Search results for "Reperfusion Injury"

showing 10 items of 140 documents

Uncoupling protein-2 (UCP2) induces mitochondrial proton leak and increases susceptibility of non-alcoholic steatohepatitis (NASH) liver to ischaemia…

2008

Background: The mechanisms of progression from fatty liver to steatohepatitis and cirrhosis are not well elucidated. Mitochondrial dysfunction represents a key factor in the progression of non-alcoholic steatohepatitis (NASH) as mitochondria are the main cellular site of fatty acid oxidation, ATP synthesis and reactive oxygen species (ROS) production. Aims: (1) To evaluate the role of the uncoupling protein 2 in controlling mitochondrial proton leak and ROS production in NASH rats and humans; and (2) to assess the acute liver damage induced by ischaemia–reperfusion in rats with NASH. Methods: Mitochondria were extracted from the livers of NASH humans and rats fed a methionine and choline de…

AdultMaleMitochondrial ROSmedicine.medical_specialtyMitochondria LiverMitochondrionBiologymedicine.disease_causeIon ChannelsMitochondrial ProteinsAdenosine TriphosphateInternal medicinemedicineAnimalsHumansUncoupling proteinUncoupling Protein 2Rats WistarBeta oxidationAdenosine TriphosphatasesMembrane Potential MitochondrialAldehydesFatty liverGastroenterologyMiddle Agedmedicine.diseaseRatsFatty LiverOxidative StressEndocrinologyMitochondrial respiratory chainLiverBiochemistryReperfusion InjuryAcute DiseaseDisease ProgressionFemaleSteatohepatitisReactive Oxygen SpeciesOxidative stressGut
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Loss of the preconditioning effect of rosuvastatin during sustained therapy: a human in vivo study

2011

Studies have demonstrated that the acute administration of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has protective effects in the setting of ischemia-reperfusion (IR). Previously, we demonstrated that a single dose of rosuvastatin prevented IR-induced endothelial dysfunction in humans through a cyclooxygenase-2-dependent mechanism. Whether the chronic administration of HMG-CoA reductase inhibitors provides similar protection remains controversial and is unknown in humans. Eighteen male volunteers were randomized to receive a single dose of rosuvastatin (20 mg) or placebo. Twenty-four hours later, endothelium-dependent, radial artery flow-mediated dilation (FMD) w…

AdultMaleTime FactorsAdolescentEndotheliumPhysiologyCoenzyme AHyperemiaPharmacologyReductaseDrug Administration ScheduleYoung Adultchemistry.chemical_compoundDouble-Blind MethodIschemiaIn vivoPhysiology (medical)medicineHumansRosuvastatinRosuvastatin CalciumOntarioAnalysis of VarianceSulfonamidesCyclooxygenase 2 Inhibitorsbiologybusiness.industryFluorobenzenesVasodilationRosuvastatin CalciumPyrimidinesmedicine.anatomical_structurechemistryCelecoxibRegional Blood FlowReperfusion InjuryRadial ArteryHMG-CoA reductasebiology.proteinCelecoxibPyrazolesHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicinebusinessBlood Flow Velocitymedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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Pentaerythrityl Tetranitrate and Nitroglycerin, but not Isosorbide Mononitrate, Prevent Endothelial Dysfunction Induced by Ischemia and Reperfusion

2007

Background— Short term exposure to nitroglycerin (GTN) has protective properties that are similar to ischemic preconditioning. Whether other organic nitrates such as pentaerithrityl tetranitrate (PETN) and isosorbide mononitrate (ISMN) have similar protective effects has not been explored. Methods and Results— In a randomized, parallel, double blind, controlled trial, 37 healthy young volunteers received no therapy (n=10), transdermal GTN 1.2 mg for 2 hours (n=9), PETN 80 mg (n=9), or ISMN 40 mg (n=9). Twenty-four hours later, endothelium-dependent flow-mediated vasodilation (FMD) was measured before and after local exposure to ischemia and reperfusion (IR). In the no therapy group, IR blu…

AdultMaleVasodilator AgentsIschemiaVasodilationPentaerythritol tetranitrateIsosorbide DinitratePharmacologyNitroglycerinchemistry.chemical_compoundDouble-Blind MethodmedicineIsosorbide mononitrateHumansPentaerythritol TetranitrateEndothelial dysfunctionIschemic PreconditioningChemistrymedicine.diseaseReperfusion InjuryAnesthesiacardiovascular systemIschemic preconditioningEndothelium VascularIsosorbide dinitrateCardiology and Cardiovascular MedicineReperfusion injurymedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
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Tolerance to nitroglycerin-induced preconditioning of the endothelium: a human in vivo study

