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Pesquisa : D27.505.519.625.120.200.700 [Categoria DeCS]
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Texto completo SciELO Chile
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Id: biblio-899682
Autor: Peña G, Pedro; Zagolin B, Mónica.
Título: Vareniclina / Varenicline
Fonte: Rev. chil. enferm. respir;33(3):212-215, set. 2017.
Idioma: es.
Resumo: Resumen Vareniclina es terapia de primera línea para la cesación del tabaquismo, y presenta la mayor efectividad demostrada ampliamente en ensayos clínicos logrando cifras de abandono al año del orden de 25-35%. En la más reciente revisión de efectividad realizada por la Cochrane se evaluaron 39 ensayos que randomizaban vareniclina contra placebo y en comparación con sustitutos de nicotina (TRN) y bupropión. Con vareniclina se objetivó un RR de 2,24 para abstinencia a 6 meses o más prolongado a dosis standard (2 mg al día) contra placebo. El RR de vareniclina versus placebo comparando con bupropión o TRN fue de 1,3 y 1,25 respectivamente mostrando su superioridad una vez más. Cuando se evaluó el uso de vareniclina por un periodo más prolongado que 12 semanas, se observó que la droga fue bien tolerada sugiriendo que es factible su uso sin intensificar los efectos adversos.

Varenicline is a first-line therapy cessation of smoking, and has the highest effectiveness widely demonstrated in clinical trials with drop-out figures per year of the order of 25-35%. In the most recent effectiveness review conducted by the Cochrane, 39 trials were evaluated that randomized varenicline versus placebo and compared with nicotine substitutes (NRT) and bupropion. With varenicline, a RR of 2.24 was observed for abstinence at 6 months or longer at standard doses (2 mg daily) versus placebo. The RR of varenicline versus placebo compared with bupropion or NRT was 1.3 and 1.25 respectively showing its superiority once again. When the use of varenicline was evaluated for a period longer than 12 weeks, it was observed that the drug was well tolerated suggesting that its use is feasible without intensifying the adverse effects.
Descritores: Tabagismo/tratamento farmacológico
Tabagismo/epidemiologia
Vareniclina/uso terapêutico
-Abandono do Hábito de Fumar
Bupropiona/uso terapêutico
Antagonistas Nicotínicos
Nicotina
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  2 / 9 LILACS  
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Texto completo SciELO Chile
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Id: lil-432434
Autor: Hatori, Eiki; Sakuraba, Shigeki; Kashiwagi, Masanori; Kuribayashi, Junya; Tsujita, Miki; Hosokawa, Yuki; Takeda, Junzo; Kuwana, Shun-Ichi.
Título: Association of nicotinic acetylcholine receptors with central respiratory control in isolated brainstem-spinal cord preparation of neonatal rats
Fonte: Biol. Res;39(2):321-330, 2006. ilus, tab.
Idioma: en.
Resumo: Nicotine exposure is a risk factor in several breathing disorders Nicotinic acetylcholine receptors (nAChRs) exist in the ventrolateral medulla, an important site for respiratory control. We examined the effects of nicotinic acetylcholine neurotransmission on central respiratory control by addition of a nAChR agonist or one of various antagonists into superfusion medium in the isolated brainstem-spinal cord from neonatal rats. Ventral C4 neuronal activity was monitored as central respiratory output, and activities of respiratory neurons in the ventrolateral medulla were recorded in whole-cell configuration. RJR-2403 (0.1-10mM), a4b2 nAChR agonist induced dose-dependent increases in respiratory frequency. Non-selective nAChR antagonist mecamylamine (0.1-100mM), a4b2 antagonist dihydro-b-erythroidine (0.1-100mM), a7 antagonist methyllycaconitine (0.1-100mM), and a-bungarotoxin (0.01-10mM) all induced dose-dependent reductions in C4 respiratory rate. We next examined effects of 20mM dihydro-b-erythroidine and 20mM methyllycaconitine on respiratory neurons. Dihydro-b-erythroidine induces hyperpolarization and decreases intraburst firing frequency of inspiratory and preinspiratory neurons. In contrast, methyllycaconitine has no effect on the membrane potential of inspiratory neurons, but does decrease their intraburst firing frequency while inducing hyperpolarization and decreasing intraburst firing frequency in preinspiratory neurons. These findings indicate that a4b2 nAChR is involved in both inspiratory and preinspiratory neurons, whereas a7 nAChR functions only in preinspiratory neurons to modulate C4 respiratory rate.
