Search results for "epoprostenol"

showing 10 items of 35 documents

Extracellular histones disarrange vasoactive mediators reléase through COX-NOS interaction in human endothelial cells

2017

Abstract Extracellular histones are mediators of inflammation, tissue injury and organ dysfunction. Interactions between circulating histones and vascular endothelial cells are key events in histone‐mediated pathologies. Our aim was to investigate the implication of extracellular histones in the production of the major vasoactive compounds released by human endothelial cells (HUVECs), prostanoids and nitric oxide (NO). HUVEC exposed to increasing concentrations of histones (0.001 to 100 μg/ml) for 4 hrs induced prostacyclin (PGI2) production in a dose‐dependent manner and decreased thromboxane A2 (TXA2) release at 100 μg/ml. Extracellular histones raised cyclooxygenase‐2 (COX‐2) and prostac…

0301 basic medicineProstacyclinHistoneschemistry.chemical_compoundThromboxane A2Cytochrome P-450 Enzyme SystemSuperoxidesEnosvascular mediatorsGenètica humanabiologySuperoxideendothelial cellsIntramolecular OxidoreductasesEndothelial stem cellMolecular MedicineOriginal ArticleThromboxane-A SynthaseSignal Transductionmedicine.drugmedicine.medical_specialtyNitric Oxide Synthase Type IIIPrimary Cell CultureNitric OxideProstacyclin synthaseNitric oxideCyclic N-OxidesThromboxane A203 medical and health sciencesInternal medicineHuman Umbilical Vein Endothelial CellsmedicineExtracellularHumansRNA MessengerprostanoidsDose-Response Relationship DrugOriginal ArticlesCell Biologybiology.organism_classificationEpoprostenolÒxid nítric030104 developmental biologyEndocrinologyGene Expression RegulationchemistryCelecoxibCyclooxygenase 2Cyclooxygenase 1biology.proteinSpin LabelsProteïnesextracellular histones
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Antiplatelet effects of intravenous iloprost in patients with peripheral arterial obliterative disease

1986

The dose-dependent inhibition of platelet aggregation by the chemically stable, prostacyclin-mimetic, iloprost, was studied in patients suffering from stage II-III peripheral arterial obliterative disease (PAOD). The study was designed as a randomized placebo-controlled cross-over trial. Iloprost was administered i.v. to six patients at doses of 0.5, 1.0, 2.0 or 3.0 ng/kg X min for 4 h, with an interval of 2-3 days between the infusions. During iloprost infusion, systolic and diastolic arterial blood pressure, heart rate and blood flow in the affected limb remained unchanged. In contrast, there was a considerable, dose-dependent inhibition of ADP- and thrombin-induced platelet aggregation a…

AdultMaleTime FactorsPlatelet AggregationDiastoleHemodynamicsArterial Occlusive DiseasesPlaceboRandom AllocationDrug DiscoveryHeart ratemedicineHumansPlateletIloprostGenetics (clinical)AgedDose-Response Relationship Drugbusiness.industryHemodynamicsCardiovascular AgentsGeneral MedicineMiddle AgedEpoprostenolBlood pressureAnesthesiaCardiovascular agentDrug EvaluationMolecular MedicineFemalelipids (amino acids peptides and proteins)businesscirculatory and respiratory physiologyIloprostmedicine.drugKlinische Wochenschrift
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Endothelium-dependent responses in human isolated thyroid arteries from donors

2004

The functional properties of the endothelium of human thyroid arteries remain unexplored. We investigated the intervention of nitric oxide (NO), prostacyclin (PGI(2)) and endothelium-derived hyperpolarizing factor (EDHF) in the responses to acetylcholine and noradrenaline in isolated thyroid arteries obtained from multi-organ donors. Artery rings were suspended in organ baths for isometric recording of tension. The contribution of NO, PGI(2) and EDHF to endothelium-dependent relaxation was determined by the inhibitory effects of N(G)-monomethyl-L-arginine (L-NMMA), indomethacin, and K(+) channel inhibitors respectively. Acetylcholine induced concentration-dependent relaxation; this effect w…

