Search results for "choline"

showing 10 items of 1138 documents

Effects of the novel polymer gel LeGoo on human internal thoracic arteries.

2011

Purpose Established hemostatic devices can injure vessel wall integrity. LeGoo (Pluromed, Woburn, MA), a novel poloxamer gel with reverse thermosensitive properties, is a new device for temporary occlusion of blood vessels. The present study investigated the effects of LeGoo on vascular function and morphology. Description The distal end of the human internal thoracic artery was used to assess vascular function of LeGoo-applied segments in organ bath experiments and by scanning electron microscopy. Evaluation After LeGoo application, both maximal contractile responses to noradrenaline and endothelium-dependent relaxant responses to acetylcholine were significantly reduced. Scanning electron…

Pulmonary and Respiratory MedicineMaleEndotheliumInternal thoracic arteryPoloxamerMuscle Smooth VascularNorepinephrinemedicine.arteryMedicineHumansNew devicePolymer gelThoracic arteryMammary ArteriesAgedbusiness.industryOrgan bathAnatomyMiddle AgedAcetylcholinemedicine.anatomical_structureSurgeryFemaleEndothelium VascularCardiology and Cardiovascular MedicinebusinessTemporary occlusionAcetylcholinemedicine.drugThe Annals of thoracic surgery
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Endurance training damages small airway epithelium in mice.

2007

RATIONALE: In athletes, airway inflammatory cells were found to be increased in induced sputum or bronchial biopsies. Most data were obtained after exposure to cold and dry air at rest or during exercise. Whether training affects epithelial and inflammatory cells in small airways is unknown. OBJECTIVES: To test whether endurance training under standard environmental conditions causes epithelial damage and inflammation in the small airways of mice. METHODS AND MEASUREMENTS: Formalin-fixed, paraffin-embedded lung sections were obtained in sedentary (n = 14) and endurance-trained (n = 16) Swiss mice at baseline and after 15, 30, and 45 days of training. The following variables were assessed (m…

Pulmonary and Respiratory MedicineMalePathologymedicine.medical_specialtyInflammationApoptosisCritical Care and Intensive Care MedicineSettore BIO/09 - FisiologiaEpitheliumEpithelial DamageLeukocyte CountMiceEndurance trainingIntensive carePhysical Conditioning AnimalProliferating Cell Nuclear AntigenmedicineLeukocytesAnimalsBronchitisCell ProliferationBasement membraneLungAerobic exercise bronchial responsivenes methacholine deep inspiration leukotrienesbusiness.industryNF-kappa Brespiratory systemImmunohistochemistryEpitheliumrespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureRespiratory epitheliummedicine.symptombusinessAmerican journal of respiratory and critical care medicine
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Association between reduced bronchodilatory effect of deep inspiration and loss of alveolar attachments.

2005

Abstract Background We have previously shown that the bronchodilatory effect of deep inspiration is attenuated in individuals with COPD. This study was designed to investigate whether the impairment in this effect is associated with loss of alveolar attachments. Methods We measured deep inspiration (DI)-induced bronchodilation in 15 individuals with and without COPD (67 ± 2.2 yrs of age, mean ± SEM) undergoing lobar resection for peripheral pulmonary nodule. Prior to surgery, we measured TLCO and determined the bronchodilatory effect of deep inspiration after constricting the airways with methacholine. The number of destroyed alveolar attachments, as well as airway wall area and airway smoo…

Pulmonary and Respiratory MedicineMalemedicine.medical_specialtyPathologyStatistics as TopicBronchial provocation testsCOPD lung inflationBronchi030204 cardiovascular system & hematologySettore MED/10 - Malattie Dell'Apparato RespiratorioBronchial Provocation Tests03 medical and health sciencesPulmonary Disease Chronic Obstructive0302 clinical medicineInternal medicinemedicineHumansLung volumesMethacholine ChlorideAgedlcsh:RC705-779COPDbusiness.industryResearchAirway smooth musclelcsh:Diseases of the respiratory systemrespiratory systemmedicine.diseaserespiratory tract diseasesPulmonary Alveoli030228 respiratory systemMethacholine chlorideInhalationAirway wallCardiologyMethacholineFemalebusinessmedicine.drugRespiratory research
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Deep inspiration-induced bronchoprotection is stronger than bronchodilation

2000

We have previously shown that in healthy subjects, deep inspiration (DI) has not only a bronchodilatory but also a bronchoprotective effect that is absent in asthmatic subjects. We conducted the study reported here to test the hypothesis that the bronchoprotective effect is stronger than the bronchodilatory effect, and to determine the extent to which these two effects are related. Ten healthy subjects underwent provocations in which single doses of methacholine, previously shown to reduce FEV(1) by 10% to 20% (Dose 1) and by 20% to 40% (Dose 2) were administered after a 20-min period devoid of DI. To measure the bronchodilator effect, DIs were performed immediately after the first spiromet…

