Search results for "Reperfusion"

showing 10 items of 210 documents

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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Ozone therapy in idiopathic carpal tunnel syndrome. Biochemical, neurophysiological and clinical aspects

2018

Purpose.
 Idiopathic Carpal Tunnel Syndrome (CTS) is the most common entrapment neuropathy; however few and only retrospective studies have been found in search engines about Ozone Therapy. 
 The aim of this paper was to evaluate clinical and neurophysiological outcome following Ozone Therapy in CTS.
 We focused the attention on the evidences concerning the role of Subsynovial Connective Tissue (SSCT) in the pathogenesis of CTS and the ozone pre-conditioning effects linked to pain and inflammatory pathways and to fibrosis induced by Ischemia-Reperfusion Injury.
 
 Materials and methods.
 Thirty-five patients, aged between 21 and 80, were stratified clinically b…

Oxidative stress Fibrosisbusiness.industryOzone therapy Carpal tunnel syndrome Ischemia reperfusion injury Oxidative stress Fibrosis TimingRetrospective cohort study:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseOzone therapyPathophysiologymedicine.anatomical_structureFibrosisAnesthesiaUNESCO::CIENCIAS MÉDICASEntrapment NeuropathyOzone therapyCarpal tunnel syndrome Ischemia reperfusion injuryMedicineCarpal tunnelTimingbusinessCarpal tunnel syndromeSensory nerve
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Infarct Size Measurement by Triphenyltetrazolium Chloride StainingVersus In VivoInjection of Propidium Iodide

1997

Infarct size delineation by triphenyltetrazolium chloride (TTC) staining is dependent on sufficient reperfusion. We therefore evaluated the possibility of using propidium iodide (PI), a reagent conventionally used in flow cytometry to fluorescently stain dead cells, for infarct size analysis after short periods of reperfusion. Forty-five rabbits were subjected to either 15 min, 2 h or 4.5 h of coronary artery occlusion without reperfusion, or to 15 min, 30 min and 2 h of coronary artery occlusion followed by 30 min, 1 h and 3 h of reperfusion. Fifteen min before terminating the experiment, PI was injected into the left atrium. Patent blue violet was used to delineate the area at risk. Follo…

Pathologymedicine.medical_specialtyCell Membrane PermeabilityMyocardial InfarctionTetrazolium SaltsMyocardial ReperfusionStainFlow cytometrychemistry.chemical_compoundIn vivoOcclusionmedicineAnimalscardiovascular diseasesPropidium iodideColoring AgentsMolecular BiologyStaining and Labelingmedicine.diagnostic_testChemistrybusiness.industryMyocardiumHistologymedicine.diseaseCoronary VesselsStainingInjections Intra-ArterialRabbitsCardiology and Cardiovascular MedicineNuclear medicinebusinessReperfusion injuryPropidiumJournal of Molecular and Cellular Cardiology
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Microvascular in vivo assessment of reperfusion injury: significance of prostaglandin E1 and I2 in postischemic “no-reflow” and “reflow-paradox”

2004

Microvascular ischemia-reperfusion (I/R) injury is characterized by failure of capillary perfusion ("no-reflow") and reoxygenation-associated phenomena ("reflow-paradox"), including activation of leukocyte-endothelium interaction with cytotoxic mediator-induced loss of endothelial integrity. The objectives of this study were to elucidate the impact of both prostaglandins E(1) (PGE(1)) and I(2) (PGI(2)) in microvascular reperfusion injury, with special focus on the distinct pathophysiology of no-reflow- and reflow-paradox phenomena.By use of the hamster dorsal skinfold preparation and in vivo fluorescence microscopy, the microcirculation of a striated skin muscle was assessed before 4 h of p…

