Search results for " Reperfusion Injury"

showing 10 items of 41 documents

Guanxin Danshen Formulation Protects against Myocardial Ischemia Reperfusion Injury-Induced Left Ventricular Remodeling by Upregulating Estrogen Rece…

2017

Background: Guanxin Danshen formulation (GXDSF) is a traditional Chinese herbal recipe recorded in the Chinese Pharmacopoeia since 1995 edition, which consists of Salviae miltiorrhizae Radix et Rhizoma, Notoginseng Radix et Rhizoma and Dalbergiae odoriferae Lignum. Our previous research suggested GXDSF had positive effect on cardiovascular disease. Therefore, the aim of this study was to elucidate the effects of GXDSF on myocardial ischemia reperfusion injury-induced left ventricular remodelling (MIRI-LVR). Methods: The effects of GXDSF on cardiac function were detected by haemodynamics and echocardiograms. The effects of GXDSF on biochemical parameters (AST, LDH and CK-MB) were analysed. H…

0301 basic medicineCardiac function curvemedicine.medical_specialtyGuanxin Danshen formulaEstrogen receptor030204 cardiovascular system & hematologyPharmacologyventricular remodeling03 medical and health sciences0302 clinical medicineFibrosisInternal medicinemedicinenetwork pharmacologyPharmacology (medical)Ventricular remodelingOriginal ResearchPharmacologyPI3K/AktEjection fractionbusiness.industryestrogen receptor βlcsh:RM1-950PHTPPmedicine.diseasemyocardial ischemia reperfusion injury030104 developmental biologylcsh:Therapeutics. PharmacologyCardiologyMyocardial fibrosisbusinessReperfusion injuryFrontiers in Pharmacology
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Changes in the spatial distribution of the Purkinje network after acute myocardial infarction in the pig

2018

Purkinje cells (PCs) are more resistant to ischemia than myocardial cells, and are suspected to participate in ventricular arrhythmias following myocardial infarction (MI). Histological studies afford little evidence on the behavior and adaptation of PCs in the different stages of MI, especially in the chronic stage, and no quantitative data have been reported to date beyond subjective qualitative depictions. The present study uses a porcine model to present the first quantitative analysis of the distal cardiac conduction system and the first reported change in the spatial distribution of PCs in three representative stages of MI: an acute model both with and without reperfusion; a subacute …

0301 basic medicineCritical Care and Emergency MedicineSwinemedicine.medical_treatmentMyocardial InfarctionInfarction030204 cardiovascular system & hematologyPathology and Laboratory MedicineVascular MedicinePurkinje Cells0302 clinical medicineAnimal CellsIschemiaMedicine and Health SciencesTissue DistributionMyocardial infarctionNeuronsCardiomyocytesMultidisciplinaryQRHeartInfarctionDisease ProgressionCardiologyMedicineCellular TypesAnatomyElectrical conduction system of the heartResearch Articlemedicine.medical_specialtyHistologyScienceCardiologyMuscle TissueIschemiaMyocardial Reperfusion InjuryCatheter ablation03 medical and health sciencesSigns and SymptomsHeart Conduction SystemDiagnostic MedicineInternal medicinemedicineAnimalscardiovascular diseasesEndocardiumMuscle Cellsbusiness.industryBiology and Life SciencesCell Biologymedicine.diseaseElectrophysiologyBiological Tissue030104 developmental biologyVacuolizationCellular NeuroscienceReperfusionCardiovascular AnatomyNerve NetbusinessEndocardiumNeuroscience
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Rosuvastatin Prevents Conduit Artery Endothelial Dysfunction Induced by Ischemia and Reperfusion by a Cyclooxygenase-2–Dependent Mechanism

2010

ObjectivesThe purpose of this study was to determine whether single-dose rosuvastatin (40 mg) protects against ischemia and reperfusion (IR)–induced endothelial dysfunction in humans and whether this effect is cyclooxygenase (COX)-2 dependent.BackgroundAnimal studies have demonstrated that rosuvastatin can limit damage and improve recovery after IR.MethodsIn a double-blind, parallel design, 20 volunteers were randomized to a single dose of oral rosuvastatin (40 mg) or placebo. Twenty-four hours later, endothelium-dependent, flow-mediated dilation (FMD) of the radial artery was measured before and after IR (15 min of upper arm ischemia followed by 15 min of reperfusion). In a separate protoc…

AdultMaleEndotheliumendotheliumAdolescentPremedicationIschemiaMyocardial Reperfusion InjuryPharmacologyPlaceboYoung AdultDouble-Blind Methodmedicineischemia reperfusionHumansRosuvastatinEndothelial dysfunctionRosuvastatin CalciumSulfonamidesCyclooxygenase 2 Inhibitorsbusiness.industryModels Cardiovascularnutritional and metabolic diseases3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitormedicine.diseaseFluorobenzenesVasodilationRosuvastatin Calciummedicine.anatomical_structurePyrimidinesCelecoxibCyclooxygenase 2AnesthesiaIschemic Preconditioning MyocardialRadial ArteryCelecoxibIschemic preconditioningPyrazolesFemaleEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessCardiology and Cardiovascular Medicinerosuvastatinmedicine.drugJournal of the American College of Cardiology
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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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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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Postnatal Overfeeding Causes Early Shifts in Gene Expression in the Heart and Long-Term Alterations in Cardiometabolic and Oxidative Parameters

