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[PMID]:12212966
[Au] Autor:Liu X; Emery CJ; Laude E; Herget J; Gill G; Cope G; Barer GR
[Ad] Endereço:Division of Clinical Sciences (S), University of Sheffield, UK.
[Ti] Título:Adverse pulmonary vascular effects of high dose tricyclic antidepressants: acute and chronic animal studies.
[So] Source:Eur Respir J;20(2):344-52, 2002 Aug.
[Is] ISSN:0903-1936
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Overdose of tricyclic antidepressants, which inhibit cellular serotonin (5-HT) uptake, sometimes causes acute respiratory syndrome-like symptoms. Their acute and chronic cardiopulmonary actions, which might be implicated, utilising both in vivo and ex vivo animal studies, were investigated in this study. Acute amitriptyline (AMI), iprindole and imipramine caused dose-dependent prolonged rises in pulmonary artery pressure and oedema in anaesthetised cats in vivo. Acute AMI, in isolated ex vivo blood-perfused rat lungs, also caused dose-dependent sustained vasoconstriction, which could be attenuated with either calcium channel inhibition or a nitric oxide donor. It was demonstrated that the pressor effects of AMI were not due to release of histamine, serotonin, noradrenaline, or the activities of cycloxygenase or lipoxygenase. After AMI, hypoxic pulmonary vasoconstriction and the pressor actions of 5-HT and noradrenaline were diminished, possibly due to uptake inhibition. Activities of the endothelial-based enzymes, nitric oxide synthase and endothelin-converting enzyme, were undiminished. Large acute doses of AMI caused oedema with rupture of capillaries and alveolar epithelium. Chronic iprindole raised pulmonary artery pressure and right ventricle (RV)/left ventricle (LV) + septal (S) weight. Chronic AMI led to attenuation of the pressor action of 5-HT, especially when associated with chronic hypoxic-induced pulmonary hypertension. RV/LV+S weight increased, attributable to LV decline. The acute and chronic effects observed might have relevance to clinical overdose, while the attenuation of acute effects offers possible therapeutic options.
[Mh] Termos MeSH primário: Amitriptilina/administração & dosagem
Amitriptilina/toxicidade
Antidepressivos Tricíclicos/administração & dosagem
Antidepressivos Tricíclicos/toxicidade
Imipramina/administração & dosagem
Imipramina/toxicidade
Iprindol/administração & dosagem
Iprindol/toxicidade
Pneumopatias/induzido quimicamente
Artéria Pulmonar/efeitos dos fármacos
Doenças Vasculares/induzido quimicamente
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Gatos
Doença Crônica
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Overdose de Drogas/complicações
Overdose de Drogas/patologia
Overdose de Drogas/fisiopatologia
Pneumopatias/patologia
Pneumopatias/fisiopatologia
Artéria Pulmonar/patologia
Artéria Pulmonar/fisiopatologia
Ratos
Ratos Wistar
Doenças Vasculares/patologia
Doenças Vasculares/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antidepressive Agents, Tricyclic); 1806D8D52K (Amitriptyline); 69U0IKR8FP (Iprindole); OGG85SX4E4 (Imipramine)
[Em] Mês de entrada:0301
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020906
[St] Status:MEDLINE


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[PMID]:9422362
[Au] Autor:Callahan B; Yuan J; Stover G; Hatzidimitriou G; Ricaurte G
[Ad] Endereço:Department of Neurology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21224, USA.
[Ti] Título:Effects of 2-deoxy-D-glucose on methamphetamine-induced dopamine and serotonin neurotoxicity.
[So] Source:J Neurochem;70(1):190-7, 1998 Jan.
[Is] ISSN:0022-3042
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mechanisms underlying the neurotoxic actions of methamphetamine (METH) and related substituted amphetamines are unknown. Previous studies with 2-deoxyglucose (2-DG) have suggested that METH-induced neurotoxicity may involve exhaustion of intracellular energy stores. However, because 2-DG also produces hypothermic effects, and because METH's neurotoxic actions are highly susceptible to thermoregulatory influence, previous findings with 2-DG are difficult to interpret. The present studies were undertaken to further examine the influence of 2-DG's glucoprivic and thermic effects in the context of METH-induced dopamine (DA) and serotonin (5-HT) neurotoxicity. 2-DG protected against METH-induced DA neurotoxicity in both rats and mice. In both species, 2-DG, alone or in combination with METH, produced hypothermic effects. METH's toxic effects on brain 5-HT neurons were either unaffected or exacerbated by 2-DG, depending on species, brain region, and dose of METH tested. These results indicate that different mechanisms may underlie METH-induced DA and 5-HT neurotoxicity, and suggest that, as compared with 5-HT neurons, DA neurons are more susceptible to temperature influence, whereas 5-HT neurons are more vulnerable than DA neurons to metabolic compromise. Additional studies are needed to further assess the role of energy stores in the neurotoxic effects of METH and related drugs.
