Search results for "toxin"

showing 10 items of 1434 documents

Lower Urinary Tract Symptoms: What's New in Medical Treatment?

2018

Abstract Context Pharmacological treatment is a cornerstone in the management of patients with lower urinary tract symptoms (LUTS). Objective To review emerging evidence in the medical treatment of LUTS. Evidence acquisition An Embase/Pubmed-based literature search was conducted in December 2017, screening for randomized controlled trials (RCTs), prospective and retrospective series, animal model studies, and reviews on medical treatment of LUTS. Evidence synthesis The main medical innovation in recent years in overactive bladder (OAB) has been the approval of the first β 3 -adrenoceptor agonists (mirabegron) and intradetrusor onabotulinum toxin A, while several other drugs such as antiepil…

Malemedicine.medical_specialtyReceptors VasopressinUrologyUrinary Bladder030232 urology & nephrologyUrologyProstatic HyperplasiaUrinary incontinenceAdrenergic beta-3 Receptor Agonistsurologic and male genital diseases03 medical and health sciences0302 clinical medicineLower Urinary Tract SymptomsLower urinary tract symptomsmedicineDesmopressin AcetateNocturiaHumansDeamino Arginine VasopressinProspective StudiesBotulinum Toxins Type ADesmopressinRandomized Controlled Trials as TopicRetrospective StudiesUrinary bladderbusiness.industryUrinary Bladder OveractiveAntidiuretic AgentsPhosphodiesterase 5 Inhibitorsmedicine.diseasefemale genital diseases and pregnancy complicationsThiazolesmedicine.anatomical_structureOveractive bladderClinical Trials Phase III as Topic030220 oncology & carcinogenesisModels AnimalAcetanilidesFemaleNocturiamedicine.symptomMirabegronbusinessmedicine.drugEuropean urology focus
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Effect of vasoactive intestinal polypeptide on the release of serotonin from the in vitro vascularly perfused small intestine of guinea pig.

1989

Isolated segments of the guinea pig small intestine were vascularly perfused and the release of endogenous serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) into the portal vein was measured. All test substances were intraarterially perfused. Vasoactive intestinal polypeptide (VIP, 1 pmol/l-100 nmol/l) inhibited the spontaneous release of 5-HT and 5-HIAA. The maximal inhibitory effect (about 60%) was seen at 100 pmol/l. The effect of VIP on the spontaneous release of 5-HT and 5-HIAA was not changed in the presence of 1 mumol/l tetrodotoxin (TTX). Raising intraluminal pressure by 500 Pa for 5 min increased the release of 5-HT and 5-HIAA by about 25%. Raising the intralu…

Malemedicine.medical_specialtySerotoninMetaboliteVasoactive intestinal peptideGuinea PigsTetrodotoxinBiologyIn Vitro TechniquesGuinea pigchemistry.chemical_compoundInternal medicineIntestine SmallmedicineAnimalsPharmacologyMuscle SmoothGeneral MedicineHydroxyindoleacetic AcidSmall intestineEndocrinologymedicine.anatomical_structurenervous systemGastrointestinal hormonechemistryEnterochromaffin cellTetrodotoxinSerotoninhormones hormone substitutes and hormone antagonistsMuscle ContractionVasoactive Intestinal PeptideNaunyn-Schmiedeberg's archives of pharmacology
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Characterization of the muscarine receptors involved in the modulation of serotonin release from the vascularly perfused small intestine of guinea pi…

1989

Isolated small intestinal segments of the guinea pig were arterially perfused and the release of 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) into the portal venous effluent measured by HPLC with electrochemical detection. Test substances were applied via the arterial perfusion medium. McN-A-343, pilocarpine and oxotremorine inhibited concentration-dependently the outflow of 5-HT and 5-HIAA. Pirenzepine (0.03-0.1 mumol/l) which can discriminate between M1 and M2-receptor subtypes antagonized completely this inhibitory effect. In the presence of 1 mumol/l tetrodotoxin (TTx), all three muscarine receptor agonists increased the outflow of 5-HT and 5-HIAA. O…

Malemedicine.medical_specialtySerotoninPopulationGuinea PigsIndomethacinTetrodotoxinIn Vitro Techniqueschemistry.chemical_compoundInternal medicineMuscarinic acetylcholine receptorIntestine SmallmedicineOxotremorineAnimalsReceptoreducationNeurotransmitterPharmacologyeducation.field_of_studyMuscarineOxotremorine(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium ChlorideGeneral MedicinePirenzepineHydroxyindoleacetic AcidPirenzepineReceptors MuscarinicPerfusionEndocrinologychemistryFemaleSerotoninmedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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Neurotransmitters adenosine triphosphate and noradrenaline induce nitric oxide release in rat vas deferens.