Descritores: Neurônios/fisiologia
Agonistas Nicotínicos/farmacologia
Antagonistas Nicotínicos/farmacologia
Receptores Nicotínicos/fisiologia
Centro Respiratório/fisiologia
-Animais Recém-Nascidos
Aconitina/análogos & derivados
Aconitina/farmacologia
Bungarotoxinas/farmacologia
Di-Hidro-beta-Eritroidina/farmacologia
Potenciais da Membrana
Mecamilamina/farmacologia
Neurônios/efeitos dos fármacos
Ratos Wistar
Receptores Nicotínicos/efeitos dos fármacos
Centro Respiratório/efeitos dos fármacos
Limites: Animais
Ratos
Responsável: BR1.1 - BIREME


  3 / 9 LILACS  
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Texto completo SciELO Brasil
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Id: lil-398182
Autor: Sampaio, L. F. S; Hamassaki-Britto, D. E; Markus, R. P.
Título: Influence of melatonin on the development of functional nicotinic acetylcholine receptors in cultured chick retinal cells
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;38(4):603-613, Apr. 2005. ilus, graf.
Idioma: en.
Projeto: Fundação de Amparo à Pesquisa do Estado de São Paulo.
Resumo: The influence of melatonin on the developmental pattern of functional nicotinic acetylcholine receptors was investigated in embryonic 8-day-old chick retinal cells in culture. The functional response to acetylcholine was measured in cultured retina cells by microphysiometry. The maximal functional response to acetylcholine increased 2.7 times between the 4th and 5th day in vitro (DIV4, DIV5), while the Bmax value for [125I]-alpha-bungarotoxin was reduced. Despite the presence of alpha8-like immunoreactivity at DIV4, functional responses mediated by alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors were observed only at DIV5. Mecamylamine (100 µM) was essentially without effect at DIV4 and DIV5, while dihydro-ß-erythroidine (10-100 µM) blocked the response to acetylcholine (3.0 nM-2.0 µM) only at DIV4, with no effect at DIV5. Inhibition of melatonin receptors with the antagonist luzindole, or melatonin synthesis by stimulation of D4 dopamine receptors blocked the appearance of the alpha-bungarotoxin-sensitive response at DIV5. Therefore, alpha-bungarotoxin-sensitive receptors were expressed in retinal cells as early as at DIV4, but they reacted to acetylcholine only after DIV5. The development of an alpha-bungarotoxin-sensitive response is dependent on the production of melatonin by the retinal culture. Melatonin, which is produced in a tonic manner by this culture, and is a key hormone in the temporal organization of vertebrates, also potentiates responses mediated by alpha-bungarotoxin-sensitive receptors in rat vas deferens and cerebellum. This common pattern of action on different cell models that express alpha-bungarotoxin-sensitive receptors probably reflects a more general mechanism of regulation of these receptors.
Descritores: Melatonina/farmacologia
Receptores Nicotínicos/biossíntese
Retina/metabolismo
-Bungarotoxinas/metabolismo
Bungarotoxinas/farmacologia
Células Cultivadas
Imuno-Histoquímica
Microquímica
Antagonistas Nicotínicos/farmacologia
Receptores Nicotínicos/efeitos dos fármacos
Retina/citologia
Retina/efeitos dos fármacos
Fatores de Tempo
Triptaminas/farmacologia
Limites: Animais
Embrião de Galinha
Responsável: BR1.1 - BIREME


  4 / 9 LILACS  
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Texto completo SciELO Brasil
Britto, Luiz R. G
Texto completo
Id: lil-320137
Autor: Torräo, Andréa S; Britto, Luiz R. G.
Título: Neurotransmitter regulation of neural development: acetylcholine and nicotinic receptors
Fonte: An. acad. bras. ciênc;74(3):453-461, Sept. 2002. ilus, tab.
Idioma: en.
Resumo: Several neurotransmitter systems have been related to developmental processes during the past decade. In this review, we discuss the evidence that the nicotinic acetylcholine receptors could have an additional function during development that may be unrelated to their role in cholinergic neurotransmission in the vertebrate brain. Both temporal expression data and in vitro and in vivo studies with nicotinic agonists and antagonists have provided direct support for a role of nicotinic receptors in neural developmental processes such as neurite outgrowth and differentiation. A similar picture has emerged for other neurotransmitter and receptor systems as well, which generates a new view of neural processes during both development and mature life
Descritores: Sistema Nervoso Central
Neurotransmissores
Sistema Nervoso Periférico
Receptores Nicotínicos
-Encéfalo
Sistema Nervoso Central
Neurotransmissores
Nicotina
Agonistas Nicotínicos
Antagonistas Nicotínicos
Sistema Nervoso Periférico
Receptores Nicotínicos
Limites: Humanos
Animais
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


  5 / 9 LILACS  
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Bondan, Eduardo Fernandes
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Id: lil-316638
Autor: Bondan, Eduardo Fernandes; Lallo, Maria Anete; Dagli, Maria Lúcia Zaidan; Pereira, Luís Antonio Violin Dias; Graça, Dominguita Luhers.