[Mh] Termos MeSH primário: Desoxiglucose/farmacologia
Dopamina/metabolismo
Metanfetamina/farmacologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurotoxinas/farmacologia
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Temperatura Corporal/efeitos dos fármacos
Corpo Estriado/citologia
Corpo Estriado/efeitos dos fármacos
Corpo Estriado/metabolismo
Relação Dose-Resposta a Droga
Iprindol/farmacologia
Masculino
Camundongos
Ratos
Ratos Sprague-Dawley
Sinaptossomos/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotoxins); 333DO1RDJY (Serotonin); 44RAL3456C (Methamphetamine); 69U0IKR8FP (Iprindole); 9G2MP84A8W (Deoxyglucose); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:9802
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:980109
[St] Status:MEDLINE


  3 / 180 MEDLINE  
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[PMID]:9360012
[Au] Autor:Lavoie PA; Beauchamp G; Elie R
[Ad] Endereço:Département de pharmacologie, Université de Montréal, QC, Canada.
[Ti] Título:Atypical antidepressants inhibit depolarization-induced calcium uptake in rat hippocampus synaptosomes.
[So] Source:Can J Physiol Pharmacol;75(8):983-7, 1997 Aug.
[Is] ISSN:0008-4212
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:The effect of the atypical antidepressants mianserin, iprindole, and fluoxetine on synaptosomal calcium uptake was tested under conditions where a selective action on voltage-dependent calcium channels can be documented. Synaptosomes from rat hippocampus were incubated with 45calcium either in choline-rich medium or in depolarizing (60 mM K+) choline-rich medium, and drug effects on calcium uptake in these two conditions, as well as on the net depolarization-induced calcium uptake, were studied in the range of concentrations 0.6-200 microM. A concentration-dependent marked inhibition of uptake in depolarizing choline medium was observed for the three antidepressants, whereas only a minor degree of inhibition of uptake in resting choline medium was present at the highest drug concentration; as a result, the concentration-effect relationships exhibited a strong concentration-dependent inhibition of net depolarization-induced calcium uptake. The IC50 values, calculated by interpolation of the last three or four points of the concentration-effect relationships, were 27, 39, and 68 microM for fluoxetine, iprindole, and mianserin, respectively. Significant degrees of calcium channel inhibition are not expected at brain concentrations of mianserin and iprindole that are likely to be encountered during clinical use; however, the fluoxetine concentration-effect relationship established in the present study, coupled with the published ratio of 20:1 for brain:plasma concentrations of fluoxetine-norfluoxetine in humans, suggests that brain calcium channel function could be appreciably reduced in some patients treated with this atypical antidepressant.
[Mh] Termos MeSH primário: Antidepressivos de Segunda Geração/farmacologia
Cálcio/metabolismo
Hipocampo/efeitos dos fármacos
Sinaptossomos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Bloqueadores dos Canais de Cálcio/farmacologia
Relação Dose-Resposta a Droga
Fluoxetina/farmacologia
Hipocampo/metabolismo
Iprindol/farmacologia
Masculino
Mianserina/farmacologia
Ratos
Ratos Sprague-Dawley
Sinaptossomos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antidepressive Agents, Second-Generation); 0 (Calcium Channel Blockers); 01K63SUP8D (Fluoxetine); 250PJI13LM (Mianserin); 69U0IKR8FP (Iprindole); SY7Q814VUP (Calcium)
[Em] Mês de entrada:9711
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:970801
[St] Status:MEDLINE


  4 / 180 MEDLINE  
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[PMID]:8870992
[Au] Autor:Carvalho F; Remião F; Amado F; Domingues P; Correia AJ; Bastos ML
[Ad] Endereço:CEQUP, Laboratório de Toxicologia, Faculdade de Farmácia da Universidade do Porto, Portugal.
