Search results for "endothelial dysfunction"

showing 10 items of 287 documents

The sodium-glucose co-transporter 2 inhibitor empagliflozin improves diabetes-induced vascular dysfunction in the streptozotocin diabetes rat model b…

2014

Objective In diabetes, vascular dysfunction is characterized by impaired endothelial function due to increased oxidative stress. Empagliflozin, as a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), offers a novel approach for the treatment of type 2 diabetes by enhancing urinary glucose excretion. The aim of the present study was to test whether treatment with empagliflozin improves endothelial dysfunction in type I diabetic rats via reduction of glucotoxicity and associated vascular oxidative stress. Methods Type I diabetes in Wistar rats was induced by an intravenous injection of streptozotocin (60 mg/kg). One week after injection empagliflozin (10 and 30 mg/kg/d) was adminis…

Blood GlucoseMalemedicine.medical_treatmentReceptor for Advanced Glycation End Productslcsh:MedicineGene ExpressionType 2 diabetesmedicine.disease_causeVascular MedicineGlucosidesMedicine and Health SciencesMedicineInsulinEndothelial dysfunctionReceptors Immunologiclcsh:ScienceMultidisciplinaryType 1 DiabetesCytokinesInflammation Mediatorsmedicine.drugSignal TransductionResearch Articlemedicine.medical_specialtyCardiologyBlood sugarStreptozocinCardiovascular PharmacologyDiabetes Mellitus ExperimentalDiabetes ComplicationsInternal medicineDiabetes mellitusEmpagliflozinDiabetes MellitusAnimalsRNA MessengerVascular DiseasesBenzhydryl CompoundsSodium-Glucose Transporter 2 InhibitorsPharmacologybusiness.industryInsulinlcsh:RHemodynamicsStreptozotocinmedicine.diseaseRatsOxidative StressEndocrinologyGlucoseMetabolic Disorderslcsh:QbusinessOxidative stressDiabetic AngiopathiesPloS one
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The Neutrophil Secretome as a Crucial Link between Inflammation and Thrombosis

2021

Cardiovascular diseases are a leading cause of death. Blood–cell interactions and endothelial dysfunction are fundamental in thrombus formation, and so further knowledge of the pathways involved in such cellular crosstalk could lead to new therapeutical approaches. Neutrophils are secretory cells that release well-known soluble inflammatory signaling mediators and other complex cellular structures whose role is not fully understood. Studies have reported that neutrophil extracellular vesicles (EVs) and neutrophil extracellular traps (NETs) contribute to thrombosis. The objective of this review is to study the role of EVs and NETs as key factors in the transition from inflammation to thrombo…

Blood Platelets0301 basic medicineQH301-705.5Neutrophilsneutrophil extracellular trapsInflammationContext (language use)Review030204 cardiovascular system & hematologyExosomesExtracellular TrapsCatalysisInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansPlateletPlatelet activationBiology (General)Physical and Theoretical ChemistryThrombusEndothelial dysfunctionQD1-999Molecular BiologySpectroscopythrombosisbusiness.industryOrganic ChemistryneutrophilGeneral MedicineNeutrophil extracellular trapsmedicine.diseaseComputer Science ApplicationsCell biologyChemistryCrosstalk (biology)secretome030104 developmental biologyinflammationplateletsmedicine.symptombusinessextracellular vesiclesSignal TransductionInternational Journal of Molecular Sciences
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Platelet-localized FXI promotes a vascular coagulation-inflammatory circuit in arterial hypertension

2017

Multicellular interactions of platelets, leukocytes, and the blood vessel wall support coagulation and precipitate arterial and venous thrombosis. High levels of angiotensin II cause arterial hypertension by a complex vascular inflammatory pathway that requires leukocyte recruitment and reactive oxygen species production and is followed by vascular dysfunction. We delineate a previously undescribed, proinflammatory coagulation-vascular circuit that is a major regulator of vascular tone, blood pressure, and endothelial function. In mice with angiotensin II-induced hypertension, tissue factor was up-regulated, as was thrombin-dependent endothelial cell vascular cellular adhesion molecule 1 ex…

Blood PlateletsMale0301 basic medicinemedicine.medical_specialtyMacrophage-1 AntigenVascular Cell Adhesion Molecule-1Blood Pressure030204 cardiovascular system & hematologyThromboplastinMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinInternal medicinemedicineAnimalsHumansPlateletRats WistarEndothelial dysfunctionBlood CoagulationFactor XIAgedMice Knockoutbusiness.industryAngiotensin IIThrombinGeneral MedicineMiddle AgedOligonucleotides Antisensemedicine.diseaseAngiotensin IIMice Inbred C57BL030104 developmental biologyEndocrinologyBlood pressuremedicine.anatomical_structurePlatelet Glycoprotein GPIb-IX ComplexPathophysiology of hypertensionHypertensionFemalebusinessmedicine.drugBlood vesselScience Translational Medicine
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The mechanisms of thrombotic risk induced by hormone replacement therapy.

