CO production. Recently, the study of CO-releasing molecules (CO-RMs) has provided a new approach for the delivery of CO. In the present study, we examined whether the cardioprotective properties of CO-RM2 in isolated rat hearts subjected to an ischemia-reperfusion (I/R) sequence were associated with the presence of CO. In addition, the antioxidant properties of CO-RM2 were evaluated. In hearts pretreated with CO-RM2, the improvement in contractile function at the end of the reperfusion period after 20 min of global total ischemia w…

MaleAntioxidantCardiotonic AgentsTime FactorsPhysiologymedicine.medical_treatmentIschemiaPharmacologyIn Vitro Techniquesmedicine.disease_causeAntioxidantsVentricular Function Left03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemSuperoxidesEthidiummedicineOrganometallic CompoundsAnimalsRats WistarComputingMilieux_MISCELLANEOUS030304 developmental biologychemistry.chemical_classification0303 health sciencesCarbon MonoxideL-Lactate DehydrogenaseSuperoxideHeartmedicine.diseaseMyocardial ContractionIn vitroRats[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemHeme oxygenaseOxidative StressEnzymechemistryBiochemistry030220 oncology & carcinogenesisReperfusion InjuryReperfusion injuryOxidative stress
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Endothelial Cell Swelling and Brain Perfusion

1997

Background: Whereas the contribution of glial swelling to no-reflow conditions in the ischemic penumbra or during reperfusion after global ischemia is widely discussed, little is known about cell volume control of endothelial cells under reperfusion conditions. Methods: The effect of extracellular acidosis-a key mediator of secondary brain damage-on cell volume was studied in the GM7373 endothelial cell line. Experiments were performed at pH = 6.0 in the presence or absence of bicarbonate, and during exposure to inhibitors of specific transport systems such as ethyl isopropyl amiloride or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. Results: Endothelial swelling to 111.1 ± 3.4% was f…

medicine.medical_specialtyCell Membrane PermeabilityBicarbonateIschemiaPharmacologyBrain IschemiaCell Linechemistry.chemical_compoundmedicineExtracellularAnimalsCell Sizebusiness.industryMicrocirculationPenumbraHydrogen-Ion Concentrationmedicine.diseaseAmilorideSurgeryEndothelial stem cellchemistryCerebrovascular CirculationReperfusion InjuryCattleEndothelium VascularSwellingmedicine.symptomAcidosisbusinessIsopropylmedicine.drugThe Journal of Trauma: Injury, Infection, and Critical Care
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Influence of the terminal complement-complex on reperfusion injury, no-reflow and arrhythmias: a comparison between C6-competent and C6-deficient rab…

1996

Objective: The complement system has been suggested to play a role in reperfusion injury which may result from an enhanced destruction of myocardial tissue or from an impairment of reflow. We investigated the influence of the C5b-9 complement complex on infarct size, reflow and arrhythmogenesis. Methods: Twenty-eight C6-competent rabbits and 18 rabbits with congenital C6 deficiency were subjected to either 30 min or 2 h of coronary artery occlusion followed by reperfusion. C6 deficiency was confirmed by the complement titration test and immunohistology. The triphenyl tetrazolium chloride method was used to delineate infarct size. Reflow into infarcted areas was evaluated histologically afte…

medicine.medical_specialtyTime FactorsPhysiologyMyocardial InfarctionIschemiaInfarctionMyocardial Reperfusion InjuryComplement Membrane Attack ComplexElectrocardiographyReperfusion therapyPhysiology (medical)Internal medicinemedicineAnimalscardiovascular diseasesComplement Activationbusiness.industryArrhythmias Cardiacmedicine.diseaseImmunohistochemistryComplement C6Complement systemRegional Blood FlowCoronary occlusionNo reflow phenomenoncardiovascular systemCardiologyRabbitsCardiology and Cardiovascular MedicineComplement membrane attack complexbusinessReperfusion injuryCardiovascular Research
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Preconditioning by Mitochondrial Reactive Oxygen Species Improves the Proangiogenic Potential of Adipose-Derived Cells-Based Therapy

2009

Objective— Transplantation of adipose-derived stroma cells (ADSCs) stimulates neovascularization after experimental ischemic injury. ADSC proangiogenic potential is likely mediated by their ability to differentiate into endothelial cells and produce a wide array of angiogenic and antiapoptotic factors. Mitochondrial reactive oxygen species (ROS) have been shown to control ADSC differentiation. We therefore hypothesized that mitochondrial ROS production may change the ADSC proangiogenic properties. Methods and Results— The use of pharmacological strategies (mitochondrial inhibitors, antimycin, and rotenone, with or without antioxidants) allowed us to specifically and precisely modulate mito…

