Search results for "drug interactions"

showing 9 items of 229 documents

Rolipram inhibits airway microvascular leakage induced by platelet-activating factor, histamine and bradykinin in guinea-pigs.

1993

Abstract Rolipram (0·1–1000 μg kg−1, i.v.) reduced the increase in microvascular permeability induced by platelet-activating factor (PAF; 50 ng kg−1, i.v.) at different sites of the guinea-pig airways. Rolipram (1–100μg kg−1, i.v.) inhibited histamine (30μg kg−1, i.v.)-and bradykinin (0·3 μg kg, i.v.)-induced airway microvascular leakage. These effects of rolipram were obtained at doses which inhibit histamine (7–20 μg kg−1 min−1)-induced bronchoconstriction (IC50 = 3 ± 1 μg kg, i.v.) without depressing arterial blood pressure in the guinea-pig. Aminophylline (50 mg kg−1) did not change the effect of PAF. The anti-exudative effect of rolipram is of potential therapeutic value in asthma.

medicine.medical_specialtyPhosphodiesterase InhibitorsGuinea PigsPharmaceutical ScienceBradykininVascular permeabilityBlood PressureBronchiBradykininCapillary Permeabilitychemistry.chemical_compoundInternal medicinemedicineAnimalsDrug InteractionsPlatelet Activating FactorRolipramPharmacologyPlatelet-activating factorMicrocirculationAminophyllinePyrrolidinonesTracheaEndocrinologymedicine.anatomical_structurechemistryBronchoconstrictionAminophyllinemedicine.symptomRolipramHistaminemedicine.drugBlood vesselEvans BlueHistamineThe Journal of pharmacy and pharmacology
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Release of non-neuronal acetylcholine from the human placenta: difference to neuronal acetylcholine

2001

The synthesis and release of non-neuronal acetylcholine, a widely expressed signaling molecule, were investigated in the human placenta. This tissue is free of cholinergic neurons, i.e. a contamination of neuronal acetylcholine can be excluded. The villus showed a choline acetyltransferase (ChAT) activity of 0.65 nmol/mg protein per h and contained 500 nmol acetylcholine/g dry weight. In the absence of cholinesterase inhibitors the release of acetylcholine from isolated villus pieces amounted to 1.3 nmol/g wet weight per 10 min corresponding to a fractional release rate of 0.13% per min. The following substances did not significantly modify the release of acetylcholine: oxotremorine (1 micr…

medicine.medical_specialtyPhysostigminePlacentaReceptors NicotinicCholine O-AcetyltransferaseNicotineInternal medicineOxotremorinemedicineHumansDrug InteractionsCholinergic neuronCholinesterasePharmacologybiologyChemistryColforsinGeneral MedicineCholine acetyltransferaseAcetylcholineElectric StimulationNeostigmineEndocrinologybiology.proteinFemaleCholinesterase InhibitorsAcetylcholinemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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Clinical pharmacokinetics of atenolol — A review

1982

Atenolol is a hydrophilic betareceptor blocking drug, which is predominantly eliminated via the kidneys, only about 5% of the atenolol is metabolised by the liver. After oral administration atenolol is incompletely absorbed from the intestine, so about 50% of the beta blocker are finally biovailable. In plasma only 3% of atenolol are protein-bound. There exists a linear relationship between the atenolol plasma levels and the degree of beta blocking effect measured by inhibition of the exercise-induced tachycardia. No correlation was found between plasma levels of atenolol and blood pressure lowering activity of the drug. After oral administration elimination half life of atenolol is calcula…

medicine.medical_specialtymedicine.drug_classAdministration OralBiological AvailabilityRenal functionPharmacologyKidneyIntestinal absorptionPropanolaminesPharmacokineticsRenal DialysisOral administrationInternal medicinemedicineHumansDrug InteractionsPharmacology (medical)cardiovascular diseasesBeta blockerPharmacologyChemistryLiver DiseasesKidney metabolismAtenololKineticsEndocrinologyAtenololIntestinal AbsorptionInjections IntravenousKidney DiseasesBiological half-lifecirculatory and respiratory physiologymedicine.drugEuropean Journal of Drug Metabolism and Pharmacokinetics
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Interaction of allopurinol with phenprocoumon in man.