2000

1. In rat vas deferens, electrical field stimulation (EFS) evoked a muscular biphasic tetrodotoxin (TTX)-sensitive contractile response. 2. The amplitude of this response increased with the frequency of stimulation. 3. After each stimulation, nitric oxide (NO) release was assayed and found to be released in a frequency-dependent manner. 4. NO release also occurred after treatment with exogenous neurotransmitters, adenosine 5'-triphosphate (ATP) and noradrenaline (NA). 5. Prazosin and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), respective antagonists of alpha1-adrenoceptors and P2x purinoceptors, inhibited NO release induced by NA and ATP. Both prazosin and PPADS inhibited…

Malemedicine.medical_specialtyStimulationTetrodotoxinIn Vitro TechniquesNitric OxideNitric oxidechemistry.chemical_compoundNorepinephrineAdenosine TriphosphateVas DeferensInternal medicinemedicinePrazosinAnimalsPPADSPharmacologyDose-Response Relationship DrugGeneral NeuroscienceVas deferensAdenosineElectric StimulationRatsEndocrinologymedicine.anatomical_structurechemistryTetrodotoxinAdenosine triphosphatemedicine.drugJournal of autonomic pharmacology
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Early-onset tolerance in rat global cerebral ischemia induced by a mitochondrial inhibitor

2000

It was studied whether a subtoxic dose of the mitochondrial neurotoxin, 3-nitropropionic acid (3-NPA), can initiate early-onset tolerance induction for subsequent ischemic injury. Wistar rats were pretreated for 3 h by intraperitoneal 3-NPA (20 mg/kg body weight; n=13) or solvent (n=12). Fifteen minutes global cerebral ischemia was induced by bilateral carotid artery occlusion and hypobaric hypotension. rCBF and tissue hemoglobin oxygen saturation were measured by laser Doppler scanning and a microspectrophotometric method. Ischemic insult and brain temperature were identical in both groups. Body weight and neurological scores recovered in the pretreated group but further deteriorated in th…

Malemedicine.medical_specialtyTime FactorsNeurotoxinsIschemiaConvulsantsMotor ActivityHippocampal formationBrain IschemiaCentral nervous system diseaseBrain ischemiaProsencephalonInternal medicinemedicineAnimalsNeurotoxinRats WistarNeuronsNeocortexbusiness.industryGeneral NeuroscienceNitro Compoundsmedicine.diseaseMitochondriaRatsTolerance inductionNeuroprotective Agentsmedicine.anatomical_structureEndocrinologyReperfusion InjuryAnesthesiaPropionatesbusinessReperfusion injuryNeuroscience Letters
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Persistent storage symptoms after TURP can be predicted with a nomogram derived from the ice water test

2019

PURPOSE To predict the persistence of storage symptoms after transurethral resection of the prostate (TURP) using a nomogram derived from the ice water test (IWT). METHODS The IWTs of 73 men with lower urinary tract symptoms and prostatic bladder outlet obstruction were retrospectively analyzed. The strength of the detrusor contraction was approximated by using the detrusor gradient of Δpdet /Δt at maximum detrusor pressure and the area under the curve. The parameters were utilized in a nomogram, which facilitated a severity categorization from 1 to 10. Patients with a positive IWT in the categories 1 to 2 were assigned to group A, categories 3 to 4 to group B and categories 5 and higher to…

Malemedicine.medical_specialtyUrologymedicine.medical_treatmentProstatic Hyperplasia030232 urology & nephrologyUrologyurologic and male genital diseasesGroup BPersistence (computer science)03 medical and health sciencesBladder outlet obstruction0302 clinical medicineLower Urinary Tract SymptomsLower urinary tract symptomsmedicineHumansAgedRetrospective StudiesTransurethral resection of the prostateAged 80 and over030219 obstetrics & reproductive medicineUrinary Bladder Overactivebusiness.industryTransurethral Resection of ProstateArea under the curveDiagnostic Techniques UrologicalMiddle AgedNomogrammedicine.diseaseBotulinum toxinUrinary Bladder Neck ObstructionNomogramsUrodynamicsNeurology (clinical)businessmedicine.drugNeurourology and Urodynamics
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Acute relaxant effects of 17-beta-estradiol through non-genomic mechanisms in rabbit carotid artery.

2002

Estrogens could play a cardiovascular protective role not only by means of systemic effects but also by means of direct effects on vascular structure and function. We have studied the acute effects and mechanisms of action of 17-beta-estradiol on vascular tone of rabbit isolated carotid artery. 17-Beta-estradiol (10, 30, and 100 microM) elicited concentration-dependent relaxation of 50 mM KCl-induced active tone in male and female rabbit carotid artery. The stereoisomer 17-alpha-estradiol showed lesser relaxant effects in male rabbits. Endothelium removal did not modify relaxation induced by 17-beta-estradiol. The NO synthase inhibitor L-NAME (100 microM) only reduced significantly relaxati…

Malemedicine.medical_specialtyVascular smooth muscleContraction (grammar)Potassium ChannelsCharybdotoxinEndotheliumMuscle RelaxationClinical BiochemistryNicardipineEstrogen receptorCycloheximideBiochemistrychemistry.chemical_compoundCalcium ChlorideNicardipineEndocrinologyInternal medicinemedicineAnimalsChannel blockerEnzyme InhibitorsMolecular BiologyPharmacologyEstradiolOrganic ChemistryCalcium Channel BlockersEndocrinologymedicine.anatomical_structureCarotid ArteriesNG-Nitroarginine Methyl EsterchemistryPotassiumCalciumFemaleCalcium ChannelsEndothelium VascularRabbitsNitric Oxide Synthasemedicine.drugSteroids
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Nitric oxide-mediated beta 2-adrenoceptor relaxation is impaired in mesenteric veins from portal-hypertensive rats.