MaleMitochondrial ROSProgrammed cell deathStromal Cells/cytology/metabolismAngiogenesisCellsReactive Oxygen Species/*metabolismNeovascularization PhysiologicBiologyMitochondrionmedicine.disease_causeMice03 medical and health sciences0302 clinical medicineAdipocytesmedicineAnimalsEndothelial Cells/*cytology/*physiologyCells CulturedNeovascularization030304 developmental biologyMitochondria/*metabolismchemistry.chemical_classificationReperfusion Injury/physiopathology0303 health sciencesReactive oxygen speciesCulturedEndothelial CellsCell DifferentiationMitochondriaCell biologyCell Differentiation/*physiologyTransplantationPhysiologic/*physiologychemistryReperfusion Injury030220 oncology & carcinogenesisImmunologyStromal CellsStem cellReactive Oxygen SpeciesCardiology and Cardiovascular MedicineOxidative stressArteriosclerosis, Thrombosis, and Vascular Biology
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Targeting antioxidants to mitochondria: a potential new therapeutic strategy for cardiovascular diseases.

2007

Mitochondria produce large amounts of free radicals and play an important role in the life and death of a cell. Thus, mitochondrial oxidative damage and dysfunction contribute to a number of cell pathologies that manifest themselves through a range of conditions including ischemia-reperfusion injury, sepsis, diabetes, atherosclerosis and, consequently, cardiovascular diseases (CVD). In fact, endothelial dysfunction, characterized by a loss of nitric oxide (NO) bioactivity, occurs early on in the development of atherosclerosis, and determines future vascular complications. Although the molecular mechanisms responsible for mitochondria-mediated disease processes are not yet clear, oxidative s…

Oxidative phosphorylationPharmacologyMitochondrionBiologymedicine.disease_causeAntioxidantsNitric oxidechemistry.chemical_compoundDrug DiscoverymedicineAnimalsHumansEndothelial dysfunctionInner mitochondrial membranePharmacologychemistry.chemical_classificationReactive oxygen speciesMolecular Structuremedicine.diseaseMitochondriaOxidative StresschemistryCardiovascular DiseasesReactive Oxygen SpeciesReperfusion injuryOxidative stressCurrent pharmaceutical design
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The role of mitochondrial transition pore, and its modulation, in traumatic brain injury and delayed neurodegeneration after TBI

2009

Following severe traumatic brain injury (TBI), a complex interplay of pathomechanism, such as exitotoxicity, oxidative stress, inflammatory events, and mitochondrial dysfunction occurs. This leads to a cascade of neuronal and axonal pathologies, which ultimately lead to axonal failure, neuronal energy metabolic failure, and neuronal death, which in turn determine patient outcome. For mild and moderate TBI, the pathomechanism is similar but much less frequent and ischemic cell death is unusual, except with mass lesions. Involvement of mitochondria in acute post-traumatic neurodegeneration has been extensively studied during the last decade, and there are a number of investigations implicatin…

Time FactorsTraumatic brain injurymedicine.medical_treatmentMitochondrionMitochondrial Membrane Transport ProteinsNeuroprotectionBrain Ischemiachemistry.chemical_compoundDevelopmental NeuroscienceCyclosporin aAnimalsHumansMedicineMitochondrial Permeability Transition Porebusiness.industryMPTPNeurodegenerationmedicine.diseasenervous system diseasesnervous systemNeurologyMitochondrial permeability transition porechemistryBrain InjuriesReperfusion InjuryAcute DiseaseChronic DiseaseNerve DegenerationAxotomybusinessNeuroscience
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The Long-Term Effect of Sevoflurane on Neuronal Cell Damage and Expression of Apoptotic Factors After Cerebral Ischemia and Reperfusion in Rats

2006

We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins of apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl and N2O/O2; control) and Group 2 (2.0 vol% sevoflurane and O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals were killed after 1, 3, 7, and 28 days. In hematoxylin and eosin-stained brain sections eosinophilic hippocampal neurons were counted. Activated caspase-3 and the apoptosis-regulating proteins Bax, Bcl-2, Mdm-2, and p53 were analyzed by i…