Pathologymedicine.medical_specialtyEndotheliummedicine.medical_treatmentIschemiaPharmacologyMicrocirculationCapillary Permeabilitychemistry.chemical_compoundIn vivoCricetinaemedicineAnimalsVascular Diseasescardiovascular diseasesAlprostadilMuscle SkeletalProstaglandin E1SkinMicroscopyMesocricetusbusiness.industryMicrocirculationmedicine.diseaseEpoprostenolPathophysiologyCapillariesChemotaxis Leukocytemedicine.anatomical_structurechemistryReperfusion InjuryModels Animalcardiovascular systemSurgeryEndothelium VascularbusinessReperfusion injuryPlatelet Aggregation InhibitorsProstaglandin EJournal of Surgical Research
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Influence of N-acetylcysteine on hepatic amino acid metabolism in patients undergoing orthotopic liver transplantation

2001

Experimental treatment with the antioxidant and glutathione precursor N-acetylcysteine (NAC) has been performed in orthotopic liver transplantation (OLT) to reduce reperfusion injury. To investigate the effect of NAC on the hepatic and intestinal amino acid metabolism, intraoperative amino acid exchange rates were studied in liver transplant recipients with high dose NAC treatment (n = 10) and in control patients (n = 9). Treatment with NAC was found to cause a loss of amino acids and increased urea nitrogen release from the liver graft. The net balance of most amino acids was shifted to increased hepatic release or decreased hepatic uptake. The initial cumulative splanchnic release of all …

PharmacologyAcetylcysteinechemistry.chemical_compoundAmino Acids AromaticmedicineHumansUreaSplanchnic CirculationAmino Acidschemistry.chemical_classificationTransplantationbusiness.industryBiological TransportMetabolismGlutathioneFree Radical ScavengersMiddle Agedmedicine.diseaseGlutathioneAmino acidAcetylcysteineLiver TransplantationTransplantationGlutamineProtein catabolismchemistryBiochemistryLiverReperfusion InjurybusinessReperfusion injuryAmino Acids Branched-Chainmedicine.drugTransplant International
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Anti-inflammatory actions of aprotinin provide dose-dependent cardioprotection from reperfusion injury

2008

Background and purpose: Myocardial injury following ischaemia and reperfusion has been attributed to activation and transmigration of polymorphonuclear leukocytes (PMNs) with release of mediators including oxygen-derived radicals and proteases causing damage. Experimental approach: We studied the serine protease inhibitor aprotinin in an in vivo rabbit model of 1 h of myocardial ischaemia followed by 3 h of reperfusion (MI+R). Aprotinin (10 000 Ukg−1) or its vehicle were injected 5 min prior to the start of reperfusion. Key results: Myocardial injury was significantly reduced with aprotinin treatment as indicated by a reduced necrotic area (11±2.7% necrosis as percentage of area at risk aft…

PharmacologyCardioprotectionProteasesNecrosisAntifibrinolyticmedicine.drug_classbusiness.industryIschemiaPharmacologymedicine.diseaseApoptosisImmunologymedicineAprotininmedicine.symptombusinessReperfusion injuryhormones hormone substitutes and hormone antagonistsmedicine.drugBritish Journal of Pharmacology
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Sodium/hydrogen exchange inhibition with cariporide reduces leukocyte adhesion via P-selectin suppression during inflammation

2008

Background and purpose: The Na+/H+ exchange (NHE) inhibitor cariporide is known to ameliorate ischaemia/reperfusion (I/R) injury by reduction of cytosolic Ca2+ overload. Leukocyte activation and infiltration also mediates I/R injury but whether cariporide reduces I/R injury by affecting leukocyte activation is unknown. We studied the effect of cariporide on thrombin and I/R induced leukocyte activation and infiltration models and examined P-selectin expression as a potential mechanism for any identified effects. Experimental approach: An in vivo rat mesenteric microcirculation microscopy model was used with stimulation by thrombin (0.5 μ ml−1) superfusion or ischaemia (by haemorrhagic shock…

PharmacologyP-selectinCariporideCell adhesion moleculeLeukocyte RollingPharmacologymedicine.diseaseExtravasationchemistry.chemical_compoundThrombinchemistryImmunologymedicineReperfusion injuryInfiltration (medical)medicine.drugBritish Journal of Pharmacology
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Pentoxifylline in liver ischemia and reperfusion.