2009

Damage and dysfunction of the vascular endothelium critically influence clinical outcomes after ischemia and reperfusion (I/R). Brief exposure to organic nitrates can protect the vascular endothelium from I/R injury via a mechanism that is similar to ischemic preconditioning and is independent of hemodynamic changes. The clinical relevance of these protective effects clearly depends on whether they can be sustained over time. Twenty-four healthy (age 25–32) male volunteers were randomized to receive 1) transdermal nitroglycerin (GTN; 0.6 mg/h) administered for 2 h on 1 day only, 2) transdermal GTN for 2 h/day for 7 days, or 3) continuous therapy with transdermal GTN for 7 days. Eight volunt…

AdultMalemedicine.medical_specialtyEndotheliumPhysiologyVasodilator AgentsIschemiaAscorbic AcidAdministration CutaneousAntioxidantsNitroglycerinIn vivoPhysiology (medical)Internal medicinemedicineHumansInfusions Intra-ArterialIschemic PreconditioningNitroglycerinDose-Response Relationship Drugbusiness.industryDrug Tolerancemedicine.diseaseAcetylcholineOrganic nitratesPlethysmographyVascular endotheliummedicine.anatomical_structureReperfusion InjuryAnesthesiaCirculatory systemcardiovascular systemCardiologyIschemic preconditioningEndothelium VascularCardiology and Cardiovascular Medicinebusinesscirculatory and respiratory physiologymedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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Release of necrosis markers and cardiovascular magnetic resonance-derived microvascular perfusion in reperfused ST-elevation myocardial infarction

2009

Abstract Introduction The association of the temporal evolution of cardiac necrosis marker release with cardiovascular magnetic resonance-derived microvascular perfusion after ST-elevation myocardial infarction is unknown. Methods We analyzed 163 patients with a first ST-elevation myocardial infarction and a patent infarct-related artery treated with thrombolysis (67%) or primary angioplasty (33%). Using first-pass perfusion CMR, abnormal perfusion was defined as a lack of contrast arrival into the infarct area in > 1 segment. Troponin I, creatine kinase MB and myoglobin were measured upon arrival and at 6, 12, 24, 48 and 96 hours after reperfusion. Results Abnormal perfusion was detected i…

AdultMalemedicine.medical_specialtyMyocardial InfarctionMyocardial Reperfusion InjuryCoronary AngiographyNecrosisReperfusion therapyInternal medicineTroponin ImedicineCreatine Kinase MB FormHumansProspective StudiesMyocardial infarctionAngioplasty Balloon CoronaryAgedmedicine.diagnostic_testbiologyMyoglobinbusiness.industryMyocardiumST elevationMagnetic resonance imagingHematologyMiddle AgedPrognosismedicine.diseaseMagnetic Resonance ImagingTroponinTroponinTreatment Outcomebiology.proteinCardiologyFemaleCreatine kinasebusinessPerfusionBiomarkersThrombosis Research
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The efficacy of N-acetylcysteine as a hepatoprotective agent in liver transplantation

1998

One of the most common complications after liver transplantation is primary graft dysfunction which results from severe deterioration of the microcirculation. The data obtained from our experimental studies indicate that N-acetylcysteine (NAC) is able to reduce the severity of ischemia/reperfusion injury and improves postoperative graft function after liver transplantation in rats. The aim of this pilot study was to evaluate the efficacy of NAC as a hepatoprotective agent under clinical conditions. A group of 30 liver transplanted patients were treated with NAC, and 30 patients (control group) were treated with a 5 % solution of glucose only. In the NAC group we observed a distinct reductio…

AdultNephrologymedicine.medical_specialtymedicine.medical_treatmentIschemiaPrimary Graft DysfunctionPilot ProjectsLiver transplantationGastroenterologyAcetylcysteineInternal medicineHumansMedicineProspective StudiesHepatoprotective AgentTransplantationbusiness.industryMiddle Agedmedicine.diseaseAcetylcysteineLiver TransplantationSurgeryReperfusion InjuryLiver functionbusinessReperfusion injurymedicine.drugTransplant International
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Application of C1-Esterase Inhibitor During Reperfusion of Ischemic Myocardium

2001

Background—Complement activation during reperfusion of ischemic myocardium augments myocardial injury, and complement inhibition with C1-esterase inhibitor (C1-INH) at the time of reperfusion exerts marked cardioprotective effects in experimental studies. Application of C1-INH in newborns, however, was recently reported to have dangerous and even lethal side effects. This study addresses the essential role of dosage in studies using C1-INH.Methods and Results—Cardioprotection by C1-INH was examined in a pig model with 60 minutes of coronary occlusion followed by 120 minutes of reperfusion. C1-INH was administered intravenously 5 to 10 minutes before coronary reperfusion without heparin at a…