AdultMalemedicine.medical_specialtyCharybdotoxinCharybdotoxinEndotheliumEndocrinology Diabetes and MetabolismIndomethacinThyroid GlandProstacyclinNitric OxideApaminOuabainNitric oxideBiological FactorsNorepinephrinechemistry.chemical_compoundEndocrinologyCulture TechniquesInternal medicinePotassium Channel BlockersmedicineHumansomega-N-MethylarginineDose-Response Relationship DrugArteriesMiddle AgedEpoprostenolAcetylcholineEndocrinologymedicine.anatomical_structureApaminchemistryVasoconstrictioncardiovascular systemFemaleEndothelium VascularNitric Oxide SynthaseSodium-Potassium-Exchanging ATPasePeptidesAcetylcholinemedicine.drugArteryJournal of Endocrinology
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The effect of two low doses of aspirin on whole blood thromboxane and prostacyclin generation in healthy subjects

1983

SummaryThe effects of two low doses of aspirin (20 mg and 100 mg) on prostacyclin and thromboxane formation during whole blood clotting were studied in 8 healthy volunteers.A single 100 mg aspirin dose caused more than 90% reduction of both serum TXB2 and 6-keto-PGF1α; a single 20 mg dose of aspirin inhibited serum TXB2 more than 6-keto-PGF1α but effects on these two products could not be completely dissociated.However, the effect of a single 20 mg aspirin dose on serum TXB2, was of much longer duration than its inhibitory effect on PGI2 synthesis during whole blood clotting.

AdultMalemedicine.medical_specialtyTime Factorsmedicine.drug_classThromboxaneAlpha (ethology)Prostacyclin6-Ketoprostaglandin F1 alphaInternal medicinemedicineHumansCyclooxygenase InhibitorsBlood CoagulationWhole bloodAspirinAspirinChemistryAnticoagulantLow doseThromboxanesHematologyHeparinEpoprostenolThromboxane B2EndocrinologyFemalelipids (amino acids peptides and proteins)circulatory and respiratory physiologymedicine.drug
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In vitro Analysis of Synergistic Effects of Fibrinolytic Agents and Prostacyclin Analogues

1997

We investigated the in vitro thrombolytic effects of streptoki-nase, urokinase, alteplase and saruplase, alone or in combination, with the prostacyclin analogues, iloprost and taprostene. Human platelet-rich plasma was stimulated with collagen (1 μg/ml) to generate thrombi containing platelets and fibrin. Following treatment with fibrinolytic agents, lysis was allowed to proceed for 30 min and was then terminated with aprotinin (2,000 ClU/ml). To evaluate the combinatory effects of fibrinolytic agents and prostacyclin analogues, we used concentrations of fibrinolytic agents which reduced thrombi weight by less than 50%. Neither iloprost nor taprostene alone demonstrated any thrombolytic eff…

AdultMalemedicine.medical_treatmentProstacyclinPharmacologyFibrinolytic AgentsPhysiology (medical)Prostaglandins SyntheticFibrinolysismedicineHumansStreptokinaseIloprostUrokinaseChemistryFibrinolysisDrug SynergismHematologyDrug interactionEpoprostenolUrokinase-Type Plasminogen ActivatorIn vitroTissue Plasminogen Activatorcardiovascular systemFemaleSaruplaseFibrinolytic agentIloprostmedicine.drugPathophysiology of Haemostasis and Thrombosis
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Prostacyclin receptor desensitization is a reversible phenomenon in human platelets.

1997

Background Long-term exposure of platelets to endogenous or exogenous prostacyclin or its analogues might result in desensitization of the platelet prostacyclin receptor in vitro and in vivo accompanied by a loss in receptor density on the platelet surface and a reduced sensitivity toward the inhibitory effects of prostacyclins. However, the reversibility of this process in platelets has not yet been investigated. Methods and Results Human platelets desensitized by the chemically stable prostacyclin analogue iloprost showed a significant reduction in [ 3 H]-iloprost binding sites that was reversed by saponin permeabilization. This indicates functionally active internalized prostacyclin rec…

AgonistBlood PlateletsMalemedicine.medical_specialtyCell Membrane Permeabilitymedicine.drug_classReceptors ProstaglandinProstaglandinProstacyclinReceptors EpoprostenolProstacyclin receptor bindingchemistry.chemical_compoundReference ValuesPhysiology (medical)Internal medicinemedicineCyclic AMPHumansPlateletIloprostProstacyclin receptorbusiness.industryEndocrinologychemistrycardiovascular systemPlatelet aggregation inhibitorlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicinebusinessPlatelet Aggregation Inhibitorsmedicine.drugIloprostCirculation
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Role of NO-synthases and cyclooxygenases in the hyperreactivity of male rabbit carotid artery to testosterone under experimental diabetes.