Pulmonary and Respiratory MedicineSpirometryAdultMaleSettore MED/10 - Malattie Dell'Apparato RespiratorioCritical Care and Intensive Care MedicineBronchial Provocation TestsPulmonary function testingRisk FactorsForced Expiratory VolumeBronchodilationmedicineHumansLung Diseases ObstructiveMethacholine ChlorideAsthmaBronchusmedicine.diagnostic_testInhalationDose-Response Relationship Drugbusiness.industryAirway Resistancemedicine.diseaseBronchodilatationBronchial Provocation Testmedicine.anatomical_structureInhalationAnesthesiaMethacholineFemalebusinessmedicine.drugHuman
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Blinded 12-week comparison of once-daily indacaterol and tiotropium in COPD.

2011

Two, once daily (q.d.) inhaled bronchodilators are available for the treatment of chronic obstructive pulmonary disease (COPD): the β(2)-agonist indacaterol and the anticholinergic tiotropium. This blinded study compared the efficacy of these two agents and assessed their safety and tolerability. Patients with moderate-to-severe COPD were randomised to treatment with indacaterol 150 μg q.d. (n=797) or tiotropium 18 μg q.d. (n=801) for 12 weeks. After 12 weeks, the two treatments had similar overall effects on "trough" (24 h post-dose) forced expiratory volume in 1 s. Indacaterol-treated patients had greater improvements in transition dyspnoea index (TDI) total score (least squares means 2.0…

Pulmonary and Respiratory MedicineSpirometryMalemedicine.drug_classScopolamine DerivativesQuinolonesSeverity of Illness IndexCholinergic AntagonistsDrug Administration ScheduleMedical Recordslaw.inventionPulmonary Disease Chronic ObstructiveRandomized controlled trialDouble-Blind MethodlawAdrenergic beta-2 Receptor AntagonistsForced Expiratory VolumemedicineAnticholinergicHumansTiotropium BromideAdverse effectAgedCOPDmedicine.diagnostic_testbusiness.industryTiotropium bromideMiddle Agedmedicine.diseaserespiratory tract diseasesBronchodilator AgentsTreatment OutcomeTolerabilitySpirometryAnesthesiaIndansIndacaterolFemalebusinessmedicine.drugThe European respiratory journal
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Maximal Response Plateau to Adenosine 5′-Monophosphate in Asthma

2009

Background No information is available on the plateau in response to adenosine 5′-monophosphate. The aims of the present study were to determine whether plateau can be detected with AMP and the relation with the plateau in response to methacholine, and to identify the relation between the plateau and indirect markers of airway inflammation, such as exhaled nitric oxide (ENO) and exhaled breath condensate (EBC) pH. Methods Airway responsiveness to high concentrations of methacholine and AMP, ENO levels, and EBC pH values were obtained in 31 subjects with well-controlled asthma. Concentration-response curves were characterized by their concentration of agonist that produces a decrease in FEV …

Pulmonary and Respiratory MedicineSpirometrymedicine.medical_specialtymedicine.diagnostic_testInhalationbusiness.industryCritical Care and Intensive Care MedicinePlateau (mathematics)medicine.diseaserespiratory tract diseasesNitric oxidechemistry.chemical_compoundEndocrinologychemistryInternal medicineAnesthesiaExhaled nitric oxidemedicineMethacholineExhaled breath condensateCardiology and Cardiovascular Medicinebusinessmedicine.drugAsthmaChest
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Aclidinium inhibits cigarette smoke-induced lung fibroblast-to-myofibroblast transition.

2012

Cigarette smoking contributes to lung remodelling in chronic obstructive pulmonary disease (COPD). As part of this remodelling, peribronchiolar fibrosis is observed in the small airways of COPD patients and contributes to airway obstruction. Fibroblast-to-myofibroblast transition is a key step in peribronchiolar fibrosis formation. This in vitro study examined the effect of cigarette smoke on bronchial fibroblast-to-myofibroblast transition, and whether aclidinium bromide inhibits this process. Human bronchial fibroblasts were incubated with aclidinium bromide (10 −9 –10 −7 M) and exposed to cigarette smoke extract. Collagen type I and α-smooth muscle actin (α-SMA) expression were measured …

Pulmonary and Respiratory MedicineTime FactorsBronchiPharmacologyCholinergic AntagonistsCollagen Type Ichemistry.chemical_compoundAclidinium bromideFibrosisSmokemedicineExtracellularCyclic AMPHumansRNA Small InterferingFibroblastMyofibroblastsLungCells CulturedInflammationbusiness.industrySmokingFibroblastsmedicine.diseaseFluoresceinsAcetylcholinesteraseFibrosisActinsrespiratory tract diseasesmedicine.anatomical_structurechemistryGene Expression RegulationMicroscopy FluorescencebusinessReactive Oxygen SpeciesMyofibroblastAcetylcholineIntracellularmedicine.drugTropanesThe European respiratory journal
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Alternative mechanisms for tiotropium

