Search results for "Drug Interaction"

showing 10 items of 246 documents

 A Mechanistic Approach to theIn VivoAnti-Inflammatory Activity of Sesquiterpenoid Compounds Isolated fromInula viscosa

2001

The present study was designed to examine the anti-inflammatory activity of the sesquiterpenoids ilicic acid and inuviscolide, isolated from Inula viscosa, on cell degranulation, leukotriene biosynthesis, neurogenic drive and glucocorticoid-like interactions. Swiss female mice were used to measure the ear oedema induced by phorbol esters or ethyl phenylpropiolate (EPP), and the paw oedema induced by phospholipase A(2) (PLA(2)) or serotonin. Drug treatment consisted of one topically-applied dose in the ear models and a subcutaneous or intraperitoneal injection in the paw models. Quantitative analysis of leukotriene B(4) (LTB(4)) formation was performed on rat peritoneal neutrophils by high p…

medicine.drug_classLeukotriene B4medicine.medical_treatmentIntraperitoneal injectionPharmaceutical SciencePharmacologyBiologyPharmacognosyLeukotriene B4Cell DegranulationAnti-inflammatoryAnalytical ChemistryInhibitory Concentration 50MiceStructure-Activity Relationshipchemistry.chemical_compoundPhospholipase A2In vivoDrug DiscoverymedicineAnimalsDrug InteractionsGlucocorticoidsInflammationPharmacologyPhospholipase ADose-Response Relationship DrugMolecular StructureAnti-Inflammatory Agents Non-SteroidalOrganic ChemistryComplementary and alternative medicineBiochemistryMechanism of actionchemistrybiology.proteinMolecular MedicineFemaleInulaPlant Preparationsmedicine.symptomSesquiterpenesPhytotherapyPlanta Medica
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Potential drug-drug interaction between duloxetine and acenocoumarol in a patient with Alzheimer's disease

2007

Abstract Background : Recent evidence suggests that duloxetine may increase the effect of warfarin, thereby increasing the possibility of bleeding. However, a MEDLINE search for articles published between 1980 and May 2007 (terms: duloxetine , anticoagulants , acenocoumarol , and interaction ; no language restriction) did not yield any reports of an interaction between concomitant use of duloxetine and acenocoumarol. Objective : The aim of this study was to describe a potential drug-drug interaction between duloxetine and acenocoumarol in a patient with Alzheimer's disease. The possible mechanism of this potential interaction is examined. Case summary : This report presents the case of a 63…

medicine.drug_classThiophenesDuloxetine Hydrochloridechemistry.chemical_compoundAlzheimer DiseasemedicineHumansDuloxetineDrug InteractionsPharmacology (medical)International Normalized Ratioduloxetine acenocoumarol international normalized ratio Alzheimer’s diseasePharmacologyAcenocoumarolbusiness.industryAcenocoumarolAnticoagulantWarfarinAnticoagulantsMiddle AgedDrug interactionDiscontinuationchemistryAnesthesiaConcomitantFemaleSettore MED/26 - NeurologiabusinessReuptake inhibitorSelective Serotonin Reuptake Inhibitorsmedicine.drugClinical Therapeutics
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Accumulation and Adverse Effects of Metoprolol and Propranolol After Concurrent Administration of Cimetidine

1983

Pharmacokinetics of metoprolol, propranolol and atenolol were investigated in six healthy volunteers following 7 days of oral monotherapy with these drugs and after 7 days concurrent administration of each of these betareceptor antagonists with cimetidine. Application of cimetidine did not lead to any interaction with atenolol, whereas mean peak plasma levels of metoprolol were increased by 70%, and those of propranolol by 95% due to concurrent administration of cimetidine (p < 0.05). The AUC of the two last mentioned beta blockers behaved similarly (p < 0.05). Measurement of exercise-induced tachycardia on the 6th day of administration showed no differences between monotherapy with the bet…

medicine.drug_classbusiness.industryPropranololPharmacologyDrug interactionAtenololPharmacokineticsmedicineCimetidinebusinessBeta blockerVolunteermedicine.drugMetoprolol
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Estradiol or genistein prevent Alzheimer's disease-associated inflammation correlating with an increase PPAR gamma expression in cultured astrocytes.

