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[PMID]:28044440
[Au] Autor:Rojas A; Ganesh T; Walker A; Dingledine R
[Ad] Endereço:Department of Pharmacology, Emory University , 1510 Clifton Road NE, Atlanta, Georgia 30322, United States.
[Ti] Título:Ethylatropine Bromide as a Peripherally Restricted Muscarinic Antagonist.
[So] Source:ACS Chem Neurosci;8(4):712-717, 2017 Apr 19.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Quaternary ammonium analogues of atropine that are unable to cross the blood-brain barrier are used to alleviate peripheral muscarinic toxicity in animal models of epilepsy produced by systemic administration of pilocarpine or diisopropylfluorophosphate (DFP). Currently, methylatropine is the most popular and potent of these quaternary derivatives; however, it is expensive and produced in limited quantity. Here, we propose the use of ethylatropine bromide as an alternative to methylatropine. The synthesis of ethylatropine bromide is simple, inexpensive and has low environmental impact. We demonstrate the efficacy of ethylatropine bromide to antagonize the carbachol induced rise in intracellular calcium in a calcium mobilization assay, and its ability to prevent pilocarpine-induced total fluid secretions in mice without blocking pilocarpine-induced seizures. The ease of synthesis, cost effectiveness, and efficacy makes ethylatropine bromide a desirable alternative to methylatropine as a peripherally restricted acetylcholine receptor antagonist.
[Mh] Termos MeSH primário: Derivados da Atropina/farmacologia
Antagonistas Muscarínicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Agonistas Muscarínicos/toxicidade
Técnicas de Patch-Clamp
Pilocarpina/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atropine Derivatives); 0 (Muscarinic Agonists); 0 (Muscarinic Antagonists); 01MI4Q9DI3 (Pilocarpine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00334


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[PMID]:27098245
[Au] Autor:Kanashiro A; Talbot J; Peres RS; Pinto LG; Bassi GS; Cunha TM; Cunha FQ
[Ad] Endereço:Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil. alex_bioquimica@yahoo.com.br.
[Ti] Título:Neutrophil Recruitment and Articular Hyperalgesia in Antigen-Induced Arthritis are Modulated by the Cholinergic Anti-Inflammatory Pathway.
[So] Source:Basic Clin Pharmacol Toxicol;119(5):453-457, 2016 Nov.
[Is] ISSN:1742-7843
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The cholinergic anti-inflammatory pathway (CAP) is a complex neuroimmune mechanism triggered by the central nervous system to regulate peripheral inflammatory responses. Understanding the role of CAP in the pathogenesis of rheumatoid arthritis (RA) could help develop new therapeutic strategies for this disease. Therefore, we investigated the participation of this neuroimmune pathway on the progression of experimental arthritis. Using antigen-induced arthritis (AIA) model, we investigated in mice the effects of vagotomy or the pharmacological treatments with hexamethonium (peripheral nicotinic receptor antagonist), methylatropine (peripheral muscarinic receptor antagonist) or neostigmine (peripheral acetylcholinesterase inhibitor) on AIA progression. Unilateral cervical vagotomy was performed 1 week before the immunization protocol with methylated bovine serum albumin (mBSA), while drug administration was conducted during the period of immunization. On day 21, 6 hr after the challenge with mBSA injection in the femur-tibial joint, the local neutrophil migration and articular mechanical hyperalgesia were assessed. Herein, we observed that vagotomy or blockade of peripheral nicotinic (but not muscarinic) receptors exacerbated the clinical parameters of this disease. Moreover, peripheral acetylcholinesterase inhibition by neostigmine treatment promoted a reduction of neutrophil recruitment in the knee joint and articular hyperalgesia. Our results demonstrated that peripheral activation of CAP modulates experimental arthritis, providing a pre-clinical evidence of a potential therapeutic strategy for RA.
