Search results for "Cardioprotection"

showing 10 items of 35 documents

Cardioprotection and natural polyphenols: An update of clinical and experimental studies

2018

Myocardial ischemia is the leading cause of death worldwide. Despite better outcomes with early coronary artery reperfusion strategies, morbidity and mortality remain significant. The principal myocardial hallmark of myocardial ischemia is cell death and the associated impairment of cardiac contractility. In this way, the use of extracts from medicinal plants versus synthetic drugs to mitigate post-ischemic damage constitutes an alternative. Despite their proven beneficial effects in cardiovascular disorders, the use of many plants is questioned. Our aim is to update the clinical and experimental studies about the actions of medicinal plants and polyphenol-enriched extracts against ischemia…

0301 basic medicineCardiotonic AgentsMyocardial ischemiaCIENCIAS MÉDICAS Y DE LA SALUDMyocardial IschemiaMEDLINE030204 cardiovascular system & hematologyFisiologíaNATURAL PRODUCTS03 medical and health sciencesISCHEMIA-REPERFUSIONCARDIOPROTECTION0302 clinical medicineWeb of knowledgeMITOCHONDRIAAnimalsHumansMedicineCardioprotective AgentMedicinal plantsBeneficial effectsCause of deathCardioprotectionClinical Trials as TopicTraditional medicinePlant Extractsbusiness.industryPolyphenolsfood and beveragesGeneral MedicineMedicina Básica030104 developmental biologybusinessFood Science
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CD40/CD40L and Related Signaling Pathways in Cardiovascular Health and Disease—The Pros and Cons for Cardioprotection

2020

The CD40–CD40 ligand (CD40L) dyad represents a scientific and clinical field that has raised many controversies in the past and cannot be clearly defined as being an either beneficial or harmful pathway. Being crucially involved in physiological immunological processes as well as pathological inflammatory reactions, the signaling pathway has been recognized as a key player in the development of both autoimmune and cardiovascular disease. Even though the possibilities of a therapeutic approach to the dyad were recognized decades ago, due to unfortunate events, detailed in this review, pharmacological treatment targeting the dyad, especially in patients suffering from atherosclerosis, is not …

0301 basic medicineCardiovascular healthMice TransgenicInflammationReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular SystemCatalysisAutoimmune DiseasesInorganic Chemistrylcsh:ChemistryMice03 medical and health sciencesTherapeutic approach0302 clinical medicineRisk Factorscardiovascular diseaseDiabetes mellitusCD40AnimalsHumansMedicineGene SilencingCD40 AntigensPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyCardioprotectionClinical Trials as Topicbusiness.industryOrganic ChemistryGeneral Medicinemedicine.diseaseComputer Science Applications030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Cardiovascular DiseasesinflammationCd40 cd40lSignal transductionmedicine.symptomCD40 ligandatherosclerosisbusinessSignal TransductionInternational Journal of Molecular Sciences
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Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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The role of mitochondrial reactive oxygen species, NO and H2S in ischaemia/reperfusion injury and cardioprotection

2020

Redox signalling in mitochondria plays an important role in myocardial ischaemia/reperfusion (I/R) injury and in cardioprotection. Reactive oxygen and nitrogen species (ROS/RNS) modify cellular structures and functions by means of covalent changes in proteins including among others S‐nitros(yl)ation by nitric oxide (NO) and its derivatives, and S‐sulphydration by hydrogen sulphide (H2S). Many enzymes are involved in the mitochondrial formation and handling of ROS, NO and H2S under physiological and pathological conditions. In particular, the balance between formation and removal of reactive species is impaired during I/R favouring their accumulation. Therefore, various interventions aimed a…

0301 basic medicineMitochondrial ROSIschemiaEndogenyheartMitochondrionRedoxNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinenitric oxidemedicinechemistry.chemical_classificationCardioprotectionreactive oxygen speciesReactive oxygen speciesVDP::Medisinske Fag: 700::Basale medisinske odontologiske og veterinærmedisinske fag: 710Cell Biologymedicine.diseaseVDP::Medical disciplines: 700::Basic medical dental and veterinary science disciplines: 710Cell biologyreperfusionmitochondria030104 developmental biologychemistry030220 oncology & carcinogenesiscardioprotectionMolecular Medicineischaemiahydrogen sulphidecardioprotection; heart; hydrogen sulphide; ischaemia; mitochondria; nitric oxide; reactive oxygen species; reperfusion
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Hypoxie et régénération cardiaque : une nouvelle approche paradoxale de la cardioprotection

