Search results for "vasodilator"

showing 10 items of 128 documents

Relaxant effects of sodium nitroprusside and NONOates in goat middle cerebral artery: delayed impairment by global ischemia-reperfusion.

1999

Global cerebral ischemia and subsequent reperfusion induce early impairment of the vasodilator responses to hypercapnia and vasoactive substances. Nitric oxide (NO) is involved in the regulation of cerebral blood flow (CBF) in both health and disease. The present study was designed to assess possible changes in the cerebrovascular reactivity to NO donors induced by cerebral ischemia-reperfusion in goats. Female goats (n = 9) were subjected to 20 min global cerebral ischemia under halothane/N2O anesthesia. Sixteen additional goats were sham-operated as a control group. One week later the effects of ischemia-reperfusion on relaxations to NO donors sodium nitroprusside (SNP), diethylamine/NO (…

NitroprussideCancer ResearchPhysiologyMuscle RelaxationClinical BiochemistryCerebral arteriesIschemiaVasodilationPharmacologyBiochemistrymedicine.arterymedicineAnimalsNitric Oxide Donorsbusiness.industryGoatsCerebral Arteriesmedicine.diseaseCerebral blood flowAnesthesiaReperfusion InjuryMiddle cerebral arteryFemaleSodium nitroprussideHalothanebusinessNitrovasodilatormedicine.drugNitric oxide : biology and chemistry
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Effects of ouabain on human bronchial muscle in vitro

2003

The effects of ouabain, an inhibitor of the plasmalemmal Na(+)/K(+)-ATPase activity, were examined in human isolated bronchus. Ouabain produced concentration-dependent contraction with -logEC(50)=7.16+/-0.11 and maximal effect of 67+/-4% of the response to acetylcholine (1 mM). Ouabain (10 microM)-induced contraction was epithelium-independent and was not depressed by inhibitors of cyclooxygenase and lipoxygenase, antagonists of muscarinic, histamine H(1)-receptors and alpha-adrenoceptors, or neuronal Na(+) channel blockade. The inhibition of ouabain contraction in tissues bathed in K(+)-free medium, and the inhibition by ouabain of the K(+)-induced relaxation confirm that the contractile a…

NitroprussideCromakalimmedicine.medical_specialtySodium-Hydrogen ExchangersTime FactorsInositol PhosphatesMuscle RelaxationVasodilator AgentsBronchiIn Vitro TechniquesOuabainMembrane Potentialschemistry.chemical_compoundSodium Potassium Chloride Symporter InhibitorsInternal medicineMuscarinic acetylcholine receptormedicineHumansVasoconstrictor AgentsNa+/K+-ATPaseOuabainInositol phosphateProtein Kinase CPharmacologychemistry.chemical_classificationForskolinColforsinIsoproterenolMuscle SmoothGeneral MedicineCalcium Channel BlockersAcetylcholineAmilorideEndocrinologychemistryCalciumSodium-Potassium-Exchanging ATPaseHistamineAcetylcholineHistaminemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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Effects of fenspiride on human bronchial cyclic nucleotide phosphodiesterase isoenzymes: functional and biochemical study.

1998

We have investigated the role of human bronchial cyclic nucleotide phosphodiesterases in the effects of fenspiride, a drug endowed with bronchodilator and anti-inflammatory properties. Functional studies on human isolated bronchi showed that fenspiride (10(-6)-3 x 10(-3) M, 30 min) induced a shift to the left of the concentration-response curves for isoprenaline and sodium nitroprusside with -logEC50 values of 4.1+/-0.1 (n = 7) and 3.5+/-0.2 (n = 8), respectively. Biochemical studies were carried out on three human bronchi in which separation of cyclic nucleotide phosphodiesterase isoenzymes was performed by ion exchange chromatography followed by determination of phosphodiesterase activity…

NitroprussideMuscle RelaxationVasodilator AgentsPhosphodiesterase 3FenspirideBronchimedicineHumansSpiro CompoundsPharmacologyCyclic nucleotide phosphodiesterasebiologyDose-Response Relationship DrugChemistryIsoproterenolPhosphodiesteraseBronchodilator AgentsIsoenzymesBiochemistryEnzyme inhibitor3'5'-Cyclic-AMP PhosphodiesterasescGMP-specific phosphodiesterase type 5biology.proteinPhosphodiesterase 2Sodium nitroprussidemedicine.drugMuscle ContractionEuropean journal of pharmacology
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Halothane inhibits endothelium-dependent relaxation elicited by acetylcholine in human isolated pulmonary arteries.