Título: Ruptura da barreira hematoencefálica após injeçäo de droga gliotóxica no tronco encefálico de ratos wistar / Blood-brain barrier breakdown following gliotoxic drug injection in the brainstem of Wistar rats
Fonte: Arq. neuropsiquiatr;60(3A):582-589, Sept. 2002. ilus.
Idioma: pt.
Resumo: O brometo de etídio (BE) determina desaparecimento astrocitário local, com ruptura da glia limitans e suposto dano na barreira hematoencefálica (BBB). Este estudo visou avaliar a integridade da BBB após injeçäo de soluçäo de BE a 0,1 por cento (grupo E) ou de salina a 0,9 por cento (grupo C) na cisterna pontis de ratos Wistar. Fragmentos do tronco encefálico foram coletados das 24 horas aos 31 dias pós-injeçäo para estudo ultra-estrutural e marcaçäo imuno-histoquímica para a GFAP. Alguns animais receberam carväo coloidal por via intravenosa nos mesmos períodos. Nos ratos do grupo C, näo houve sinal de perda astrocitária, nem extravasamento vascular de carväo no sítio da injeçäo. No grupo E, o desaparecimento astrocitário começou às 48 horas e algumas áreas estavam ainda destituídas de processos astrocíticos 31 dias após. Extravasamento de partículas de carväo nas lesöes foi visto de 48 horas até 7 dias, näo sendo detectada qualquer alteraçäo ultra-estrutural das junçöes oclusivas pela falta de astrócitos perivasculares
Descritores: Astrócitos
Barreira Hematoencefálica
Tronco Encefálico
Etídio
Proteína Glial Fibrilar Ácida
Cloreto de Sódio
-Astrócitos
Tronco Encefálico
Modelos Animais de Doenças
Imuno-Histoquímica
Injeções
Antagonistas Nicotínicos
Ratos Wistar
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


  6 / 9 LILACS  
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Id: lil-278441
Autor: Duarte, Danilo Freire.
Título: Curarizantes: das suas origens aos dias de hoje / Curare and curare-like drugs: from the beginning to the present days
Fonte: Rev. bras. anestesiol;50(4):330-6, jul.-ago. 2000. tab.
Idioma: pt.
Descritores: Fármacos Neuromusculares não Despolarizantes/história
Anestesiologia
Antagonistas Nicotínicos/história
-Atracúrio
Succinilcolina
Brometo de Vecurônio
Limites: Humanos
Responsável: BR14.1 - Biblioteca Central


  7 / 9 LILACS  
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Id: lil-241340
Autor: Wacyk, Jurij; Fuenzalida, Marcela; Morales, Miguel; Acuña, Olga; Lemus, David.
Título: Effect of cholinergic agonists on muscular tonus of the lizard small intestine and esophagus
Fonte: Biol. Res;32(1):29-33, 1999. tab, graf.
Idioma: en.
Resumo: The underlying mechanisms of acetycholine-induced intestinal relaxation in the lizard Liolaemus tenuis tenuis are still unknows. By using a classical model of intestinal recording of isometric contraction and relaxation in conjunction with specific pharmacological tools, this article studies the possible influence of EDRF/NO and nicotinic ganglionar receptors on the Ach-induced relaxation in an effort to elucidate the probable mechanisms involved in ACh effect. It was observed that the relaxation of the lizard intestine elicited by ACh (10(-7) - 4 x 10(-4) M) was not affected by hexametonium (5 x 10(4) M) or tetrodotoxin (10(-6) M). Nicotine (10(-7) to 10(-4) M) induced relaxation was significantly antagonized by hexametonium; however, it was not influenced by tetrodotoxin. These results allow us to discard a neuronal pathway in cholinergic-induced relaxation, suggesting a more direct cholinergic effect on the smooth muscle, perhaps mediated by an unknown substance released by some specialized tissue. N-nitro-L-arginine, used to block NO-synthase and NO production, induced no changes in ACh-induced relaxation. Methylene blue, a soluble guanylate cyclase inhibitor, induced no changes in ACh-induced relaxation. These results allow us to dicard a probable role of EDRF/nitric oxide in the ACh-induced relaxation of lizard small intestine, providing evidence that this mechanism could be different from reported on other species.
Descritores: Agonistas Colinérgicos/farmacologia
Esôfago/efeitos dos fármacos
Intestino Delgado/efeitos dos fármacos
Relaxamento Muscular/efeitos dos fármacos
Tono Muscular/efeitos dos fármacos
-Inibidores Enzimáticos/farmacologia
Hexametônio/farmacologia
Lagartos
Azul de Metileno/farmacologia
Nicotina/farmacologia
Agonistas Nicotínicos/farmacologia
Antagonistas Nicotínicos/farmacologia
Óxido Nítrico Sintase
Nitroarginina/farmacologia
Tetrodotoxina/farmacologia
Limites: Animais
Masculino
Feminino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  8 / 9 LILACS  
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Id: lil-238969
Autor: Zago, W. M; Markus, R. P.