2009

Inflammation has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD). The main inflammatory players in AD are the glial cells which initiate the inflammatory response. One of the earliest neuropathological changes in AD is the accumulation of astrocytes at sites of A beta deposition. It is desirable to find methods of tipping the balance towards anti-inflammatory state. Estrogenic compounds have shown anti-inflammatory and also antioxidant activity. Astrocytes were pretreated with 17-beta estradiol or with genistein, and 48 h later treated with 5 microM amyloid beta (A beta) for 24 h. We found that A beta induces inflammatory mediators, such as cyclooxygenase 2 (…

medicine.medical_specialtyAmyloid betaInterleukin-1betaGenisteinPeroxisome proliferator-activated receptorNitric Oxide Synthase Type IIInflammationEnzyme-Linked Immunosorbent Assaychemistry.chemical_compoundInternal medicinemedicineAnimalsDrug InteractionsMolecular BiologyProtein Kinase InhibitorsCells Culturedchemistry.chemical_classificationCerebral CortexAmyloid beta-PeptidesbiologyDose-Response Relationship DrugEstradiolTumor Necrosis Factor-alphaGeneral NeuroscienceInterleukinEstrogensGenisteinPeptide FragmentsRatsPPAR gammaEndocrinologymedicine.anatomical_structurechemistryGene Expression RegulationCyclooxygenase 2Astrocytesbiology.proteinNeurogliaTumor necrosis factor alphaNeurology (clinical)medicine.symptomDevelopmental BiologyAstrocyteBrain research
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Different mechanism of relaxation induced by aporphine alkaloids in rat uterus.

1993

Abstract We have examined the uterine relaxant action of three aporphine molecules (S-glaucine, S-boldine and R-apomorphine) in two experimental conditions, with and without calcium in the bathing solution, and compared these effects with those obtained with the calcium antagonists verapamil and diltiazem. The present study shows that the alkaloids relax the uterine muscle but with different mechanisms of action. In Ca2+-containing solution all three alkaloids relaxed the uterus previously contracted by KCl or acetylcholine, but in Ca2+-free medium only R-apomorphine was able to relax oxytocin-induced contraction. The calcium antagonists, verapamil and diltiazem, relaxed KCl- or acetylcholi…

medicine.medical_specialtyAporphinesApomorphineMuscle RelaxationPharmaceutical Sciencechemistry.chemical_elementCalciumIn Vitro TechniquesOxytocinUterine contractionPotassium Chloridechemistry.chemical_compoundUterine ContractionInternal medicinemedicineBoldineAnimalsDrug InteractionsDiltiazemAporphineRats WistarPharmacologyCalcium Channel BlockersGlaucineAcetylcholineCulture MediaRatsEndocrinologyMuscle relaxationchemistryBiophysicsVerapamilCalciumFemalemedicine.symptommedicine.drugThe Journal of pharmacy and pharmacology
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Severe Tremor After Cotrimoxazole-Induced Elevation of Venlafaxine Serum Concentrations in a Patient With Major Depressive Disorder

2013

: We describe a female patient who was an extensive metabolizer of cytochrome P450 isoenzyme (CYP) 2D6 and an intermediate metabolizer of CYP2C19 (genotype: CYP2C19 *1/*2). She exhibited high serum concentrations of venlafaxine and O-desmethylvenlafaxine and developed severe tremor after comedication with cotrimoxazole (sulfamethazole/trimethoprim). Venlafaxine is mainly metabolized by O- and N-demethylation. O-demethylation is catalyzed by the highly polymorphic CYP2D6 and N-demethylation by several enzymes, CYP2C19, CYP2C9, and CYP3A4. The observed overall pharmacokinetic effect was most probably the result of decreased N-demethylation of venlafaxine by (1) reduced expression of CYP2C19 d…

medicine.medical_specialtyCYP2D6Venlafaxine HydrochlorideVenlafaxineCYP2C19Severity of Illness IndexGastroenterologyAnti-Infective AgentsInternal medicineTremorTrimethoprim Sulfamethoxazole Drug CombinationHumansMedicineDrug InteractionsPharmacology (medical)PsychiatryCYP2C9PharmacologyDepressive Disorder MajorCYP3A4business.industryVenlafaxine HydrochlorideMiddle AgedCyclohexanolsmedicine.diseaseTrimethoprimCytochrome P-450 CYP2C19Cytochrome P-450 CYP2D6Major depressive disorderFemaleAryl Hydrocarbon HydroxylasesbusinessSelective Serotonin Reuptake Inhibitorsmedicine.drugTherapeutic Drug Monitoring
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Mucosa-dependent muscarinic liberation of prostaglandins from rat isolated trachea.

1995

1. The present study examined whether cholinoceptor stimulation modulates the release of arachidonic acid-derived mediators from rat isolate tracheae. 2. Tracheae were preincubated with [3H]-arachidonic acid and the outflow of 3H-compounds was determined. Acetylcholine and the muscarinic agonist, carbachol but not nicotine, increased the rate of tritium outflow maximally by about 30%. The M3 receptor-preferring antagonist rho-fluoro-hexahydrosiladiphenidol was more effective than pirenzepine and methoctramine in antagonizing the effect of acetylcholine. 3. High performance liquid chromatography analysis (methanol gradient) of the released 3H-compounds showed that one peak, co-eluting with […

medicine.medical_specialtyCarbacholAcetonitrilesMuscarinic AntagonistsIn Vitro TechniquesMuscarinic AgonistsMuscarinic agonistRats Sprague-Dawleychemistry.chemical_compoundPiperidinesInternal medicineMuscarinic acetylcholine receptormedicineMethoctramineAnimalsDrug InteractionsAcetylcholine receptorPharmacologyArachidonic AcidDose-Response Relationship DrugMuscarinic acetylcholine receptor M1PirenzepineAcetylcholineRatsTracheaEndocrinologychemistryProstaglandinslipids (amino acids peptides and proteins)FemaleAcetylcholinemedicine.drugResearch Article
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Expert opinion on managing chronic HCV in patients with cardiovascular disease

