Search results for "endothelial dysfunction"

showing 7 items of 287 documents

COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up

2020

Coronavirus disease-2019 (COVID-19), a viral respiratory illness caused by the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), may predispose patients to thrombotic disease, both in the venous and arterial circulations, because of excessive inflammation, platelet activation, endothelial dysfunction, and stasis. In addition, many patients receiving antithrombotic therapy for thrombotic disease may develop COVID-19, which can have implications for choice, dosing, and laboratory monitoring of antithrombotic therapy. Moreover, during a time with much focus on COVID-19, it is critical to consider how to optimize the available technology to care for patients without COVID-19 who hav…

medicine.medical_specialtymedicine.drug_classantithrombotic therapyCoronavirus disease 2019; SARS-CoV-2; anticoagulant; antiplatelet; antithrombotic therapy; thrombosisDisease030204 cardiovascular system & hematologyantiplateletPathogenesis03 medical and health sciences0302 clinical medicineAntithromboticEpidemiologyMedicine030212 general & internal medicinePlatelet activationEndothelial dysfunctionIntensive care medicinethrombosisCoronavirus disease 2019SARS-CoV-2business.industryanticoagulantAnticoagulantmedicine.diseaseThrombosisCardiology and Cardiovascular MedicinebusinessJournal of the American College of Cardiology
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Cigarette smoke-induced pulmonary endothelial dysfunction is partially suppressed by sildenafil.

2009

Abstract Cigarette smoke mediated oxidative stress and endothelial dysfunction are important processes in the pathogenesis of several lung disorders. In this study we evaluated the effect of PDE5 inhibition on pulmonary artery endothelial dysfunction induced by cigarette smoke in vitro . Human pulmonary artery endothelial cells (HPAEC) were incubated in the absence or presence of PDE5 inhibitor sildenafil (10 nM–1 μM), PKG agonist 8-Br-cGMP (1 mM), or the antioxidants dyphenyleneiodonium (DPI 1 μM) and N -acetylcysteine (NAC 1 mM) for 30 min. Then, cigarette smoke extract (CSE) was added for 24 h. CSE (2.5–10%)-induced ROS generation was suppressed by DPI, and partially reversed by sildenaf…

medicine.medical_specialtymedicine.drug_mechanism_of_actionSildenafilVasodilator AgentsPharmaceutical ScienceEnzyme-Linked Immunosorbent Assaymedicine.disease_causeNitric OxidePolymerase Chain ReactionPiperazinesSildenafil CitrateAcetylcysteinechemistry.chemical_compoundInternal medicineSmokeparasitic diseasesTobaccomedicineHumansSulfonesEndothelial dysfunctionPhosphodiesterase inhibitorLungCells CulturedDNA PrimersbiologyBase Sequencebusiness.industrymedicine.diseaseEndothelial stem cellEndocrinologychemistryEnzyme inhibitorPurinescardiovascular systembiology.proteinEndothelium VascularbusinessPhosphodiesterase 5 inhibitorOxidative stressmedicine.drugEuropean journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
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An update on the relationships between rheumatoid arthritis and atherosclerosis

2010

Rheumatoid arthritis is a chronic inflammatory disease. Cardiovascular events are the most important cause of mortality and morbidity in patients with rheumatoid arthritis. Beyond the traditional cardiovascular risk factors, chronic systemic inflammation has been shown to be a crucial factor in atherosclerosis development and progression from endothelial dysfunction to plaque rupture and thrombosis. Many studies have shown that atherosclerosis is not a passive event like accumulation of lipids in the vessel walls; by contrast, it represents an active inflammation of the vessels. Inflammatory cells such as macrophages, monocytes and T cells play important roles in the development of both rhe…

musculoskeletal diseasesT-LymphocytesAtherosclerosis Rheumatoid arthritis Inflammation Cardiovascular risk10265 Clinic for Endocrinology and DiabetologyInflammation610 Medicine & healthComorbiditySystemic inflammationModels BiologicalMonocytes2705 Cardiology and Cardiovascular MedicineArthritis RheumatoidRisk FactorsImmunopathologymedicineHumansEndothelial dysfunctionAutoimmune diseaseInflammationbusiness.industryVascular diseaseMacrophagesmedicine.diseaseAtherosclerosisThrombosisOxidative StressCardiovascular DiseasesRheumatoid arthritisImmunologyDisease Progressionmedicine.symptomInsulin ResistanceCardiology and Cardiovascular Medicinebusiness
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Effect of Non-Surgical Periodontal Treatment on Oxidative Stress Markers in Leukocytes and Their Interaction with the Endothelium in Obese Subjects w…