MaleMethyl Ethersmedicine.medical_specialtyH&E stainIschemiaCell CountHippocampal formationHippocampusNeuroprotectionSevofluraneBrain IschemiaRats Sprague-DawleySevofluraneInternal medicineEosinophilicmedicineAnimalsNeuronsCaspase 3business.industrymedicine.diseaseImmunohistochemistryRatsEnzyme ActivationNeuroprotective AgentsAnesthesiology and Pain MedicineBlood pressureEndocrinologyCaspasesCerebrovascular CirculationReperfusion InjuryAnesthesiaAnesthetics InhalationApoptosis Regulatory ProteinsbusinessBlood Flow VelocityImmunostainingmedicine.drugAnesthesia & Analgesia
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P4613Long-term impact of postnatal nutritional programming on cardiac sensitivity to ischemia-reperfusion injury in vivo and on cardio-protective pat…

2019

Abstract Introduction Nutritional disturbances during the postnatal period may be responsible for a predisposition, or “programming”, to increased cardio-metabolic risk and to a progressive alteration of left ventricular contractility in adulthood. This nutritional perinatal programming may also lead to an alteration of cellular pathways involved in cardiac protection, such as the specific RISK and SAFE pathways, highlighted during pre- and post-ischemic conditioning or those of sirtuins (SIRT), histone deacetylases involved in the regulation of essential biological process. Purpose Our aim was to evaluate in mice the impact of postnatal overfeeding (PNOF) on cardiac sensitivity to ischemia…

medicine.medical_specialtybusiness.industryCardio protectiveIschemiaInfarctionmedicine.diseaseOvernutritionReperfusion therapyIn vivoInternal medicineCardiologymedicineCardiology and Cardiovascular MedicinebusinessLigationReperfusion injuryEuropean Heart Journal
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Area at Risk and Viability after Myocardial Ischemia and Reperfusion Can Be Determined by Contrast-Enhanced Cardiac Magnetic Resonance Imaging

2008

<i>Background/Aims:</i> Clinical differentiation between infarcted and viable myocardium in the ischemic area at risk is controversial. We investigated the potential of contrast-enhanced cardiac magnetic resonance imaging (ceCMRI) in determining the area at risk 24 h after ischemia. <i>Methods:</i> Myocardial ischemia was induced by percutaneous coronary intervention of the left anterior descending coronary artery in pigs. Coronary occlusion time was 30 min in group A, which caused little myocardial infarction and 45 min in group B, which led to irreversible damage. 24 h after reperfusion ceCMRI was performed at 2 and 15 min after administration of gadolinium-diethyl…

Gadolinium DTPAMalemedicine.medical_specialtyCell SurvivalSwinemedia_common.quotation_subjectMyocardial Reperfusion InjuryCoronary AngiographyMicrocirculationArea at riskNecrosisText miningCardiac magnetic resonance imagingInternal medicinemedicineAnimalsContrast (vision)cardiovascular diseasesMyocardial infarctionmedia_commonTissue Survivalmedicine.diagnostic_testbusiness.industryMyocardiumMagnetic resonance imagingmedicine.diseaseMagnetic Resonance Imagingcardiovascular systemCardiologyFemaleSurgeryRadiologybusinessReperfusion injuryEuropean Surgical Research
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Pharmacology of Ischemia-Reperfusion. Translational Research Considerations.

2016

Ischemia-reperfusion (IRI) is a complex physiopathological mechanism involving a large number of metabolic processes that can eventually lead to cell apoptosis and ultimately tissue necrosis. Treatment approaches intended to reduce or palliate the effects of IRI are varied, and are aimed basically at: inhibiting cell apoptosis and the complement system in the inflammatory process deriving from IRI, modulating calcium levels, maintaining mitochondrial membrane integrity, reducing the oxidative effects of IRI and levels of inflammatory cytokines, or minimizing the action of macrophages, neutrophils, and other cell types. This study involved an extensive, up-to-date review of the bibliography …

NeutrophilsIschemiaApoptosis030204 cardiovascular system & hematologyPharmacologyurologic and male genital diseasesAntioxidantsProinflammatory cytokineTranslational Research Biomedical03 medical and health sciences0302 clinical medicinemedicineHumanscardiovascular diseasesIschemic PreconditioningOpiate alkaloidurogenital systemMechanism (biology)business.industryTumor Necrosis Factor-alphaMacrophagesOpiate AlkaloidsfungiNF-kappa BComplement System Proteinsmedicine.diseaseApoptosis030220 oncology & carcinogenesisReperfusion InjuryAnesthetics InhalationIschemic preconditioningCytokinesSurgeryTumor necrosis factor alphaInflammation MediatorsbusinessReperfusion injuryJournal of investigative surgery : the official journal of the Academy of Surgical Research
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