[Mh] Termos MeSH primário: Artrite Experimental/imunologia
Artrite Reumatoide/imunologia
Neurônios Colinérgicos/imunologia
Vias Eferentes/imunologia
Hiperalgesia/tratamento farmacológico
Neuroimunomodulação/efeitos dos fármacos
Infiltração de Neutrófilos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antígenos/efeitos adversos
Artrite Experimental/tratamento farmacológico
Artrite Experimental/etiologia
Artrite Reumatoide/tratamento farmacológico
Derivados da Atropina/farmacologia
Inibidores da Colinesterase/farmacologia
Hexametônio/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Antagonistas Muscarínicos/farmacologia
Neostigmina/farmacologia
Antagonistas Nicotínicos/farmacologia
Soroalbumina Bovina
Vagotomia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Atropine Derivatives); 0 (Cholinesterase Inhibitors); 0 (Muscarinic Antagonists); 0 (Nicotinic Antagonists); 0 (methylated bovine serum albumin); 27432CM55Q (Serum Albumin, Bovine); 3982TWQ96G (Neostigmine); 3C9PSP36Z2 (Hexamethonium); 80719I460H (methylatropine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1111/bcpt.12611


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[PMID]:27085086
[Au] Autor:Beau AB; Montastruc JL; Lacroix I; Montastruc F; Hurault-Delarue C; Damase-Michel C
[Ad] Endereço:Service de Pharmacologie Médicale et Clinique, Centre Midi-Pyrénées de Pharmacovigilance, Pharmacoépidémiologie et d'Informations sur le Médicament, Pharmacopôle Midi-Pyrénées, INSERM U 1027 CHU et Faculté de Médecine de Toulouse, France.
[Ti] Título:Atropinic burden of drugs during pregnancy and psychological development of children: a cohort study in the EFEMERIS database.
[So] Source:Br J Clin Pharmacol;82(2):478-86, 2016 Aug.
[Is] ISSN:1365-2125
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: The aim of this study was to evaluate the potential effect of in utero exposure to drugs with atropinic properties on infant psychological development using atropinic burden (AB) scales. METHODS: Women from the EFEMERIS cohort, a French database including prescribed and dispensed reimbursed drugs during pregnancy and pregnancy outcomes, delivering between 2004 and 2010 were included (n = 43 740). Each drug was classified as having no (score = 0), few (score = 1) or strong (score = 3) atropinic properties. AB per woman was calculated by adding the atropinic scores of drugs prescribed during pregnancy. AB was categorized as exposure or no exposure. Secondary analyses were performed by dividing the exposure into four scores = [0], [1-8], [9-17] and [≥18]. Data for psychological development were extracted from children's medical certificates completed at 9 and 24 months. RESULTS: Thirty-four% (n = 14 925) of women received at least one atropinic drug during pregnancy. Women with AB ≥1 were older and received more drugs during pregnancy than unexposed women. At 24 months, more infants of mothers with AB ≥1 had difficulties to 'name a picture' (ORa , 1.18, 95% CI 1.03, 1.36) and to 'understand instructions' (ORa , 1.61, 95% CI 1.13, , 2.30]) compared with infants of unexposed women. Analyses of four groups of exposure and analyses excluding women receiving psychotropics led to similar results. CONCLUSIONS: The study showed significant association between in utero exposure to drugs with atropinic properties and fewer infant cognitive acquisitions at 24 months. Further exploring the potential effect of simultaneous use of drugs with atropinic effects among pregnant women will bring into consideration whether such prescriptions could be inappropriate for the child.
[Mh] Termos MeSH primário: Derivados da Atropina/efeitos adversos
Resultado da Gravidez
Efeitos Tardios da Exposição Pré-Natal/epidemiologia
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Derivados da Atropina/administração & dosagem
Desenvolvimento Infantil/efeitos dos fármacos
Pré-Escolar
Estudos de Coortes
Bases de Dados Factuais
Feminino
Seguimentos
França
Seres Humanos
Lactente
Recém-Nascido
Masculino
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atropine Derivatives)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160417
[St] Status:MEDLINE
[do] DOI:10.1111/bcp.12978


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[PMID]:26769133
[Au] Autor:Sayin H; Chapuis B; Chevalier P; Barrès C; Julien C
[Ad] Endereço:Neurocardiology Unit, Medical School Lyon East, University Claude Bernard Lyon 1, Lyon, France.
[Ti] Título:Assessment of cardiac autonomic tone in conscious rats.
[So] Source:Auton Neurosci;194:26-31, 2016 Jan.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cardiac autonomic tone can be assessed either by estimating separately vagal and sympathetic tones or by evaluating the net effect of their interaction, the so-called sympathovagal balance (SVB). To compare the most commonly used methods in rats, telemetric recordings of the electrocardiogram were performed in normotensive WKY rats, and in groups of spontaneously hypertensive (SHR) rats that were either untreated or chronically treated with the cholinesterase inhibitor, pyridostigmine, to enhance vagal tone. Cardiac autonomic blockers were administered alone and in combination, so that heart rate (HR) could be measured (1) under resting conditions, (2) with either autonomic branch blocked, and (3) with both branches blocked (which provided intrinsic HR, iHR). SVB was assessed as the ratio of resting HR to iHR. This calculation pointed to a sympathetic predominance in untreated SHRs and even more so in WKY rats, and to a marked vagal predominance in pyridostigmine-treated SHRs. By contrast, the ratio between low and high frequency components (LF/HF) of RR interval spectra did not significantly differ between the groups. Each autonomic tone was quantified as the HR change induced by its selective blocker or as the difference between iHR and HR after blockade of its counterpart. Both pharmacological methods indicated vagal enhancement in treated SHRs, but provided opposite results in terms of vagal vs. sympathetic predominance. These data seriously question the use of the LF/HF ratio as an index of SVB, and the possibility to reliably estimate vagal and sympathetic tones separately through current pharmacological approaches in conscious rats.