2001

Abstract Objective : To review the available information on the action of hormones on the mechanisms involved in thrombotic risk. Results and Conclusions : Thrombosis plays a crucial role in the genesis and progression of both coronary heart disease (CHD) and venous thromboembolic disease (VTED), the two main forms of cardiovascular disease. Two main determinants of the thromboembolic phenotype, hypercoagulable state and altered endothelium, accumulate much of the work performed on the influence of hormones on thrombosis. Information has accumulated mainly for oestrogens, but increasing evidences support a role for progestogens. The sensitivity of each of the three components of the hemosta…

Blood PlateletsMalemedicine.medical_specialtyArteriosclerosismedicine.medical_treatmentCoronary DiseaseDiseaseBioinformaticsFibrinogenGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundRisk FactorsInternal medicineFibrinolysismedicineHumansHormone replacement therapyEndothelial dysfunctionAgedVenous ThrombosisHemostasisFactor VIIbusiness.industryAntithrombinEstrogen Replacement TherapyObstetrics and GynecologyEstrogensMiddle Agedmedicine.diseasePostmenopauseEndocrinologyPhenotypechemistryHemostasisFemaleEndothelium Vascularbusinessmedicine.drugMaturitas
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A single loading dose of clopidogrel causes dose-dependent improvement of endothelial dysfunction in patients with stable coronary artery disease: Re…

2006

Clinical studies have demonstrated beneficial effects for clopidogrel in patients with atherothrombotic disease. Recent in vitro studies identified stimulating effects of clopidogrel on endothelial cells, pointing towards mechanisms of action beyond the inhibition of platelet aggregation. We hypothesized that in vivo use of clopidogrel improves endothelial dysfunction in patients with coronary artery disease (CAD). Fifty-eight patients with CAD were randomly assigned to double-blinded oral administration of one single dose of clopidogrel 300 mg (C300) or 600 mg (C600), respectively. Endothelial function was assessed by measurement of flow-mediated dilation (FMD) of the brachial artery befor…

Blood PlateletsMalemedicine.medical_specialtyTiclopidineCoronary Artery DiseaseLoading doseCoronary artery diseaseP2Y12Double-Blind MethodSuperoxidesmedicine.arteryInternal medicinePurinergic P2 Receptor AntagonistsHumansMedicinePlateletcardiovascular diseasesBrachial arteryEndothelial dysfunctionAgedbusiness.industryVascular diseaseMicrofilament ProteinsMiddle AgedPhosphoproteinsmedicine.diseaseClopidogrelReceptors Purinergic P2Y12ClopidogrelAnesthesiaCardiologyFemaleEndothelium VascularCardiology and Cardiovascular MedicinebusinessCell Adhesion MoleculesDilatation Pathologiccirculatory and respiratory physiologymedicine.drugAtherosclerosis
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Increased Platelet Sensitivity toward Platelet Inhibitors during Physical Exercise in Patients with Coronary Artery Disease

1999

Generalized atherosclerosis and coronary artery disease (CAD) are associated with endothelial dysfunction and during acute myocardial ischemia platelet activation has been reported. Activated platelets exert activated fibrinogen receptors (GP IIb/IIIa) and express CD 62p being regarded as reliable marker for platelet activation. Patients with angiographically proven CAD performed a bicycle exercise test until the onset of angina or ST-segment depression. We studied the ischemia-induced alterations in fibrinogen binding to activated platelet GP IIb/IIIa receptors and CD 62p expression. Therefore, the basal fibrinogen binding to GP IIb/IIIa and CD 62p expression and the thrombin-concentration…