2018

International audience; Extrahepatic manifestations of chronic HCV infection include cardiovascular diseases and an increase in cardiovascular mortality. The pathogenic mechanisms by which HCV contributes to cardiovascular disease are not well defined, however, it is likely that systemic inflammation, and the promotion of other metabolic diseases are involved. In this Review, the evidence for HCV infection as a non-traditional risk factor for cardiovascular disease is evaluated. Furthermore, practical advice to evaluate cardiovascular disease risk and disease in chronic hepatitis C patients are included for help in daily clinical practice. Despite the advances in therapies for the treatment…

medicine.medical_specialtyCardiotonic AgentsHepacivirusDisease030204 cardiovascular system & hematologySystemic inflammationAntiviral Agents03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemRisk Factors[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesOdds RatioHumansMedicineDrug InteractionsPharmacology (medical)In patient030212 general & internal medicineRisk factorIntensive care medicineExpert TestimonyCardiovascular mortalityInflammationPharmacologybusiness.industryDisease progressionDisease ManagementHepatitis C Chronic3. Good healthInfectious DiseasesCardiovascular DiseasesExpert opinionPractice Guidelines as TopicDisease riskmedicine.symptombusiness
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Special Considerations for Antihypertensive Agents in Dialysis Patients

2010

Hypertension is present in most patients with end-stage renal disease and likely contributes to the premature cardiovascular disease in dialysis patients. Previous practice guidelines have recommended that, in patients on chronic dialysis, blood pressure (BP) should be reduced below 130/80 mm Hg. This is based on opinions but not strong evidence, since no concrete information exists about which BP values should be the parameter to follow and which should be the target BP values. The majority of the antihypertensive agents can be used in this population, but the pharmacokinetics altered by the impaired kidney function and dialyzability influence the appropriate dosage as well as the time and…

medicine.medical_specialtyCardiotonic AgentsHypertension RenalCombination therapyMetabolic Clearance Ratemedicine.drug_classVasodilator Agentsmedicine.medical_treatmentAdrenergic beta-AntagonistsPopulationAngiotensin-Converting Enzyme InhibitorsCardiotonic AgentsRenal DialysisInternal medicinemedicineHumansDrug InteractionsDiureticseducationAntihypertensive drugAntihypertensive AgentsDialysisRandomized Controlled Trials as Topiceducation.field_of_studybusiness.industryHematologyGeneral MedicineCalcium Channel Blockersmedicine.diseaseEndocrinologyBlood pressureCardiovascular DiseasesNephrologyPractice Guidelines as TopicPolypharmacyKidney Failure ChronicDrug Therapy CombinationHemodialysisbusinessAngiotensin II Type 1 Receptor BlockersKidney diseaseBlood Purification
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Intermittent ethanol exposure induces inflammatory brain damage and causes long-term behavioural alterations in adolescent rats

2007

Adolescent brain development seems to be important for the maturation of brain structures and behaviour. Intermittent binge ethanol drinking is common among adolescents, and this type of drinking can induce brain damage. Because we have demonstrated that chronic ethanol treatment induces inflammatory processes in the brain, we investigate whether intermittent ethanol intoxication enhances cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in adolescent rats, and whether these mediators induce brain damage and cause permanent cognitive dysfunctions. Adolescent rats were exposed to ethanol (3.0 g/kg) for two consecutive days at 48-h intervals over 14 days. Levels of COX-2, iN…

medicine.medical_specialtyCerebellumProgrammed cell deathIndomethacinHippocampusNitric Oxide Synthase Type IIInflammationBrain damageMotor ActivityNeuropsychological TestsDiscrimination Learningchemistry.chemical_compoundindomethacinInternal medicineintermittent ethanol intoxicationmedicineAnimalsDrug InteractionsRats WistarAnalysis of VarianceNeocortexEthanolbiologyBehavior AnimalCell DeathEthanolCaspase 3General NeuroscienceAnti-Inflammatory Agents Non-SteroidalBrainRecognition PsychologyRatsNitric oxide synthasemedicine.anatomical_structureEndocrinologychemistryAnimals NewbornneurobehaviourCyclooxygenase 2inflammationAnesthesiabiology.proteinEncephalitisadolescencemedicine.symptomPsychologyPsychomotor Performance
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