2013

International audience; Background: Postnatal overfeeding (OF) in rodents induces a permanent moderate increase in body weight in adulthood. However, the repercussions of postnatal OF on cardiac gene expression, cardiac metabolism and nitro-oxidative stress are less well known. Methodology/Principal Findings: Immediately after birth, litters of C57BL/6 mice were either maintained at 10 (normal-fed group, NF), or reduced to 3 in order to induce OF. At weaning, mice of both groups received a standard diet. The cardiac gene expression profile was determined at weaning and cardiac metabolism and oxidative stress were assessed at 7 months. The cardiac expression of several genes, including membe…

Blood GlucoseAnatomy and PhysiologyTime FactorsMouseMicroarrays[SDV]Life Sciences [q-bio]Myocardial InfarctionGene Expressionlcsh:Medicine030204 cardiovascular system & hematologyCardiovascularmedicine.disease_causeCardiovascular SystemMiceOvernutrition0302 clinical medicineBlood plasmaInsulinlcsh:Science2. Zero hungerRegulation of gene expression0303 health sciencesMultidisciplinaryEjection fractionVentricular RemodelingHeartAnimal ModelsReactive Nitrogen Species[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemApelin[SDV] Life Sciences [q-bio]Body CompositionMedicineFemaleDisease SusceptibilityOxidation-ReductionResearch ArticlePhysiogenomicsmedicine.medical_specialtyDiastoleEndocrine SystemMyocardial Reperfusion InjuryBiology03 medical and health sciencesModel Organisms[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsWeaningVentricular remodelingBiology030304 developmental biologyEndocrine Physiology[ SDV ] Life Sciences [q-bio]Gene Expression ProfilingMyocardiumBody Weightlcsh:RComputational Biologymedicine.diseaseOxidative StressEndocrinologyGene Expression Regulationlcsh:QOxidative stress
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C1-esterase inhibitor in ischemia and reperfusion.

2002

Summary Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte en…

Cardiotonic AgentsImmunologyIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryPharmacologyComplement C1 Inactivator ProteinsProinflammatory cytokineClassical complement pathwayIschemiamedicineImmunology and AllergyAnimalsHumansAnaphylatoxinComplement Pathway ClassicalCardioprotectionbusiness.industryHeartHematologymedicine.diseaseC1 esteraseComplement systemAnesthesiaModels AnimalbusinessPerfusionComplement C1 Inhibitor ProteinImmunobiology
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Cardioprotection by gene therapy: A review paper on behalf of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of…

2015

Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…

CardiotoxinIschemic heart diseaseCardiologyMyocardial IschemiaPreconditioningMyocardial Reperfusion InjuryCardioprotectionRemote conditioningCardiotoxinsPostconditioningGene therapyMedicalHumansMyocardialIschemic PreconditioningSocieties MedicalCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioning; Cardiology; Cardiotoxicity; Cardiotoxins; Gene Targeting; Genetic Therapy; Humans; Ischemic Preconditioning Myocardial; Italy; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidative Stress; Societies MedicalCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioning; Cardiology; Cardiotoxicity; Cardiotoxins; Gene Targeting; Genetic Therapy; Humans; Ischemic Preconditioning; Myocardial; Italy; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidative Stress; Societies; Medical; Cardiology and Cardiovascular MedicineOxidative StreGenomicsGenetic TherapyCardioprotection Gene therapy Genomics Ischemic heart disease Postconditioning Preconditioning Remote conditioningCardiotoxicityOxidative StressCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioningItalyIschemic Preconditioning MyocardialGene TargetingGenomicSocietiesCardiology and Cardiovascular MedicineHuman
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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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Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function

2001

Up-regulation of proapoptotic genes has been reported in heart failure and myocardial infarction. To determine whether caspase genes can affect cardiac function, a transgenic mouse was generated. Cardiac tissue-specific overexpression of the proapoptotic gene Caspase3 was induced by using the rat promoter of α-myosin heavy chain, a model that may represent a unique tool for investigating new molecules and antiapoptotic therapeutic strategies. Cardiac-specific Caspase3 expression induced transient depression of cardiac function and abnormal nuclear and myofibrillar ultrastructural damage. When subjected to myocardial ischemia–reperfusion injury, Caspase3 transgenic mice showed increased inf…

Genetically modified mouseCardiac function curveDNA ComplementaryTransgeneRecombinant Fusion ProteinsMyocardial InfarctionMyocardial IschemiaCaspase 3ApoptosisMice TransgenicMyocardial Reperfusion InjuryDNA FragmentationContractilityMiceVentricular Dysfunction LeftmedicineAnimalsHumansGenetic Predisposition to DiseaseMyocardial infarctionCaspaseMultidisciplinarybiologyCaspase 3MyocardiumBiological Sciencesmedicine.diseasePhenotypeGene Expression RegulationEchocardiographyOrgan SpecificityHeart failureCaspasesCancer researchbiology.proteincardiovascular system
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