[Ti] Título:d-Amphetamine interaction with glutathione in freshly isolated rat hepatocytes.
[So] Source:Chem Res Toxicol;9(6):1031-6, 1996 Sep.
[Is] ISSN:0893-228X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatocellular damage has been reported as a consequence of amphetamine intake for which little is known about the respective biological mechanisms involved. To give a better insight of cellular d-amphetamine effects, the present study was performed to evaluate d-amphetamine effects on glutathione homeostasis, in vitro, using freshly isolated rat hepatocytes. Cell viability and lipid peroxidation were also evaluated. Incubation of freshly isolated rat hepatocytes with d-amphetamine (0.08, 0.20, 0.40, and 2.00 mM) induced a concentration dependent glutathione depletion which was observed at all times (1, 2, and 3 h of incubation). After 3 h of incubation, cellular GSH decreased to 85%, 78%, 71% and 47% of control levels for the referred concentrations, respectively. At the third hour of incubation, GSSG levels were only slightly increased for the three higher concentrations of d-amphetamine. The mass spectral study of the methanolic supernatants obtained from hepatocytes incubated with all d-amphetamine concentrations revealed the presence of the p-hydroxyamphetamine glutathione adduct (glutathion-S-yl)-p-hydroxyamphetamine. Pretreatment of hepatocytes with the P450 inhibitors metyrapone (1 mM) and iprindole (10 microM) significantly prevented the glutathione depletion induced by d-amphetamine. This inhibition was more effective for iprindole than for metyrapone. Incubation of isolated hepatocytes with p-hydroxyamphetamine (0.10 mM) for 3 h did not result in any modification of cell viability or GSH or GSSG levels. Also, in the mass spectrum study performed on these samples, the characteristic adduct obtained for d-amphetamine incubations was not detected. The above data suggest that the observed glutathione depletion induced by d-amphetamine is at least in part due to the conversion of d-amphetamine into (glutathion-S-yl)-p-hydroxyamphetamine and that P450 2D seems to have an important role in this metabolism. In spite of the results obtained, showing glutathione homeostasis alterations, incubation of freshly isolated rat hepatocytes with d-amphetamine did not result in any modification of cell viability or lipid redox status.
[Mh] Termos MeSH primário: Dextroanfetamina/farmacologia
Glutationa/metabolismo
Fígado/metabolismo
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Inibidores das Enzimas do Citocromo P-450
Sistema Enzimático do Citocromo P-450/metabolismo
Glutationa/análogos & derivados
Dissulfeto de Glutationa
Homeostase/efeitos dos fármacos
Técnicas In Vitro
Iprindol/farmacologia
Peroxidação de Lipídeos/efeitos dos fármacos
Fígado/citologia
Fígado/efeitos dos fármacos
Masculino
Oxirredução
Ratos
Ratos Wistar
p-Hidroxianfetamina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytochrome P-450 Enzyme Inhibitors); 69U0IKR8FP (Iprindole); 9035-51-2 (Cytochrome P-450 Enzyme System); FQR280JW2N (p-Hydroxyamphetamine); GAN16C9B8O (Glutathione); TZ47U051FI (Dextroamphetamine); ULW86O013H (Glutathione Disulfide)
[Em] Mês de entrada:9701
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960901
[St] Status:MEDLINE


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[PMID]:8870052
[Au] Autor:Vogel G; Hagler M
[Ad] Endereço:Department of Psychiatry, Emory University School of Medicine, Atlanta 30306, USA.
[Ti] Título:Effects of neonatally administered iprindole on adult behaviors of rats.
[So] Source:Pharmacol Biochem Behav;55(1):157-61, 1996 Sep.
[Is] ISSN:0091-3057
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In past studies, administration of the antidepressant drugs clorimipramine, zimeldine, or desipramine to neonatal rats produced abnormalities in adult rats that modeled some behavioral and/or REM sleep features of human endogenous depression. Although these three drugs affected different neurotransmitter systems, all caused REM sleep deprivation (RSD). This suggested the hypothesis that RSD of neonatal rats caused their adult depression. One prediction of this hypothesis is that neonatally administered iprindole, an antidepressant drug that does not produce RSD, will not produce adult rats that model depression. The present study tested this hypothesis. Iprindole was administered to neonatal experimental rats and saline was administered to neonatal control rats. When the rats matured, compared with control rats, experimental rats were not significantly different in aggressive behavior (shock induced fighting), sexual behaviors, open field locomotion, and REM sleep. In our previous studies on rats, all these adult behaviors were affected in a depressive-like way by neonatally administered clorimipramine. Because iprindole does not decrease REM sleep, the present results support the hypothesis that in rats neonatal RSD causes adult depression.
