Search results for "Myocardial reperfusion"

showing 10 items of 58 documents

Resultados de la estrategia farmacoinvasiva y de la angioplastia primaria en la reperfusión del infarto con elevación del segmento ST. Estudio con re…

2011

[EN] Introduction and objectives: Pharmacoinvasive strategy represents an attractive alternative to primary angioplasty. Using cardiovascular magnetic resonance imaging we compared the left ventricular outcome of the pharmacoinvasive strategy and primary angioplasty for the reperfusion of ST-segment elevation myocardial infarction. Methods: Cardiovascular magnetic resonance was performed 1 week and 6 months after infarction in two consecutive cohorts of patients included in a prospective university hospital ST-segment elevation myocardial infarction registry. During the period 2004-2006, 151 patients were treated with pharmacoinvasive strategy (thrombolysis followed by routine non-immediate…

MaleCardiac CatheterizationPropensity scoremedicine.medical_treatmentLeftHeart left ventricleCoronaryMyocardial InfarctionInfarctionMagnetic resonance angiographyVentricular Dysfunction LeftHeart infarction sizeVentricular DysfunctionMedicineThrombolytic TherapyMyocardial infarctionProspective StudiesAngioplasty Balloon Coronarycomparative studyeducation.field_of_studyEjection fractionmedicine.diagnostic_testGeneral MedicineMiddle AgedMagnetic Resonance ImagingThrombolysisDeathNuclear magnetic resonance imagingTreatment OutcomeHeart left ventricle endsystolic volumeCardiologyFemaleTIMIHumanmedicine.medical_specialtyHeart CatheterizationEndpoint DeterminationFibrinolytic agentPopulationMyocardial Reperfusion InjuryMajor clinical studyArticleTECNOLOGIA ELECTRONICAMagnetic resonance imagingInternal medicineAngioplastyHumansBlood clot lysisProspective studyeducationPrimary angioplastyAgedUniversity hospitalST segment elevation myocardial infarctionbusiness.industryAngioplastymedicine.diseaseSurgeryST-segment elevation myocardial infarctionOutcome assessmentHeart catheterizationReperfusionHeart muscle reperfusionbusinessControlled studyBalloonMagnetic Resonance AngiographyFollow-Up Studies
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Limitations of Myocardial Blush Grade in the Evaluation of Myocardial Perfusion in Patients With Acute Myocardial Infarction and TIMI Grade 3 Flow

2006

Introduction and objectives An analysis was made of variability in the measurement of the angiographic index blush between a university hospital and an independent core laboratory, as well as its correlation with perfusion analised by intracoronary myocardial contrast echocardigraphy (MCE) and the ventricular function at the sixth month. Methods The study comprised 40 patients with a first ST-segment elevation myocardial infarction, single-vessel disease and open infarct-related artery. Perfusion was quantified by angiography (median fifth day, range 3-7) with blush in our laboratory and in an independent core laboratory. MCE was performed. Ejection fraction at the sixth month was determine…

MaleCardiac Catheterizationmedicine.medical_specialtyMyocardial InfarctionInfarctionMyocardial ReperfusionCoronary AngiographyElectrocardiographyCoronary CirculationInternal medicinemedicineHumansThrombolytic TherapyMyocardial infarctionAgedEjection fractionmedicine.diagnostic_testbusiness.industryStroke VolumeMagnetic resonance imagingGeneral MedicineMiddle Agedmedicine.diseaseMagnetic Resonance Imagingmedicine.anatomical_structureEchocardiographyAngiographyCardiologyFemalebusinessNuclear medicinePerfusionTIMIArteryRevista Española de Cardiología (English Edition)
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Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse

2015

Myocardial ischaemia-reperfusion (MIR) triggers a sterile inflammatory response important for myocardial healing, but which may also contribute to adverse ventricular remodelling. Such inflammation is initiated by molecular danger signals released by damaged myocardium, which induce innate immune responses by activating toll-like receptors (TLRs). Detrimental roles have been recently reported for TLR2, TLR3 and TLR4. The role of other TLRs is unknown. We therefore evaluated the role of TLR5, expressed at high level in the heart, in the development of myocardial damage and inflammation acutely triggered by MIR. TLR5−/− and wild-type (WT) mice were exposed to MIR (30 min ischaemia, 2 h reperf…

MaleChemokinemedicine.medical_specialtyGenotypep38 mitogen-activated protein kinasesMyocardial InfarctionMyocardial Reperfusion InjuryInflammation030204 cardiovascular system & hematologyBiologyp38 Mitogen-Activated Protein KinasesVentricular Function LeftProinflammatory cytokineVentricular Dysfunction Left03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsPhosphorylationProtein kinase B030304 developmental biologyInflammationMice Knockout0303 health sciencesToll-like receptorMyocardiumGeneral MedicineImmunity Innate3. Good healthMice Inbred C57BLDisease Models AnimalOxidative StressToll-Like Receptor 5CXCL2PhenotypeEndocrinologybiology.proteinTLR4Inflammation Mediatorsmedicine.symptomProto-Oncogene Proteins c-aktClinical Science
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Acute in vivo administration of a fish oil-containing emulsion improves post-ischemic cardiac function in n-3-depleted rats