2020

Aim: The primary objective of this pilot study was to evaluate the effect of non-surgical periodontal treatment. The secondary aim was to evaluate the effect of dietary therapy on both parameters of oxidative stress in leukocytes and leukocyte-endothelial cell interactions in an obese population. Methods: This was a pilot study with a before-and-after design. Forty-nine obese subjects with periodontitis were randomized by means of the minimization method and assigned to one of two groups, one of which underwent dietary therapy while the other did not. All the subjects underwent non-surgical periodontal treatment. We determined periodontal, inflammatory and oxidative stress parameters&mdash

obesityPopulationlcsh:MedicineLeukocyte homeostasis030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeArticleendothelial dysfunctionSuperoxide dismutase03 medical and health scienceschemistry.chemical_compound0302 clinical medicineoxidative stressMedicineEndothelial dysfunctioneducationperiodontitisreactive oxygen specieschemistry.chemical_classificationPeriodontitisReactive oxygen specieseducation.field_of_studydietary therapybiologybusiness.industrySuperoxidelcsh:R030206 dentistryGeneral Medicinemedicine.diseaseperiodontal treatmentchemistrybiology.proteinbusinessOxidative stressJournal of Clinical Medicine
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Study of the mechanisms of oxidative stress, mitochondrial function and endoplasmic reticulum stress in obesity. Role in subclinical atherosclerosis …

2019

El aumento alarmante de la prevalencia de obesidad a nivel mundial y la enorme carga de enfermedad asociada ha generado una creciente demanda de estrategias para frenar la epidemia y / o mitigar los efectos dañinos de la obesidad sobre la salud. Para ello se requiere un compromiso firme y sinérgico por parte de todas las fuerzas sociales, no sólo para desarrollar estrategias preventivas, sino también para contribuir al conocimiento de los eventos patológicos y los mecanismos involucrados en el desarrollo de esta enfermedad. Por ello, el objetivo principal de la presente tesis doctoral es profundizar en los mecanismos subyacentes de la obesidad, especialmente en aquellos relacionados con el …

obesityleukocytes activationUNESCO::CIENCIAS DE LA VIDA::Biología molecularchronic periodontitis:CIENCIAS MÉDICAS ::Medicina interna::Endocrinología [UNESCO]pinitolendothelial dysfunction:CIENCIAS DE LA VIDA::Biología molecular [UNESCO]mitochondriaUNESCO::CIENCIAS MÉDICAS ::Patología::Arteriosclerosisinflammationcardiovascular diseasebotanical compoundsoxidative stresscaloric restriction:CIENCIAS DE LA VIDA::Fisiología humana ::Fisiología endocrina [UNESCO]:CIENCIAS MÉDICAS ::Patología::Arteriosclerosis [UNESCO]metabolismUNESCO::CIENCIAS MÉDICAS ::Medicina interna::EndocrinologíaUNESCO::CIENCIAS DE LA VIDA::Fisiología humana ::Fisiología endocrina
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Correlation between a marker of oxidative stress and a few indexes of endothelial dysfunction in essential hypertensive patients.

2005

oxidative stress endothelial dysfunction hypertension
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Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis.

2005

Objective— Sedentary lifestyle is associated with increased cardiovascular events. The underlying molecular mechanisms are incompletely understood. Reactive oxygen species (ROS) contribute to endothelial dysfunction and atherosclerosis. An important source of vascular ROS is the NADPH oxidase. Methods and Results— C57BL6 mice were subjected to regular housing (physical inactivity) or voluntary training on running wheels (6 weeks). Inactivity increased vascular lipid peroxidation to 148±9% and upregulated superoxide release to 176±17% (L-012 chemiluminescence) and 188±29% (cytochrome C reduction assay), respectively. ROS production was predominantly increased in the endothelium and the medi…

rac1 GTP-Binding Proteinmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIArteriosclerosisNitric Oxide Synthase Type IIBiologymedicine.disease_causechemistry.chemical_compoundMiceApolipoproteins EInternal medicinePhysical Conditioning AnimalmedicineAnimalsNADH NADPH OxidoreductasesRNA MessengerEndothelial dysfunctionLife Stylechemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseSuperoxideNeuropeptidesNADPH Oxidase 1NADPH Oxidasesmedicine.diseasePhosphoproteinsMice Mutant Strainsrac GTP-Binding ProteinsMice Inbred C57BLVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologychemistryNOX1biology.proteinNADPH Oxidase 1Endothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressArteriosclerosis, thrombosis, and vascular biology
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