Search results for " reperfusion"

showing 10 items of 68 documents

Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR‐1‐dependent pathway

2019

The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member …

Male0301 basic medicineCell SurvivalMyocardial InfarctionIschemiaConnexinMyocardial Reperfusion InjuryPharmacologymiR‐1telmisartanCell Lineconnexin 43Rats Sprague-Dawleyhypoxic H9c2 cells03 medical and health sciences0302 clinical medicineIn vivomedicineAnimalsBcl-2Myocytes CardiacKCNQ1ChemistryBcl‐2Original ArticlesCell BiologyTransfectionHypoxia (medical)medicine.diseasemiR-1Cell HypoxiaIn vitroRatsMicroRNAsmyocardial ischaemia/reperfusion030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisKCNQ1 Potassium ChannelMolecular Medicinehypoxic H9c2 cellOriginal Articlemedicine.symptomTelmisartanReperfusion injurymedicine.drugJournal of Cellular and Molecular Medicine
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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Sex differences in anthracycline-induced cardiotoxicity: the benefits of estrogens

2019

Anthracyclines are the cornerstone for many oncologic treatments, but their cardiotoxicity has been recognized for several decades. Female subjects, especially before puberty and adolescence, or after menopause, seem to be more at increased risk, with the prognostic impact of this sex issue being less consistent compared to other cardiovascular risk factors. Several studies imply that sex differences could depend on the lack of the protective effect of sex hormones against the anthracycline-initiated damage in cardiac cells, or on differential mitochondria-related oxidative gene expression. This is also reflected by the results obtained with different diagnostic methods, such as cardiovascu…

MaleCardiac & Cardiovascular SystemsMagnetic Resonance Spectroscopyand protection from anthracycline cardiotoxicitymedicine.disease_causeBioinformaticsRisk FactorsAnthracycline cardiotoxicityGender differenceGender differencesAnthracyclinesGonadal Steroid Hormones1102 Cardiorespiratory Medicine and HaematologyAMERICAN SOCIETYCardioprotectionSex CharacteristicsHeartPrognosisMitochondriaMenopauseEchocardiographyReperfusion InjuryHEART-FAILUREAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicity; Anthracyclines; Biomarkers; Cardiotonic Agents; Cardiotoxicity; Echocardiography; Female; Gonadal Steroid Hormones; Heart; Heart Failure; Humans; Magnetic Resonance Spectroscopy; Male; Mitochondria; Nuclear Medicine; Oxidative Stress; Prognosis; Reperfusion Injury; Risk Factors; Sex CharacteristicsFemaleCardiology and Cardiovascular MedicineLife Sciences & BiomedicinePOSITION PAPERCARDIAC DYSFUNCTIONCardiotonic AgentsAnthracyclineSPECKLE-TRACKINGIschemiaDRUG CARDIOTOXICITYPathophysiologymedicineHumansCHILDHOOD-CANCER SURVIVORSBREAST-CANCERPathophysiology monitoring and protection from anthracycline cardiotoxicityHeart FailureCardiotoxicityScience & Technologybusiness.industryWORKING GROUPmedicine.diseaseCardiotoxicityOxidative StressmonitoringCardiovascular System & HematologyHeart failureCardiovascular System & CardiologyRISK-FACTORSNuclear MedicinebusinessOxidative stressAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicityBiomarkersHormone
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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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