2009

Tiotropium is commonly used in the treatment of chronic obstructive pulmonary disease. Although largely considered to be a long-acting bronchodilator, its demonstrated efficacy in reducing the frequency of exacerbations and preliminary evidence from early studies indicating that it might slow the rate of decline in lung function suggested mechanisms of action in addition to simple bronchodilation. This hypothesis was examined in the recently published UPLIFT study and, although spirometric and other clinical benefits of tiotropium treatment extended to four years, the rate of decline in lung function did not appear to be reduced by the addition of tiotropium in this study. This article summ…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyANTICHOLINERGIC BRONCHODILATORmedicine.drug_classRespiratory SystemScopolamine DerivativesPulmonary diseaseIPRATROPIUM BROMIDEIpratropium bromideOBSTRUCTIVE PULMONARY-DISEASEMUCOCILIARY CLEARANCECholinergic AntagonistsRECEPTORS MEDIATE STIMULATIONParasympathetic Nervous SystemAIRWAY SMOOTH-MUSCLEBronchodilatorBronchodilationMechanismsBRONCHIAL EPITHELIAL-CELLSAnimalsHumansMedicineCOPDPharmacology (medical)Tiotropium BromideIntensive care medicineLungLung functionInflammationCOPDbusiness.industryTiotropiumBiochemistry (medical)RemodellingTiotropium bromidemedicine.diseaseAcetylcholineBronchodilator Agentsrespiratory tract diseasesMucusClinical researchNONNEURONAL CHOLINERGIC SYSTEMCoughPOLYSPECIFIC CATION TRANSPORTERSAnesthesiaLUNG FIBROBLAST PROLIFERATIONbusinesshuman activitiesmedicine.drugPulmonary Pharmacology & Therapeutics
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Aclidinium inhibits human lung fibroblast to myofibroblast transition

2011

Background Fibroblast to myofibroblast transition is believed to contribute to airway remodelling in lung diseases such as asthma and chronic obstructive pulmonary disease. This study examines the role of aclidinium, a new long-acting muscarinic antagonist, on human fibroblast to myofibroblast transition. Methods Human bronchial fibroblasts were stimulated with carbachol (10 −8 to 10 −5  M) or transforming growth factor-β1 (TGF-β1; 2 ng/ml) in the presence or absence of aclidinium (10 −9 to 10 −7  M) or different drug modulators for 48 h. Characterisation of myofibroblasts was performed by analysis of collagen type I and α-smooth muscle actin (α-SMA) mRNA and protein expression as well as α…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyCarbacholChronic Obstructive Pulmonary DiseaseBronchiMuscarinic AntagonistsBiologyCholinergic AgonistsCollagen Type ITransforming Growth Factor beta1Downregulation and upregulationWestern blotanticholinergicCell MovementInternal medicinemedicineCOPDHumans1506RNA MessengerAutocrine signallingFibroblastMyofibroblastsCells CulturedCell Proliferationmedicine.diagnostic_testDose-Response Relationship Drugairway epitheliumCell Differentiationasthmainterstitial fibrosisFibroblastsAdenosineMolecular biologymyofibroblastActinsUp-RegulationEndocrinologymedicine.anatomical_structurePhosphorylationFibroblastCarbacholMyofibroblastmedicine.drugTropanesThorax
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Muscarinic M2 receptors in acetylcholine-isoproterenol functional antagonism in human isolated bronchus

2002

The muscarinic functional antagonism of isoproterenol relaxation and the contribution of muscarinic M2 receptors were examined in human isolated bronchus. In intact tissues, acetylcholine (ACh) precontraction decreased isoproterenol potency and maximal relaxation (−log EC50 shift = −1.49 ± 0.16 and Emax inhibition for 100 μM ACh = 30%) more than the same levels of histamine contraction. The M2receptor-selective antagonist methoctramine (1 μM) reduced this antagonism in ACh- but not histamine-contracted tissues. Similar results were obtained for forskolin-induced relaxation. After selective inactivation of M3 receptors with 4-diphenylacetoxy- N-(2-chloroethyl)piperadine hydrochloric acid (3…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyLung NeoplasmsPhysiologyMuscle RelaxationBronchiMuscarinic AntagonistsIn Vitro Techniqueschemistry.chemical_compoundPiperidinesPhysiology (medical)Internal medicineIsoprenalineMuscarinic acetylcholine receptorCyclic AMPmedicineMethoctramineHumansNeurotransmitterAcetylcholine receptorReceptor Muscarinic M2BronchusColforsinIsoproterenolMuscle SmoothMuscarinic acetylcholine receptor M2Cell BiologyReceptors MuscarinicAcetylcholinemedicine.anatomical_structureEndocrinologychemistryAcetylcholineMuscle Contractionmedicine.drugAmerican Journal of Physiology-Lung Cellular and Molecular Physiology
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