[Mh] Termos MeSH primário: Animais Recém-Nascidos/fisiologia
Antidepressivos Tricíclicos/farmacologia
Comportamento Animal/efeitos dos fármacos
Iprindol/farmacologia
[Mh] Termos MeSH secundário: Agressão/efeitos dos fármacos
Animais
Eletrochoque
Masculino
Atividade Motora/efeitos dos fármacos
Polissonografia
Ratos
Ratos Sprague-Dawley
Sono REM/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antidepressive Agents, Tricyclic); 69U0IKR8FP (Iprindole)
[Em] Mês de entrada:9701
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960901
[St] Status:MEDLINE


  6 / 180 MEDLINE  
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[PMID]:8736071
[Au] Autor:Erez M; Varon D
[Ad] Endereço:Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Israel.
[Ti] Título:A new class of antiarrhythmic--defibrillatory compounds.
[So] Source:J Basic Clin Physiol Pharmacol;5(1):59-66, 1994 Jan-Mar.
[Is] ISSN:0792-6855
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ventricular fibrillation (VF) is a major cause of sudden cardiac death in humans. Currently used antiarrhythmic drugs are aimed at preventing initiation of VF by decreasing the incidence of arrhythmias which can lead to VF. This approach today seems to be insufficient. On the basis of reports that VF can terminate spontaneously in various mammals, and even in humans, we propose pharmaceutical enhancement of self-ventricular defibrillation as a new therapeutical approach. Data obtained over the last decade indicate that a high cardiac extraneuronal noepinephrine level during VF facilitates self-defibrillation. Dibenzazepines (tricyclic antidepressants) and phenothiazines elevate norepinephrine level by inhibiting norepinephrine reuptake and were found to exhibit defibrillatory activity. The relationship of chemical structure to defibrillatory activity was studied in a group of dibenzazepine and phenothiazine compounds.
[Mh] Termos MeSH primário: Antiarrítmicos/uso terapêutico
Antidepressivos Tricíclicos/uso terapêutico
Antipsicóticos/uso terapêutico
Fibrilação Ventricular/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antiarrítmicos/administração & dosagem
Antiarrítmicos/farmacologia
Antidepressivos Tricíclicos/administração & dosagem
Antidepressivos Tricíclicos/farmacologia
Antipsicóticos/administração & dosagem
Antipsicóticos/farmacologia
Gatos
Clorpromazina/farmacologia
Clorpromazina/uso terapêutico
Desipramina/farmacologia
Desipramina/uso terapêutico
Dibenzazepinas/farmacologia
Dibenzazepinas/uso terapêutico
Estimulação Elétrica
Imipramina/farmacologia
Imipramina/uso terapêutico
Iprindol/farmacologia
Iprindol/uso terapêutico
Maprotilina/farmacologia
Maprotilina/uso terapêutico
Mianserina/farmacologia
Mianserina/uso terapêutico
Moricizina/farmacologia
Moricizina/uso terapêutico
Norepinefrina/metabolismo
Relação Estrutura-Atividade
Trifluoperazina/farmacologia
Trifluoperazina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Antidepressive Agents, Tricyclic); 0 (Antipsychotic Agents); 0 (Dibenzazepines); 214IZI85K3 (Trifluoperazine); 250PJI13LM (Mianserin); 2GT1D0TMX1 (Moricizine); 2U1W68TROF (Maprotiline); 510SJZ1Y6L (dibenzepin); 69U0IKR8FP (Iprindole); OGG85SX4E4 (Imipramine); TG537D343B (Desipramine); U42B7VYA4P (Chlorpromazine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:9610
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:940101
[St] Status:MEDLINE


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[PMID]:8204417
[Au] Autor:Aspeslet LJ; Baker GB; Coutts RT; Torok-Both GA
[Ad] Endereço:Department of Psychiatry and Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Canada.