2006

International audience; A novel i.v. lipid preparation (MCT:FO) containing 80% medium chain-triacylglycerols and 20% fish oil was recently developed to rapidly replenish cell membrane phospholipids with omega 3 (n-3) polyunsaturated fatty acids (PUFA). In regard of this property, we investigated the effect of a single i.v. administration of MCT:FO on the recovery of cardiac function after ischemia in control and n-3-depleted rats. Results were compared with those obtained either with a control preparation, where FO was replaced by triolein (MCT:OO), or with saline. Saline (1 ml) or lipid preparation (also 1 ml) was injected as a bolus via the left saphenous vein. After 60 min the heart was …

MaleFat EmulsionsTime Factorsmedicine.medical_treatmentMyocardial IschemiaWistar030204 cardiovascular system & hematologyPharmacologyLIPID PREPARATIONchemistry.chemical_compound0302 clinical medicineBolus (medicine)MESH: Fatty Acids Omega-3Heart Rate[SDV.IDA]Life Sciences [q-bio]/Food engineeringMedicineMESH: AnimalsMESH: Oxygen ConsumptionTrioleinMESH: Heart RateSalineOMEGA3-DEFICIENCYOmega-3chemistry.chemical_classification0303 health sciencesFatty AcidsHeartGeneral Medicine[SDV.IDA] Life Sciences [q-bio]/Food engineeringFish oilMESH: Myocardial Reperfusion Injury3. Good healthLactatesMESH: Myocardial IschemiaIntravenousPolyunsaturated fatty acidCardiac function curveFat Emulsions Intravenousmedicine.medical_specialtyMESH: Rats[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process EngineeringACIDE GRAS POLYINSATURE OMEGA3IschemiaMESH: Fish OilsMyocardial Reperfusion InjuryMESH: Coronary CirculationMESH: Lactates03 medical and health sciencesISCHEMIA-REPERFUSIONFish OilsOxygen ConsumptionIn vivoCoronary CirculationMESH: Analysis of VarianceFatty Acids Omega-3[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyGeneticsAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringRats WistarLANGENDORFF030304 developmental biologyAnalysis of Variancebusiness.industryBody WeightMESH: Time FactorsMESH: Rats Wistarmedicine.diseaseMESH: MaleRatsMESH: Body WeightMESH: Fat Emulsions IntravenousSurgeryMESH: Heartchemistrybusiness
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Postconditioning or preconditioning, which should be promoted for protecting from ischemic reperfusion injury? Response to letter IJC-D-14-02875

2014

MaleIschemic reperfusion injurymedicine.medical_specialtybusiness.industryMicrocirculationMyocardial InfarctionMyocardial Reperfusionmedicine.diseaseDisease Models AnimalInternal medicineCardiologyAnimalsHumansMedicineFemaleMyocardial infarctionIschemic PostconditioningCardiology and Cardiovascular MedicinebusinessPerfusionInternational Journal of Cardiology
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Endothelial kinin B1‐receptors are induced by myocardial ischaemia‐reperfusion in the rabbit

2001

Kinin B1-receptors are induced by various inflammatory stimuli. Since myocardial ischaemia-reperfusion results in inflammation, we questioned whether it could induce B1-receptor-dependent responses to des-Arg9-bradykinin (DBK). Thirty-six rabbits were submitted either to a 30 min coronary occlusion followed by a 3 h reperfusion or to a sham operation. The response to DBK was then tested in vivo on mean arterial pressure (MAP) and in vitro on isolated hearts and arterial rings. DBK induced a dose-dependent decrease in MAP in the ischaemia-reperfusion group (DBK, 10 μg kg−1, intra-arterial: -12 ± 2 vs. -5 ± 2 mmHg in the sham group, P < 0.02), which was significantly antagonised by [Leu8]-des…

MaleMean arterial pressuremedicine.medical_specialtyEndotheliumPhysiologyBlotting WesternBradykininBlood PressureMyocardial Reperfusion InjuryInflammationIn Vitro TechniquesBradykininReceptor Bradykinin B1Muscle Smooth Vascularchemistry.chemical_compoundIsometric ContractionInternal medicinemedicineAnimalsMesenteric arteriesDose-Response Relationship Drugbiologybusiness.industryReceptors BradykininAngiotensin-converting enzymeOriginal ArticlesKininImmunohistochemistryMyocardial ContractionPerfusionmedicine.anatomical_structureEndocrinologychemistryImmunologybiology.proteinCoronary perfusion pressureEndothelium VascularRabbitsmedicine.symptombusinessThe Journal of Physiology
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Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits

2001

Abstract Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic agents, adhesion molecule expression, release of cytokines and oxygen-derived free radicals, and subsequent neutrophil accumulation. In the present study the cardioprotective effects of a novel highly selective small molecule C1s inhibitor (C1s-INH-248, Knoll) were examined in a rabbit model of myocardial ischemia (I) and reperfusion (R; i.e., 60 min I + 180 min R). In in vitro tests (enzyme activity and SRBC lysis) C1s-INH-248 demonstrated profound inhibitory potency. In vivo C1s-INH-248 (1 mg/kg body weight) administered 5 min before reperfusion significantly attenuated m…