Título: Melatonin modulation of presynaptic nicotinic acetylcholine receptors located on short noradrenergic neurons of the rat vas deferens: a pharmacological characterization
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;32(8):999-1006, Aug. 1999.
Idioma: en.
Resumo: Melatonin, the pineal hormone produced during the dark phase of the light-dark cycle, modulates neuronal acetylcholine receptors located presynaptically on nerve terminals of the rat vas deferens. Recently we showed the presence of high affinity nicotine-binding sites during the light phase, and low and high affinity binding sites during the dark phase. The appearance of the low affinity binding sites was due to the nocturnal melatonin surge and could be mimicked by exposure to melatonin in vitro. The aim of the present research was to identify the receptor subtypes responsible for the functional response during the light and the dark phase. The rank order of potency of agonists was dimethylphenylpiperazinium (DMPP) = cytisine > nicotine > carbachol and DMPP = nicotine = cytisine > carbachol, during the light and dark phase, respectively, due to an increase in apparent affinity for nicotine. Mecamylamine similarly blocked the DMPP response during the light and the dark phase, while the response to nicotine was more efficiently blocked during the light phase. In contrast, methyllycaconitine inhibited the nicotine-induced response only at 21:00 h. Since = 7 nicotinic acetylcholine receptors (nAChRs) have low affinity for nicotine in binding assays, we suggest that a mixed population composed of alpha 3 Beta 4 - plus alpha7-bearing nAChR subtypes is present at night. This plasticity in receptor subtypes is probably driven by melatonin since nicotine-induced contraction in organs from animals sacrificed at 15:00 h and incubated with melatonin (100 pg/ml, 4 h) is not totally blocked by mecamylamine. Thus melatonin, by acting directly on the short adrenergic neurons that innervate the rat vas deferens, induces the appearance of the low affinity binding site, probably an alpha nAChR subtype
Descritores: Melatonina/metabolismo
Neurônios/efeitos dos fármacos
Agonistas Nicotínicos/farmacologia
Antagonistas Nicotínicos/farmacologia
Receptores Nicotínicos/efeitos dos fármacos
Ducto Deferente/metabolismo
-Ratos Wistar
Limites: Animais
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  9 / 9 LILACS  
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Texto completo SciELO Brasil
Texto completo
Id: lil-212871
Autor: Fernandes, C. G; Graça, D. L; Pereira, L. A. V. D.
Título: Inflammatory response of the spinal cord to multiple episodes of blood-brain barrier disruption and toxic demyelination in Wistar rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;31(7):933-6, jul. 1998. ilus.
Idioma: en.
Projeto: CNPq.
Resumo: Multiple episodes of blood-brain barrier disruption were induced by sequential intraspinal injections of ethidium bromide. In addition to the barrier disruption, there was toxic demyelination and exposure of myelin components to the immune system. Twenty-seven 3-month-old Wistar rats received 2, 3 or 4 injections of 1 mul of either 0.1 percent ethidium bromide in normal saline (19 rats) or 0.9 percent saline (8 rats) at different levels of the spinal cord. The time intervals between the injections ranged from 28 to 42 days. Ten days after the last injection, all rats were perfused with 2.5 percent glutaraldehyde. The spinal sections were evaluated macroscopically and by light and transmission electron microscopy. All the lesions demonstrated a mononuclear phagocytic infiltrate apparently removing myelin. Lymphocytes were not conspicuos and were found in only 34 percent of the lesions. No perivascular cuffings were detected. In older lesions (38 days and older) they were found only within Virchow-Robin spaces. This result suggests that multiple blood-brain barrier disruptions with demyelination and exposure of myelin components to the immune system were not sufficient to induce an immune-mediated reaction in the central nervous system.
Descritores: Barreira Hematoencefálica/imunologia
Doenças Desmielinizantes/induzido quimicamente
Doenças Desmielinizantes/imunologia
Etídio/toxicidade
Esclerose Múltipla/imunologia
Antagonistas Nicotínicos/toxicidade
Medula Espinal/imunologia
-Sistema Nervoso Central/imunologia
Sistema Nervoso Central/patologia
Doenças Desmielinizantes/patologia
Etídio/metabolismo
Injeções Espinhais
Linfócitos/ultraestrutura
Microscopia Eletrônica
Esclerose Múltipla/patologia
Proteína Básica da Mielina
Antagonistas Nicotínicos/metabolismo
Ratos Wistar
Limites: Animais
Ratos
Feminino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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