[Ti] Título:The effects of desipramine and iprindole on levels of enantiomers of fluoxetine in rat brain and urine.
[So] Source:Chirality;6(2):86-90, 1994.
[Is] ISSN:0899-0042
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The antidepressant fluoxetine (FLU) and its N-demethylated metabolite, norfluoxetine (NFLU), each contains a chiral center. The combination of FLU and desipramine (DMI), another antidepressant, has been reported to be useful in treatment of depression, to dramatically increase plasma levels of DMI and also to produce more rapid beta-adrenergic receptor down-regulation in brain than caused by DMI alone. We have now begun studies on the effects of this drug combination on the levels of FLU and NFLU enantiomers in the rat. In addition, the combination of FLU and iprindole (IPR) was also investigated. Male Sprague-Dawley rats were treated intraperitoneally with either normal saline vehicle, DMI (5 mg/kg/day), (R,S)-FLU (10 mg/kg/day) or DMI (5 mg/kg/day) + (R,S)-FLU (10 mg/kg/day) for 4 days. Following the last treatment, 24 h urine samples were collected. Rats were sacrificed and brains were removed. For the IPR study, rats were pretreated with either saline or IPR-HCl (11.2 mg/kg) and then treated 1 h later with (R,S)-FLU. After 5 h, the rats were sacrificed and brains were removed. Brain and urine samples were analyzed by gas chromatography with electron-capture detection for free (R)-and (S)-FLU and (R)- and (S)-NFLU after extraction and reaction with (-)-(S)-N-(trifluoroacetyl)prolyl chloride. The results from the brains of the rats treated with DMI/FLU indicate that levels of enantiomers of both FLU and NFLU were significantly increased over those seen in the animals receiving (R,S)-FLU alone.(ABSTRACT TRUNCATED AT 250 WORDS)
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Desipramina/farmacologia
Fluoxetina/farmacocinética
Iprindol/farmacologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Cromatografia Gasosa
Fluoxetina/urina
Masculino
Ratos
Ratos Sprague-Dawley
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
01K63SUP8D (Fluoxetine); 69U0IKR8FP (Iprindole); TG537D343B (Desipramine)
[Em] Mês de entrada:9407
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:940101
[St] Status:MEDLINE


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[PMID]:8174513
[Au] Autor:Ganry H; Bourin M
[Ad] Endereço:Département de Pharmacologie et Gis Médicament, Faculté de Médecine, Nantes.
[Ti] Título:[Iprindole: a functional link between serotonin and noradrenaline systems?].
[Ti] Título:Iprindole: lien fonctionnel entre systèmes sérotoninergique et noradrénergique?.
[So] Source:Encephale;20(1):7-11, 1994 Jan-Feb.
[Is] ISSN:0013-7006
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:Iprindole is an active antidepressant in clinical practice but its mechanism of action has never been clearly defined. Serotoninergic regulation of noradrenergic neurons of locus coeruleus depends on 5-HT2 receptors. This regulatory action of the 5-HT system appears to facilitate the down-regulation of beta receptors. In behavioural tests involving the noradrenergic system, the role of iprindole, administered in subactive doses, was evaluated in the presence of subactive doses of fluvoxamine, a serotonin uptake inhibitor. Yohimbine is an alpha2 antagonist, inducing a dose-dependent toxicity. This test allows a rapid and selective screening of antidepressants with direct and indirect beta-agonist properties. Administration of iprindole displayed a toxicity of fluvoxamine in the presence of yohimbine. A 5-day pre-treatment of iprindole antagonized this potentiation unmasked after acute administration of iprindole. The down-regulation of beta receptors induced by a chronic treatment by iprindole could prevent the adrenergic expression of yohimbine's toxicity. But the down-regulation of 5-HT2 receptors also obtained with chronic treatment by iprindole, can explain this antagonism preventing fluvoxamine's action. Hypothermia induced by a high dose of apomorphine, depends on an activation of the noradrenergic system. During the interaction with fluvoxamine, iprindole unmasked an antagonism of this hypothermia due to apomorphine. The activity of a subactive dose of salbutamol, a direct beta-agonist, was evaluated in the presence of fluvoxamine on hypothermia induced by a high dose of apomorphine. The aim of this interaction was to define the beta-adrenergic property of iprindole more precisely.(ABSTRACT TRUNCATED AT 250 WORDS)
[Mh] Termos MeSH primário: Nível de Alerta/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Iprindol/farmacologia
Receptores Adrenérgicos/efeitos dos fármacos
Receptores de Serotonina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apomorfina/farmacologia
Nível de Alerta/fisiologia
Regulação da Temperatura Corporal/efeitos dos fármacos
Relação Dose-Resposta a Droga
Dose Letal Mediana
Masculino
Camundongos
Norepinefrina/fisiologia
Receptores Adrenérgicos/fisiologia
Receptores de Serotonina/fisiologia
Serotonina/fisiologia
Ioimbina/farmacologia
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Adrenergic); 0 (Receptors, Serotonin); 2Y49VWD90Q (Yohimbine); 333DO1RDJY (Serotonin); 69U0IKR8FP (Iprindole); N21FAR7B4S (Apomorphine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:9406
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:940101
[St] Status:MEDLINE


  9 / 180 MEDLINE  
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[PMID]:8356178
[Au] Autor:Zieba A; Pawlowski L
[Ad] Endereço:Kliniki Psychiatrii Doroslych AM w Krakowie.