2017

IF 2.331; International audience

0301 basic medicinemedicine.medical_specialtyReactive oxygen species metabolismTranscription GeneticCardiac pathologyEnergy metabolismCardiac metabolismCardioprotectionHypoxie03 medical and health sciencesInternal medicinemedicineRégénérationAnimalsHumansRegenerationMyocytes CardiacTissue survivalHypoxiaCoeurCell ProliferationCardioprotectionHeart FailureTissue Survivalbusiness.industryOxygen metabolismHeartGeneral MedicineRecovery of FunctionHypoxia (medical)[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemCell HypoxiaOxygenOxidative Stress030104 developmental biologyGene Expression RegulationAnesthesiaCardiologymedicine.symptomCardiology and Cardiovascular MedicinebusinessEnergy MetabolismReactive Oxygen SpeciesSignal TransductionArchives of cardiovascular diseases
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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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Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardioto…

2015

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal model…

Cardiac function curveACE inhibitorsCardiotonic AgentsNeuregulin-1CardiomyopathyAntineoplastic AgentsPreclinical modelsCardioprotectionCardiotonic AgentsPharmacologyBioinformaticsmedicine.disease_causeCancer therapy-induced cardiac injury ;Preclinical modelsMitochondria HeartBeta-blockersNeoplasmsCancer therapy-induced cardiac injuryMedicineAnimalsHumansCardiac stem cellsCardioprotectionCardiotoxicityACE inhibitors; Beta-blockers; Cancer therapy-induced cardiac injury; Cardiac stem cells; Cardioprotection; Mitochondria; Neuregulin-1; Oxidative stress; Preclinical models; Statinsbusiness.industryStatinsCancermedicine.diseaseCardiotoxicityMitochondriaCancer therapy-induced cardiac injury Preclinical models Cardioprotection Mitochondria Neuregulin-1 Oxidative stress Statins Beta-blockers ACE inhibitors Cardiac stem cellsDisease Models AnimalOxidative StressHeart failureCardiology and Cardiovascular MedicinebusinessOxidative stress
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Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and…

1997

Background 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, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing reperfusion damage by the application of C1 esterase inhibitor (C1-INH). Methods and Results Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of coronary occlusion, followed by 120 minutes of reperfusion. C1-INH was administered during the first 5 minutes of coronary reperfusion…

Cardiac function curveMalemedicine.medical_specialtyAnaphylatoxinsNecrosisSwinePartial PressureIschemiaMyocardial IschemiaMyocardial ReperfusionComplement C1 Inactivator ProteinsCreatineInjectionschemistry.chemical_compoundNecrosisTroponin TPhysiology (medical)Internal medicinemedicineAnimalsMyocardial infarctionLactic AcidCreatine KinaseCardioprotectionTroponin Tbusiness.industryMyocardiumHemodynamicsHeartmedicine.diseaseCoronary VesselsTroponinOxygenchemistryCoronary occlusionAnesthesiaCardiologyFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessCirculation
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Differential responses to docosahexaenoic acid in primary and immortalized cardiac cells

2013

Abstract The importance of dietary polyunsaturated fatty acids (PUFAs) in the reduction of cardiovascular disease has been recognized for many years. Docosahexaenoic acid (22:6n3, DHA) is an n-3 PUFA known to affect numerous biological functions and provide cardioprotection; however, the exact molecular and cellular protective mechanism(s) remain unknown. In contrast, DHA also possesses many anti-tumorgenic properties including suppressing cell growth and inducing apoptosis. In the present study, we investigated the effect of DHA toward H9c2 cells (an immortalized cardiac cell line) and neonatal primary cardiomyocytes (NCM). Cells were treated with 0 μM, 10 μM or 100 μM DHA for upto 48 h. C…

CardioprotectionDocosahexaenoic AcidsbiologyCaspase 3Cell SurvivalInterleukin-6Cell growthCytochrome cBlotting WesternCytochromes cGeneral MedicineMitochondrionToxicologyMitochondria HeartCell LineRatsCell biologyDocosahexaenoic acidApoptosiscardiovascular systembiology.proteinAnimalsMyocytes CardiacViability assayCaspaseToxicology Letters
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