Search results for " Epoprostenol"

showing 3 items of 3 documents

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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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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Combination Therapy with Oral Treprostinil for Pulmonary Arterial Hypertension:A Double-Blind Placebo-controlled Clinical Trial

2020

Rationale: Oral treprostinil improves exercise capacity in patients with pulmonary arterial hypertension (PAH), but the effect on clinical outcomes was unknown.\ud \ud Objectives: To evaluate the effect of oral treprostinil compared with placebo on time to first adjudicated clinical worsening event in participants with PAH who recently began approved oral monotherapy.\ud \ud Methods: In this event-driven, double-blind study, we randomly allocated 690 participants (1:1 ratio) with PAH to receive placebo or oral treprostinil extended-release tablets three times daily. Eligible participants were using approved oral monotherapy for over 30 days before randomization and had a 6-minute-walk dista…

MaleAdministration OralOral treprostinilCritical Care and Intensive Care MedicinePulmonary arterial hypertension[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractcombination therapyoralepoprostenol0302 clinical medicinepulmonary arterial hypertensionmiddle agedClinical endpointdouble-blind methodMESH: Double-Blind MethodFamilial Primary Pulmonary Hypertension030212 general & internal medicinehumansMESH: AgedMESH: Middle AgedEpoprostenol/analogs & derivativesadultHazard ratioMiddle Aged[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciencesantihypertensive agents3. Good healthagedfemaleMESH: Young Adultoral treprostinilMESH: Administration Oralyoung adultFemalePulmonary Arterial Hypertension/drug therapymedicine.drugAdultPulmonary and Respiratory MedicineMESH: Pulmonary Arterial Hypertensionmedicine.medical_specialtyRandomizationAdolescentclinical study; combination therapy; oral treprostinil; pulmonary arterial hypertension; sequential therapy; administration oral; adolescent; adult; aged; antihypertensive agents; double-blind method; epoprostenol; female; humans; male; middle aged; placebos; pulmonary arterial hypertension; young adultSequential therapyMESH: PlacebosMESH: EpoprostenolLower riskPlaceboadministrationClinical studyYoung Adult03 medical and health sciencesDouble-Blind Method[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmaleInternal medicineplacebosmedicineHumansCombination therapyAdverse effectPlacebos/therapeutic useAgedMESH: AdolescentPulmonary Vascular DiseaseMESH: Antihypertensive AgentsMESH: Humanssequential therapybusiness.industryMESH: AdultOriginal Articlesclinical studyMESH: MaleClinical trial030228 respiratory systemadolescentAntihypertensive Agents/administration & dosagebusinessMESH: FemaleTreprostinil
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