1997

This study examined whether a clinically relevant concentration of the volatile anaesthetic halothane modifies the endothelium-dependent relaxation produced by acetylcholine (3 nM-10 microM), histamine (1 pM-0.1 microM) and anti-human immunoglobulin E (1:1000) in human isolated pulmonary arteries submaximally precontracted with noradrenaline. An inhibitor of nitric oxide formation, N(G)-nitro-L-arginine (100 microM), attenuated acetylcholine-induced relaxation but failed to inhibit histamine- and anti-human immunoglobulin E-induced relaxation. Indomethacin (2.8 microM, a cyclooxygenase inhibitor) preferentially reduced the relaxation to histamine and anti-human IgE. Halothane (2%) significa…

Nitroprussidemedicine.medical_specialtyCromakalimEndotheliumArginineVasodilator AgentsDrug Evaluation PreclinicalProstaglandinVasodilationIn Vitro TechniquesPulmonary ArteryNitric oxidechemistry.chemical_compoundInternal medicinemedicineHumansBenzopyransPyrrolesPharmacologyColforsinImmunoglobulin EAcetylcholineEnzyme ActivationEndocrinologymedicine.anatomical_structurechemistryGuanylate CyclaseAnesthetics InhalationEndothelium VascularHalothaneHalothaneAcetylcholineHistaminemedicine.drugAdenylyl CyclasesEuropean journal of pharmacology
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The effects of the nitric oxide donors molsidomine and SIN-1 on human polymorphonuclear leucocyte functionin vitro andex vivo

1992

The nitrovasodilator and nitric oxide donor molsidomine and its metabolite SIN-I dilate vascular smooth muscle and inhibit platelet activation by increasing intracellular concentrations of cyclic GMP We have therefore studied the effects of molsidomine and SIN-I on isolated human polymorphonuclear leucocytes (PMN)in vitro andex vivo. In vitro molsidomine dose-dependently reducedβ-glucuronidase release and the generation of superoxide anions from non-activated and from FMLP- or PAF-stimulated human PMNs. SIN-1 was equally effective in reducing (β-glucuronidase release and totally inhibited oxygen radical generation at a concentration of 580 μmol · l−1. In a double-blind, placebo-controlled, …

PharmacologyMolsidomineChemistrySuperoxideMetabolitehemic and immune systemsGeneral MedicinePharmacologyNitric oxidechemistry.chemical_compoundBiochemistryIn vivomedicinePharmacology (medical)Platelet activationNitrovasodilatorEx vivomedicine.drugEuropean Journal of Clinical Pharmacology
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Number of nitrate groups determines reactivity and potency of organic nitrates: a proof of concept study in ALDH-2−/− mice

2007

Background and purpose: Mitochondrial aldehyde dehydrogenase (ALDH-2) has been shown to provide a pathway for bioactivation of organic nitrates and to be prone to desensitization in response to highly potent, but not to less potent, nitrates. We therefore sought to support the hypothesis that bioactivation by ALDH-2 critically depends on the number of nitrate groups within the nitrovasodilator. Experimental approach: Nitrates with one (PEMN), two (PEDN; GDN), three (PETriN; glyceryl trinitrate, GTN) and four (pentaerithrityl tetranitrate, PETN) nitrate groups were investigated. Vasodilatory potency was measured in isometric tension studies using isolated aortic segments of wild type (WT) an…

Pharmacologychemistry.chemical_classificationbiologyAldehyde dehydrogenasePentaerythritol tetranitrateDehydrogenaseNitric oxidechemistry.chemical_compoundEnzymeBiochemistrychemistrymedicinebiology.proteinStructure–activity relationshipPotencyNitrovasodilatormedicine.drugBritish Journal of Pharmacology
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Explaining the phenomenon of nitrate tolerance.

2005

During the last century, nitroglycerin has been the most commonly used antiischemic and antianginal agent. Unfortunately, after continuous application, its therapeutic efficacy rapidly vanishes. Neurohormonal activation of vasoconstrictor signals and intravascular volume expansion constitute early counter-regulatory responses (pseudotolerance), whereas long-term treatment induces intrinsic vascular changes, eg, a loss of nitrovasodilator-responsiveness (vascular tolerance). This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase …

PhysiologyVasodilator AgentsPharmacologymedicine.disease_causeNitric OxideProstacyclin synthaseNitric oxidechemistry.chemical_compoundNitroglycerinSuperoxidesPeroxynitrous AcidmedicineCyclic GMP-Dependent Protein KinasesAnimalsHumansBiotransformationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyChemistrySuperoxidePhosphoric Diester HydrolasesAldehyde Dehydrogenase MitochondrialDrug ToleranceAldehyde DehydrogenaseCyclic Nucleotide Phosphodiesterases Type 1VasodilationOxidative StressBiochemistryVasoconstrictioncardiovascular systembiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseReactive Oxygen SpeciesPeroxynitriteOxidative stressSignal TransductionCirculation research
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Inhaled iloprost to control residual pulmonary hypertension following pulmonary endarterectomy.