1996

Abstract BACKGROUND & AIMS: beta-Adrenergic relaxation seems to be mediated by nitric oxide. The aim of this study was to evaluate changes induced by portal hypertension in beta 2-adrenergic vasorelaxation. METHODS: Isolated rat mesenteric veins were relaxed by salbutamol, and nerve- mediated vasocontractions were induced by electrical field stimulation. Responses were evaluated in the presence of NG-nitro-L-arginine methyl ester (L-NAME) or tetrodotoxin. Immunocytochemical techniques were used for localization of neuronal NO synthase. RESULTS: Salbutamol-induced relaxations were decreased in rings from portal-hypertensive animals. L- NAME reduced these relaxations, but its effects were mor…

Malemedicine.medical_specialtyVasodilator AgentsStimulationVasodilationTetrodotoxinIn Vitro TechniquesS-Nitroso-N-AcetylpenicillamineNitric OxideNitric oxideRats Sprague-Dawleychemistry.chemical_compoundMesenteric VeinsInternal medicinePapaverineHypertension PortalReceptors Adrenergic betamedicineAnimalsAlbuterolHepatologybiologyPenicillamineGastroenterologyAdrenergic beta-AgonistsImmunohistochemistryElectric StimulationRatsNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl EsterchemistryTetrodotoxinbiology.proteinS-Nitroso-N-acetylpenicillamineNitric Oxide SynthaseFree nerve endingBlood vesselGastroenterology
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Effects of endotoxin on neurally-mediated gastric acid secretion in the rat.

1998

Abstract The effects of a peripheral administration of E. coli endotoxin on neurally-mediated gastric acid secretion and the role of endogenous opioids or PAF receptors in endotoxin effects have been evaluated in the continuously perfused stomach of the anaesthetized rat. Gastric acid secretion stimulated by distension (20 cm H2O) was reduced dose-dependently by single intravenous bolus injection of endotoxin (0.1–10 μg kg−1). Doses of 5 μg kg−1 induced a peak reduction of distension-stimulated acid output and significantly reduced the secretory response induced by an intravenous bolus of 2-deoxy-d-glucose (150 mg kg−1). This dose of endotoxin did not significantly modify mean systemic arte…

Malemedicine.medical_specialtymedicine.drug_classNarcotic AntagonistsPharmaceutical ScienceBlood PressureReceptors Cell Surface(+)-NaloxonePlatelet Membrane GlycoproteinsDistensionDeoxyglucoseReceptors G-Protein-CoupledGastric AcidOpioid receptorInternal medicinemedicineEscherichia coliAnimalsRats WistarEndogenous opioidPharmacologyDose-Response Relationship Drugbusiness.industryNaloxoneGastric distensionStomachAntagonistAzepinesTriazolesReceptor antagonistRatsEndotoxinsEndocrinologyOpioid PeptidesReceptors OpioidGastric acidFemalemedicine.symptombusinessPlatelet Aggregation InhibitorsThe Journal of pharmacy and pharmacology
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Nitric Oxide Modulates the Acute Increase of Gastrointestinal Transit Induced by Endotoxin in Rats: a Possible Role for Tachykinins

1997

Abstract Because of the evidence that endogenous nitric oxide (NO) plays an essential role in the physiological regulation of gastrointestinal motility we have investigated, by use of the NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), the role of endogenous NO in the acute endotoxin-induced changes of gastrointestinal transit. Pre-treatment with E. coli endotoxin (100 μg kg−, i.v.) induced a significant increase in the gastrointestinal transit of a charcoal suspension in anaesthetized rats. Previous administration of the NO synthase inhibitor, l-NAME (10 mg kg−, i.v.) significantly prevented the effects of endotoxin. l-arginine (200 mg kg−, i.v.) and the substance P antag…

Malemedicine.medical_specialtymedicine.medical_treatmentAnti-Inflammatory AgentsPharmaceutical ScienceMotilityEndogenySubstance PBiologyNitric OxideDexamethasoneNitric oxidePathogenesischemistry.chemical_compoundTachykininsInternal medicineNeuromodulationmedicineAnimalsEnzyme InhibitorsRats WistarGastrointestinal TransitDexamethasonePharmacologyRatsEndotoxinsNG-Nitroarginine Methyl EsterEndocrinologyCytokinemedicine.anatomical_structurechemistryToxicityNitric Oxide Synthasemedicine.drugJournal of Pharmacy and Pharmacology
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