Blood Plateletsmedicine.medical_specialtyMyocardial IschemiaCoronary DiseaseProstacyclinPlatelet Glycoprotein GPIIb-IIIa ComplexNitric OxideFibrinogenThrombinRisk FactorsInternal medicinemedicineHumansPlateletcardiovascular diseasesPlatelet activationEndothelial dysfunctionbusiness.industryThrombinFibrinogen bindingHematologyMiddle AgedPlatelet Activationmedicine.diseaseEpoprostenolRadiographyP-SelectinEndocrinologyExercise TestCardiologybusinessPlatelet Aggregation Inhibitorsmedicine.drugIloprostThrombosis Research
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Blood pressure and glycaemia, not insulin-resistance, influence endothelial dysfunction in metabolic syndrome

2005

Blood pressure endothelial dysfunction metabolic syndrome
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Progressive Development of Renal Vascular Dysfunction in Brain Death Implicates Reversible Alterations of Nitric Oxide Metabolism

2011

Vascular endothelial dysfunction occurs in the kidney graft from marginal brain death (BD) donors and may be responsible for a low success rate after transplantation.BD was induced in 16 dogs for 6 hours. Immediately after the inflation of the intracranial balloon, the treated group (n = 8) received 40 mg/kg bolus followed by 3 mg/kg/min infusion of L-arginine for 30 minutes. Renal vascular function and hemodynamic and biochemical parameters were determined.BD caused vasoconstriction, increase in renal venous nitrite (4.9 ± 0.8 versus 2.6 ± 0.1, P.05) and myeloperoxidase levels (1.43 ± 0.04 versus 2.43 ± 0.23, P.001), and reduced vasodilatation of renal artery to acetylcholine. Larginine di…

Brain Deathmedicine.medical_specialtyHemodynamicsKidneyNitric Oxidechemistry.chemical_compoundDogsBolus (medicine)Internal medicinemedicineAnimalsNitriteEndothelial dysfunctionTransplantationKidneybusiness.industryHemodynamicsNitric oxide metabolismmedicine.diseaseTransplantationmedicine.anatomical_structureEndocrinologychemistryAnesthesiaDisease ProgressionBlood VesselsSurgerymedicine.symptombusinessVasoconstrictionTransplantation Proceedings
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2015

The recombinant form of tissue plasminogen activator (rt-PA) is the only curative treatment for ischemic stroke. Recently, t-PA has been linked to the metabolism of brain-derived neurotrophic factor (BDNF), a major neurotrophin involved in post-stroke neuroplasticity. Thus, the objective of our study was to investigate the impact of rt-PA treatment on post-stroke circulating BDNF levels in humans and in animals. Serum BDNF levels and t-PA/plasmin activity were measured at hospital admission and at up to 90 days in stroke patients receiving (n = 24) or not (n = 14) rt-PA perfusion. We investigated the relationships between serum BDNF with concurrent t-PA/plasmin activity, neurological outcom…

Brain-derived neurotrophic factor0303 health sciencesmedicine.medical_specialtyPathologyMultidisciplinaryPlasminbusiness.industrymedicine.diseaseTissue plasminogen activator3. Good healthBrain ischemia03 medical and health sciences0302 clinical medicineEndocrinologyBlood pressurenervous systemInternal medicinemedicineEndothelial dysfunctionbusinessStroke030217 neurology & neurosurgeryFibrinolytic agent030304 developmental biologymedicine.drugPLOS ONE
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Buerger`s Disease and Hyperhomocysteinemia: Is there a Relationship?

2009

Thromboangiitis obliterans, also known as Buerger's disease, is a cause of juvenile lower limb ischaemia. Buerger's disease is idiopathic and one of diagnostic criteria is the absence of atherosclerotic risk factors other than smok- ing. A possible involvement of thrombophilia has been investigated and the role of hyperhomocysteinemia is still matter of discussion. We describe 9 patients with Buerger's disease followed-up for the past 3 years. We found a significant in- crease in circulating homocysteine levels (mean: 31.6 in patients vs 8.2 μmol/L in control subjects). We also analyzed the C677T mutation of MTHFR; 5/9 Buerger's patients were heterozygotes and 4/9 homozygotes for the mutati…

Buerger's diseasemedicine.medical_specialtyHyperhomocysteinemiaPathologyHomocysteinebiologybusiness.industryDiseasemedicine.diseaseThrombophiliaGastroenterologyPathogenesischemistry.chemical_compoundchemistrythrombophilia hyperhomocysteinemia MTHFR Buerger's diseaseInternal medicineMethylenetetrahydrofolate reductasemedicinebiology.proteinEndothelial dysfunctionbusinessThe Open Atherosclerosis & Thrombosis Journal
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