2005

Objective: Pulmonary endarterectomy (PEA) is the standard therapy for patients with chronic thromboembolic pulmonary hypertension (CTEPH). In the immediate postoperative period, persistent pulmonary hypertension increases the risk of acute respiratory or right heart failure. In pulmonary arterial hypertension, prostanoid inhalation has been found to improve pulmonary hemodynamics, right ventricular function, gas exchange, and clinical outcome. We report the results of a double-blinded randomized trial with the aerosolized prostacyclin analogue iloprost in patients with residual pulmonary hypertension after PEA. Methods: Twenty-two patients (age, 55 � 13 years; 8 females; propofol- and sufen…

Pulmonary and Respiratory MedicineAdultMalemedicine.medical_specialtymedicine.medical_treatmentHypertension PulmonaryPartial PressureVasodilator AgentsEndarterectomyPulmonary ArteryDouble-Blind MethodInternal medicineAdministration InhalationmedicineHumansIloprostProspective StudiesEndarterectomyAgedMechanical ventilationLungbusiness.industryPulmonary Gas ExchangeRespiratory diseaseHemodynamicsGeneral MedicineCarbon DioxideMiddle Agedmedicine.diseasePulmonary hypertensionOxygenmedicine.anatomical_structureTreatment OutcomeAnesthesiaCirculatory systemVascular resistanceCardiologySurgeryFemaleCardiology and Cardiovascular MedicinebusinessIloprostmedicine.drugEuropean journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
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Inhaled iloprost in patients with chronic thromboembolic pulmonary hypertension: effects before and after pulmonary thromboendarterectomy.

2003

Abstract Background In primary pulmonary hypertension, aerosolized prostanoids selectively reduce pulmonary vascular resistance and improve right ventricular function. In this study, hemodynamic effects of inhaled iloprost, a stable prostacyclin analogue, were evaluated in patients with chronic thromboembolic pulmonary hypertension (CTEPH) before and early after pulmonary thromboendarterctomy (PTE). Methods Ten patients (mean age 49 years old [32 to 70 years old], New York Heart Association functional class III and IV) received a dose of 33 μg aerosolized iloprost immediately before surgery (T1), after intensive care unit admission (T2), and 12-hours postoperatively (T3). Effects on pulmona…

Pulmonary and Respiratory MedicineAdultMalemedicine.medical_treatmentHypertension PulmonaryVasodilator AgentsHemodynamicsEndarterectomymedicine.arteryAdministration InhalationPreoperative CaremedicineHumansIloprostPostoperative PeriodEndarterectomyAgedPulmonary thromboendarterectomybusiness.industryRespiratory diseaseMiddle Agedmedicine.diseasePulmonary hypertensionmedicine.anatomical_structureAnesthesiaPulmonary arteryChronic DiseaseVascular resistanceSurgeryFemaleCardiology and Cardiovascular MedicinebusinessPulmonary EmbolismIloprostmedicine.drugThe Annals of thoracic surgery
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Síndrome hepatopulmonar en paciente con adenocarcinoma de colon con metástasis hepáticas y sin hepatopatía crónica conocida

2006

El sindrome hepatopulmonar comprende una triada clinica caracterizada por desoxigenacion arterial, dilataciones vasculares intrapulmonares y hepatopatia. Se han descrito tanto casos agudos como cronicos, y la causa mas frecuente es la cirrosis. El mecanismo fisiopatologico principal es la dilatacion de los vasos pulmonares, que produce una alteracion del intercambio gaseoso. Se ha implicado la mayor produccion pulmonar de oxido nitrico como mecanismo patogenico principal de la vasodilatacion, aunque tambien se ha relacionado el desequilibrio entre sustancias vasodilatadoras y vasoconstrictoras. Describimos un caso en el que se produjo un sindrome hepatopulmonar en un paciente afectado de un…

Pulmonary and Respiratory MedicineGynecologymedicine.medical_specialtybusiness.industrymedicinebusinessPulmonary vasodilatorsArchivos de Bronconeumología
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