MaleNecrosisEndotheliumNeutrophilsG proteinImmunologyMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryComplement C1 Inactivator ProteinsPharmacologyHemolysisLeukocyte CountClassical complement pathwaySuperoxidesIn vivomedicineAnimalsImmunology and AllergyComplement Activationbusiness.industryHemodynamicsmedicine.diseaseComplement systemmedicine.anatomical_structureAnesthesiaEndothelium VascularRabbitsmedicine.symptombusinessReperfusion injuryThe Journal of Immunology
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Controlled reperfusion after hypothermic heart preservation inhibits mitochondrial permeability transition-pore opening and enhances functional recov…

2006

We investigated whether low-pressure reperfusion may attenuate postischemic contractile dysfunction, limits necrosis and apoptosis after a prolonged hypothermic ischemia, and inhibits mitochondrial permeability transition-pore (MPTP) opening. Isolated rats hearts ( n = 72) were exposed to 8 h of cold ischemia and assigned to the following groups: 1) reperfusion with low pressure (LP = 70 cmH2O) and 2) reperfusion with normal pressure (NP = 100 cmH2O). Cardiac function was assessed during reperfusion using the Langendorff model. Mitochondria were isolated, and the Ca2+resistance capacity (CRC) of the MPTP was determined. Malondialdehyde (MDA) production, caspase-3 activity, and cytochrome c …

MaleNecrosisPhysiologyIschemiaHeart preservationMyocardial IschemiaMyocardial ReperfusionPharmacologyBiologyMitochondrionMitochondrial Membrane Transport ProteinsMitochondria HeartPermeabilityHypothermia InducedPhysiology (medical)MalondialdehydemedicinePressureAnimalsRats WistarCaspase 3Mitochondrial Permeability Transition PoreMyocardiumCytochromes cRecovery of Functionmedicine.diseaseFunctional recoveryRatsMitochondrial permeability transition poreApoptosisAnesthesiaCalciummedicine.symptomCardiology and Cardiovascular MedicineAmerican journal of physiology. Heart and circulatory physiology
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Proteome analysis of myocardial tissue following ischemia and reperfusion--effects of complement inhibition.

2006

Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic mediators, release of cytokines, leukocyte accumulation, and subsequent severe tissue injury. In this regard, activation of transcription factors (i.e., NFkappaB) and de novo protein synthesis or inflammatory protein degradation seems to play an important role. In the present study, we analyzed the cardiac protein expression following myocardial ischemia (60 min) and reperfusion (180 min) in a rabbit model utilizing two-dimensional electrophoresis and nanoHPLC/ESI-MS/MS for biochemical protein identification. To achieve cardioprotective effects, we used a novel highly selective smal…

MaleProteomeG proteinNeutrophilsMolecular Sequence DataBiophysicsIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryProtein degradationComplement C1 Inactivator ProteinsBiochemistryAnalytical ChemistrySuperoxide dismutaseClassical complement pathwayElectrocardiographyNecrosismedicineProtein biosynthesisAnimalsAmino Acid SequenceMolecular BiologyCreatine KinasebiologySuperoxide DismutaseMyocardiumalpha-Crystallin B ChainComplement System Proteinsmedicine.diseaseMolecular biologyComplement systembiology.proteinCreatine kinaseRabbitsMicrotubule-Associated ProteinsBiomarkersBiochimica et biophysica acta
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Beneficial effects of C1 esterase inhibitor in ST-elevation myocardial infarction in patients who underwentsurgical reperfusion: a randomized double-…

2007

Background: The inflammatory cascade has been hypothesized to be an important mechanism of post-ischaemic myocardial reperfusion injury and several studies demonstrated that C1 esterase inhibitor (C1 -INH) is effective in post-ischaemia myocardial protection. Therefore, we aimed to investigate prospectively in a randomised double-blind study the cardioprotective effects of C1-INH in ST segment elevation myocardial infarction (STEMI) in patients who underwent emergent reperfusion with coronary artery bypass grafting (CABG). Methods: In this study, we enrolled 80 patients affected with STEMI who underwent emergent CABG. Patients were assigned in two groups (C1-INH group: receive 1000 Ul of C1…

MalePulmonary and Respiratory MedicineCardiac function curvemedicine.medical_specialtyMean arterial pressureCardiotonic AgentsMyocardial InfarctionCardiac indexMyocardial ReperfusionComplement C1 Inactivator ProteinsCoronary artery bypass surgeryReperfusion therapyDouble-Blind MethodInternal medicinemedicineHumansProspective StudiesMyocardial infarctionCoronary Artery BypassInfusions IntravenousSTEMI patients CABG C1 esterase inhibitor Reperfusion injury Complement cascade Myocardial function recoverybusiness.industryST elevationTroponin IComplement C4aGeneral MedicineMiddle Agedmedicine.diseaseMyocardial ContractionComplement Inactivating AgentsTreatment OutcomeComplement C3aCardiologyFemaleSurgeryCardiology and Cardiovascular MedicinebusinessReperfusion injury
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