Anaphylatoxinsmedicine.medical_specialtyNecrosisSwineHeart VentriclesPartial PressureMyocardial IschemiaIschemiaComplement C1 Inactivator ProteinsPharmacologyNecrosisTroponin TCoronary CirculationPhysiology (medical)Internal medicineAnimalsMedicineLactic AcidMyocardial infarctionCardiac OutputCreatine KinaseCardioprotectionDose-Response Relationship Drugbiologybusiness.industryMyocardiumHemodynamicsHeparinmedicine.diseaseComplement systemOxygenMicroscopy ElectronEndocrinologyCoronary occlusionEnzyme inhibitorReperfusion Injurybiology.proteinBlood Gas Analysismedicine.symptomCardiology and Cardiovascular Medicinebusinessmedicine.drugCirculation
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Antioxidant activity and cardioprotective effect of a nonalcoholic extract of Vaccinium meridionale Swartz during ischemia-reperfusion in rats

2013

Our objective was to assess the antioxidant properties and the effects against the reperfusion injury of a nonalcoholic extract obtained by fermentation from the Colombian blueberry, mortiño (Vaccinium meridionale Swartz, Ericaceae). Antioxidant properties were assessed by in vitro systems. To examine the postischemic myocardial function, isolated rat hearts were treated 10 min before ischemia and during the first 10 min of reperfusion with the extract. To analyze the participation of nitric oxide (NO), other experiments were performed in the presence of nitric oxide synthase (NOS) inhibition with NG-nitro-L-arginine methyl ester (L-NAME). In cardiac tissue thiobarbituric acid reactive subs…

AntioxidantCIENCIAS MÉDICAS Y DE LA SALUDJuicesArticle Subjectmedicine.medical_treatmentNITRIC OXIDASE SYNTHASEPharmacologyEndothelial NOSFisiologíaNitric oxideAnthocyaninschemistry.chemical_compoundISCHEMIA-REPERFUSIONEnosANTIOXIDANTTBARSMedicineVACCINIUM MERIDIONALE SWCardioprotectionbiologybusiness.industry//purl.org/becyt/ford/3.1 [https]lcsh:Other systems of medicinelcsh:RZ201-999medicine.diseasebiology.organism_classificationNitric oxide synthaseMedicina BásicaComplementary and alternative medicineBiochemistrychemistryCiencias Médicasbiology.protein//purl.org/becyt/ford/3 [https]Anthocyanin degradationbusinessReperfusion injuryResearch Article
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Melatonin protects against ischemia-reperfusion injury and inhibits apoptosis in isolated working rat heart.

2003

INTRODUCTION: Melatonin (MEL), a pineal hormone, is well known as a potent antioxidant in a variety of ischemia-reperfusion models. Recent studies have assumed a pivotal role of reactive oxygen species (ROS) in the development of apoptosis. There are few pieces of information concerning a possible protective role of MEL against apoptosis in ischemia-reperfusion injury of myocardium. METHODS: We conducted an in vitro experiment: (1) to study the effect of MEL in the model of isolated and perfused working rat heart; (2) to evaluate the antioxidant capacity of MEL by a simple fluorescence test; and (3) to analyze the extent of apoptosis inhibition by MEL. Four groups of male Wistar rat were us…

Antioxidantmedicine.medical_treatmentIschemiaPharmacologymedicine.disease_causePathology and Forensic MedicineMelatonin03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesPhysiology (medical)medicineneoplasms030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesTUNEL assaymedicine.disease3. Good healthchemistryApoptosisAnesthesiaReperfusion injury030217 neurology & neurosurgeryOxidative stressmedicine.drugPathophysiology : the official journal of the International Society for Pathophysiology
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Some aspects of cardiac antioxidant defence: Ebselen (PZ 51) treatment increases glutathione peroxidase activity in the rat heart

1990

Ebselcn (PZ 5 1 : 2-phenyl1.2-benzisoelenazol-3-( 2H)-one 1 is ii synthetic organoselenium compound with anti-inflammatory activity ( I . 21, which exhibits glutathione peroxidase (GSH-Px)-like activity, catalysing the reduction o f hydrogen peroxide as well as other organic peroxides [3-5]. Its antiinflammatory effect may be mediated by either the GSH-Px activity, the inhibition of leukotriene B4 formation [6], the antioxidant capacity, or a combination of all of them. Many attempts have been made to increase the antioxidant capacity of the myocardium, since free radical generation has been demonstrated in ischaemia-reperfusion damage [7, 81; superoxide dismutase (SOD) and catalase have be…

AzolesAntioxidantmedicine.medical_treatmentMyocardial Reperfusion InjuryIsoindolesPharmacologyBiochemistryAntioxidantsSuperoxide dismutaseSeleniumchemistry.chemical_compoundOrganoselenium CompoundsmedicineAnimalsHydrogen peroxidechemistry.chemical_classificationGlutathione PeroxidasebiologyChemistryEbselenMyocardiumGlutathione peroxidaseHeartRats Inbred StrainsGlutathioneRatsBiochemistryCatalasebiology.proteinPeroxidase
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