1977

Conditions in two patients on long-term phenprocoumon (Marcumar®) treatment are reported who had signs of phenprocoumon overdosage when given simultaneously allopurinol. The determination of phenprocoumon plasma concentrations in one patient showed that phenprocoumon accumulates for several weeks during treatment with allopurinol. Signs of phenprocoumon overdosage thus can appear long time after starting allopurinol treatment.

musculoskeletal diseasesAdultMalecongenital hereditary and neonatal diseases and abnormalitiesAllopurinolMyocardial InfarctionAllopurinolPharmacologyPhenprocoumonDrug DiscoveryMedicineHumansDrug InteractionsBlood CoagulationGenetics (clinical)integumentary systembusiness.industrynutritional and metabolic diseasesGeneral Medicine4-HydroxycoumarinsDrug interactionMiddle AgedPlasma concentrationPhenprocoumonMolecular MedicineBlood Coagulation TestsbusinessMathematicsmedicine.drugKlinische Wochenschrift
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Significant interaction between high-dose methotrexate and high-dose piperacillin-tazobactam causing reversible neurotoxicity and renal failure in an…

2020

Introduction Pharmacokinetic interaction of high-dose methotrexate (MTX) and other concomitantly administered renally secreted medicinal products may lead to insufficient methotrexate serum level decrease and significant MTX toxicity. Case report We report the case of an 18-year-old male patient treated with high-dose MTX for an osteosarcoma and with high-dose piperacillin-tazobactam at the same time. MTX serum levels were severely elevated 24 hours after the MTX infusion and did not decrease in accordance with the specific calcium folinate rescue protocol. The patient experienced renal failure accompanied by neurological symptoms, most consistent with MTX-related renal and CNS toxicity. Ma…

musculoskeletal diseasesMaleAntimetabolites AntineoplasticAdolescentBone Neoplasms030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicinemedicineHumansPharmacology (medical)Drug InteractionsRenal InsufficiencyPiperacillinOsteosarcomabusiness.industryNeurotoxicitymedicine.diseaseHigh dose methotrexateAnti-Bacterial AgentsMethotrexateOncology030220 oncology & carcinogenesisPiperacillin/tazobactamOsteosarcomaMethotrexateNeurotoxicity SyndromesbusinessPharmacokinetic interactionmedicine.drugJournal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners
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The Major Heat Shock Proteins, Hsp70 and Hsp90, in 2-Methoxyestradiol-Mediated Osteosarcoma Cell Death Model

2020

2-Methoxyestradiol is one of the natural 17&beta

neuronal nitric oxide synthaseProgrammed cell death2-methoxyestradiolLactams MacrocyclicAntineoplastic AgentsBone NeoplasmsModels BiologicalArticleCatalysisHsp90 inhibitorNitric oxidelcsh:ChemistryInorganic Chemistrychemistry.chemical_compoundDownregulation and upregulationosteosarcomaHeat shock proteinBenzoquinonesAnimalsHumansDrug InteractionsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsPhysical and Theoretical Chemistrygeldanamycinlcsh:QH301-705.5Molecular BiologySpectroscopyAntibiotics AntineoplasticbiologyOrganic ChemistryGeneral MedicineGeldanamycinHsp90Computer Science ApplicationsHsp70lcsh:Biology (General)lcsh:QD1-999chemistryCancer researchbiology.proteinInternational Journal of Molecular Sciences
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Inhibition of small G proteins of the Rho family by statins orClostridium difficiletoxin B enhances cytokine-mediated induction of NO synthase II