2013

Pentoxifylline is a methylxanthine compound which was first filed in 1973 and registered in 1974 in the United States by Sanofi-Aventis Deustchland Gmbh for the treatment of intermittent claudication for chronic occlusive arterial disease. This methylxanthine was later discovered to be a phosphodiesterase inhibitor. Furthermore, its hemorheological properties and its function as an inhibitor of inflammatory cytokines, like TNF- α, allowed researchers to study its effects in organ ischemia and reperfusion and transplantation. Although this drug has demonstrated beneficial effects, the mechanisms by which Pentoxifylline exerts a protective effect are not fully understood. This paper focuses o…

Phosphodiesterase InhibitorsIschemiaApoptosisPharmacologyPentoxifyllineProinflammatory cytokineIschemiamedicineAnimalsHumansPhosphodiesterase inhibitorPentoxifyllinebusiness.industryTumor Necrosis Factor-alphaLiver Diseasesmedicine.diseaseIntermittent claudicationLiver TransplantationTransplantationLiverAnesthesiaReperfusion InjurySurgeryTumor necrosis factor alphamedicine.symptombusinessReperfusion injurymedicine.drugJournal of investigative surgery : the official journal of the Academy of Surgical Research
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Targeting Mitochondria: A New Promising Approach for the Treatment of Liver Diseases

2010

Mitochondrial dysfunction acts as a common pathogenetic mechanism in several acute and chronic liver diseases, such as Alcoholic and Non-Alcoholic Fatty Liver Disease (NAFLD), drug-induced steatohepatitis, viral hepatitis, biliary cirrhosis, hepatocellular carcinoma, ischemia/reperfusion injury and transplant rejection. In particular mitochondrial uncoupling has been recently identified to play a determinant role in the pathogenesis of liver diseases by causing decrease of mitochondrial proton motive force and ATP depletion. Damaged mitochondria present defects in lipid homeostasis, bioenergetics impairment and overproduction of Reactive Oxygen Species (ROS), leading to lipid accumulation a…

Programmed cell deathMitochondrionBiologymedicine.disease_causeBiochemistryLiver diseaseDrug Delivery SystemsDrug DiscoverymedicineAnimalsHumansPharmacologychemistry.chemical_classificationReactive oxygen speciesCell DeathLiver DiseasesOrganic ChemistryFatty livermedicine.diseaseMitochondriaOxidative StressBiochemistrychemistryCancer researchMolecular MedicineSteatohepatitisReactive Oxygen SpeciesReperfusion injuryOxidative stressCurrent Medicinal Chemistry
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Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits

2020

Simple Summary Ischemic heart disease is one of the leading causes of death. A series of processes occur during acute myocardial infarction that contribute to the development of ventricular dysfunction, with subsequent heart failure and ventricular arrhythmias, which account for most episodes of sudden cardiac death in these patients. These complications are associated with the adverse cardiac remodeling that occurs during the healing process following an acute episode. The remodeling causes the appearance of a substrate that can trigger life-threatening arrhythmias, such as tachycardia and/or ventricular fibrillation. The development of experimental models for analyzing the basic mechanism…

Programmed stimulationmedicine.medical_specialtyLong term follow upmedicine.medical_treatment030204 cardiovascular system & hematologyischemia/reperfusion injuryventricular remodelingArticle03 medical and health sciencesexperimental surgery0302 clinical medicineRisk areaInternal medicinelcsh:ZoologymedicineMyocardial infarctionlcsh:QL1-991cardiovascular diseasesVentricular remodelingLigature030304 developmental biology0303 health scienceslcsh:Veterinary medicineGeneral Veterinarybusiness.industryExperimental modelventricular arrhythmiasInfarct sizemedicine.diseasemyocardial infarctionCardiologycardiovascular systemlcsh:SF600-1100Animal Science and Zoologycardiac mappingbusinessAnimals : an Open Access Journal from MDPI
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