2009

Abstract Cardiovascular disease is the major cause of morbidity and mortality in diabetic patients, which in turn is also associated with low levels of serum testosterone. The working hypothesis was that diabetes might modify the mechanisms involved in the vascular actions of testosterone in isolated rabbit carotid arteries. Testosterone (10 −8 –3 × 10 −4  M) induced a concentration-dependent relaxation of precontracted carotid arteries, which was higher in diabetic than in control rabbits. In control rabbits neither endothelium removal nor the nitric oxide synthase (NOS) inhibitor N G -nitro- l -arginine ( l -NOArg, 10 −5  M) modified the relaxant action of testosterone, and the cyclooxyge…

Blood GlucoseCarotid Artery DiseasesMalemedicine.medical_specialtyArginineEndotheliumCharybdotoxinNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIVasodilationProstacyclinNitric OxideNitroarginineDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Internal medicinemedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsTestosteronePharmacologybiologyDose-Response Relationship Drugbusiness.industryTestosterone (patch)EpoprostenolNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureCarotid ArteriesApaminCyclooxygenase 2cardiovascular systembiology.proteinPotassiumCalciumCyclooxygenaseEndothelium VascularRabbitsbusinessDiabetic Angiopathiesmedicine.drugPharmacological research
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Involvement of prostacyclin and potassium channels in the diabetes-induced hyporeactivity of the rabbit carotid artery to B-type natriuretic peptide

2012

The relation between diabetes and stroke is bidirectional: diabetes is an important risk factor for ischemic stroke, and acute stroke frequently induces hyperglycemia. On the other hand, plasma B-type natriuretic peptide (BNP) levels are raised in diabetes and stroke. The purpose was to study how alloxan-induced diabetes might modify the effects of BNP in rabbit carotid arteries and the mechanisms involved in such actions. To do this, isometric tension in isolated rabbit carotid artery was recorded and prostanoids release and plasma NT-proBNP were measured by enzyme immunoassay. BNP induced a relaxation of phenylephrine-precontracted carotid arteries, and this relaxation was lower in diabet…

Blood GlucoseMalemedicine.medical_specialtyPotassium ChannelsEndotheliummedicine.drug_classProstacyclinNitric OxideGlibenclamideThromboxane A2chemistry.chemical_compoundDiabetes mellitusInternal medicineNatriuretic Peptide BrainDiabetes MellitusmedicineNatriuretic peptideAnimalscardiovascular diseasesEndothelial dysfunctionStrokePharmacologyDose-Response Relationship Drugbusiness.industryBody Weightmedicine.diseaseEpoprostenolPeptide FragmentsCarotid Arteriesmedicine.anatomical_structureEndocrinologychemistryPotassiumcardiovascular systemRabbitsbusinessReceptors Atrial Natriuretic Factorhormones hormone substitutes and hormone antagonistsmedicine.drugEuropean Journal of Pharmacology
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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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Altered expression of inflammation-related genes in human carotid atherosclerotic plaques.

2011

Abstract Objective Inflammation is a pivotal process in atherosclerosis development and progression, but the underlying molecular mechanisms remain largely obscure. We have conducted an extensive expression study of atherosclerotic plaques to identify the inflammatory pathways involved in atherosclerosis. Methods We studied 11 human carotid plaques, their respective adjacent regions and 7 control arteries from different subjects. Expression of 92 genes was studied by TaqMan low-density array human inflammation panel. Human aortic endothelial and smooth muscle cells were used for in vitro experiments. Results The mRNA levels of 44/92 genes (48%) differed significantly between the tissues exa…

Carotid Artery DiseasesMalemedicine.medical_specialtyMyocytes Smooth MuscleReceptors ProstaglandinPTGS1InflammationReceptors EpoprostenolSettore MED/22 - Chirurgia VascolareMuscle Smooth VascularCytochrome P-450 Enzyme SystemInternal medicineGene expressionmedicineHumansRNA MessengerReceptors CytokineCells CulturedAgedRegulation of gene expressionInflammationbiologyTumor Necrosis Factor-alphaGene Expression ProfilingMacrophagesEndothelial CellsMiddle AgedCoculture TechniquesPlaque AtheroscleroticGene expression profilingLipoproteins LDLEndocrinologyEicosanoidEicosanoid pathwayGene Expression RegulationItalyAtherosclerosiCase-Control StudiesArachidonate 5-lipoxygenasebiology.proteinCancer researchOxidative streTumor necrosis factor alphaFemaleGene expressionmedicine.symptomInflammation MediatorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesAtherosclerosis
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