2000

In order to investigate the involvement of Ras and/or Rho proteins in the induction of the inducible isoform of nitric oxide synthase (NOS II) we used HMG-CoA reductase inhibitors (statins) and Clostridium difficile toxin B (TcdB) as pharmacological tools. Statins indirectly inhibit small G proteins by preventing their essential farnesylation (Ras) and/or geranylgeranylation (Rho). In contrast, TcdB is a glucosyltransferase and inactivates Rho-proteins directly. Human A549/8- and DLD-1 cells as well as murine 3T3 fibroblasts were preincubated for 18 h with statins (1–100 μM) or TcdB (0.01–10 ng ml−1). Then NOS II expression was induced by cytokines. NOS II mRNA was measured after 4–8 h by R…

rho GTP-Binding ProteinsG proteinBacterial ToxinsMevalonic AcidNitric Oxide Synthase Type IISmall G ProteinClostridium difficile toxin BBiologyGene Expression Regulation EnzymologicMiceGeranylgeranylationBacterial ProteinsPolyisoprenyl PhosphatesPrenylationGTP-Binding ProteinsGene expressionAtorvastatinTumor Cells CulturedAnimalsHumansDrug InteractionsPyrrolesLovastatinPromoter Regions GeneticPharmacology3T3 CellsTransfectionMolecular biologyHeptanoic AcidsEnzyme InductionPapersCytokinesHydroxymethylglutaryl-CoA Reductase InhibitorsNitric Oxide SynthaseSignal transductionBritish Journal of Pharmacology
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Safety and potential interaction of immunosuppressive drugs for the treatment of inflammatory bowel disease in elderly patients

2021

Inflammatory bowel diseases, including Crohn's disease and ulcerative colitis, are chronic diseases associated with increased morbidity and reduced quality of life. Age may represent a risk factor for adverse events, due to the multimorbidity and polypharmacy, common in elderly patients. Elderly are often not included in clinical trials evaluating efficacy and safety of study drugs for the treatment of inflammatory bowel diseases. Several drugs, such as aminosalicylates, systemic corticosteroids, immunosuppressant drugs, biological drugs and Janus Kinase inhibitors, are available for the management of inflammatory bowel diseases. With the increasing spectrum of therapeutic options, it is th…

safetyPolypharmacydrug-drug interactionsmedicine.medical_specialtybusiness.industryEndocrinology Diabetes and MetabolismInflammatory bowel disease elderly patients safety drug-drug interactionsGastroenterologyDiseaseelderly patientsmedicine.diseaseInflammatory bowel diseaseUlcerative colitisInflammatory bowel diseaseVedolizumabClinical trialUstekinumabInternal MedicinemedicineAdverse effectIntensive care medicinebusinessmedicine.drugMinerva Gastroenterology
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Tenapanor for the treatment of irritable bowel syndrome with constipation.

2020

Introduction: Irritable bowel syndrome with constipation is associated with higher rates of functional impairment, as compared to other subtypes of the syndrome. Conventional laxative-based pharmacologic therapy of IBS-C, which is mostly symptom-based, is often unsatisfactory. Tenapanor represents a first-in-class orally available inhibitor of NHE3, which is minimally absorbed in the GI tract, what constitutes a significant therapeutic benefit, as it may act on the drug target. Areas covered: Aim of this article is to sum up the evidences about pharmacodynamics and pharmacokinetics of tenapanor, focusing on animal models and in vitro studies, but also discuss clinical trials on tenapanor's …

safetymedicine.medical_specialtyFunctional impairmentConstipationmedicine.medical_treatmentefficacyLaxative030226 pharmacology & pharmacyGastroenterologyIrritable Bowel Syndrome03 medical and health scienceschemistry.chemical_compound0302 clinical medicineGastrointestinal AgentsInternal medicinemedicineAnimalsHumansPharmacology (medical)Pharmacologic therapyDrug InteractionsGeneral Pharmacology Toxicology and PharmaceuticsTenapanorIrritable bowel syndromeSulfonamidesbusiness.industrySodium-Hydrogen Exchanger 3General Medicinemedicine.diseaseIsoquinolinestenapanor.chemistry030220 oncology & carcinogenesismedicine.symptombusinessConstipationExpert review of clinical pharmacology
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