[Ti] Título:[Current views of the mechanism of action of antidepressants].
[Ti] Título:Aktualne poglady na mechanizm dzialania leków przeciwdepresyjnych..
[So] Source:Psychiatr Pol;27(3):317-24, 1993 May-Jun.
[Is] ISSN:0033-2674
[Cp] País de publicação:Poland
[La] Idioma:pol
[Ab] Resumo:Considering the ever growing number of new discoveries and changes in ideas in the field of psychopharmacology, the authors present the actual state of knowledge about the mechanism of action of antidepressant drugs. Three periods characterize the research and the development of antidepressants. In the first period the presynaptic monoamine neuron was considered as the target structure both with respect to the search for the origin of depression and the mechanism of action of antidepressants. Two types of antidepressants, monoamine uptake inhibitors and monoamine oxidase inhibitors (IMAO) are representative of this period. In the second period, the research focused its interest primarily on monoaminergic receptors, anticipating that they were critically involved in the pathophysiology of depression. Such research sought to explain the antidepressant properties of iprindole and mianserine which are neither monoamine uptake inhibitors nor inhibitors of MAO. The onset of the third period is recent and it is characterized by the shift in research emphasis to intracellular transmission events. This period started with the discovery of the antidepressant properties of the phosphodiesterase inhibitor rolipram.
[Mh] Termos MeSH primário: Antidepressivos/farmacologia
Transtorno Depressivo/tratamento farmacológico
Levodopa/farmacologia
Ácido gama-Aminobutírico/farmacologia
[Mh] Termos MeSH secundário: Antidepressivos/uso terapêutico
Transtorno Depressivo/psicologia
Feminino
Seres Humanos
Iprindol/farmacologia
Masculino
Inibidores da Monoaminoxidase/farmacologia
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Monoamine Oxidase Inhibitors); 46627O600J (Levodopa); 56-12-2 (gamma-Aminobutyric Acid); 69U0IKR8FP (Iprindole)
[Em] Mês de entrada:9309
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:930501
[St] Status:MEDLINE


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[PMID]:8271622
[Au] Autor:Koyama T; Abe M; Matsubara S; Yamashita I
[Ad] Endereço:Department of Psychiatry and Neurology, Hokkaido University School of Medicine, Sapporo.
[Ti] Título:Iprindole treatment increases extracellular concentrations of NA nd DA in the medial prefrontal cortex: evidence that iprindole increases availability of synaptic catecholamine in vivo.
[So] Source:Jpn J Psychiatry Neurol;47(2):424-5, 1993 Jun.
[Is] ISSN:0912-2036
[Cp] País de publicação:Japan
[La] Idioma:eng
[Mh] Termos MeSH primário: Dopamina/metabolismo
Iprindol/farmacologia
Norepinefrina/metabolismo
Córtex Pré-Frontal/efeitos dos fármacos
Sinapses/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Epinefrina/metabolismo
Espaço Extracelular/efeitos dos fármacos
Espaço Extracelular/metabolismo
Masculino
Microdiálise
Ratos
Ratos Sprague-Dawley
Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
333DO1RDJY (Serotonin); 69U0IKR8FP (Iprindole); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:9401
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:930601
[St] Status:MEDLINE



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