[Mh] Termos MeSH primário: Sistema Nervoso Autônomo/fisiologia
Estado de Consciência
[Mh] Termos MeSH secundário: Animais
Atenolol/farmacologia
Atropina/farmacologia
Derivados da Atropina/farmacologia
Sistema Nervoso Autônomo/efeitos dos fármacos
Eletrocardiografia
Frequência Cardíaca/efeitos dos fármacos
Masculino
Antagonistas Muscarínicos/farmacologia
Parassimpatolíticos/farmacologia
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Simpatolíticos/farmacologia
Fatores de Tempo
Nervo Vago/efeitos dos fármacos
Nervo Vago/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atropine Derivatives); 0 (Muscarinic Antagonists); 0 (Parasympatholytics); 0 (Sympatholytics); 50VV3VW0TI (Atenolol); 7C0697DR9I (Atropine); 80719I460H (methylatropine)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160116
[St] Status:MEDLINE


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[PMID]:25920465
[Au] Autor:Piermartiri TC; Pan H; Chen J; McDonough J; Grunberg N; Apland JP; Marini AM
[Ad] Endereço:Molecular and Cellular Biology Graduate Student Program, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD, 20814, USA.
[Ti] Título:Alpha-Linolenic Acid-Induced Increase in Neurogenesis is a Key Factor in the Improvement in the Passive Avoidance Task After Soman Exposure.
[So] Source:Neuromolecular Med;17(3):251-69, 2015 Sep.
[Is] ISSN:1559-1174
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exposure to organophosphorous (OP) nerve agents such as soman inhibits the critical enzyme acetylcholinesterase (AChE) leading to excessive acetylcholine accumulation in synapses, resulting in cholinergic crisis, status epilepticus and brain damage in survivors. The hippocampus is profoundly damaged after soman exposure leading to long-term memory deficits. We have previously shown that treatment with three sequential doses of alpha-linolenic acid, an essential omega-3 polyunsaturated fatty acid, increases brain plasticity in naïve animals. However, the effects of this dosing schedule administered after a brain insult and the underlying molecular mechanisms in the hippocampus are unknown. We now show that injection of three sequential doses of alpha-linolenic acid after soman exposure increases the endogenous expression of mature BDNF, activates Akt and the mammalian target of rapamycin complex 1 (mTORC1), increases neurogenesis in the subgranular zone of the dentate gyrus, increases retention latency in the passive avoidance task and increases animal survival. In sharp contrast, while soman exposure also increases mature BDNF, this increase did not activate downstream signaling pathways or neurogenesis. Administration of the inhibitor of mTORC1, rapamycin, blocked the alpha-linolenic acid-induced neurogenesis and the enhanced retention latency but did not affect animal survival. Our results suggest that alpha-linolenic acid induces a long-lasting neurorestorative effect that involves activation of mTORC1 possibly via a BDNF-TrkB-mediated mechanism.
[Mh] Termos MeSH primário: Aprendizagem da Esquiva/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Neurogênese/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Soman/toxicidade
Ácido alfa-Linolênico/farmacologia
[Mh] Termos MeSH secundário: Animais
Antígenos Nucleares/biossíntese
Antígenos Nucleares/genética
Derivados da Atropina/uso terapêutico
Aprendizagem da Esquiva/fisiologia
Dano Encefálico Crônico/etiologia
Dano Encefálico Crônico/fisiopatologia
Fator Neurotrófico Derivado do Encéfalo/biossíntese
Fator Neurotrófico Derivado do Encéfalo/genética
Replicação do DNA/efeitos dos fármacos
Diazepam/uso terapêutico
Eletrochoque
Comportamento Exploratório/efeitos dos fármacos
Hipocampo/fisiopatologia
Masculino
Alvo Mecanístico do Complexo 1 de Rapamicina
Proteínas Associadas aos Microtúbulos/biossíntese
Proteínas Associadas aos Microtúbulos/genética
Complexos Multiproteicos/antagonistas & inibidores
Complexos Multiproteicos/biossíntese
Complexos Multiproteicos/genética
Proteínas do Tecido Nervoso/biossíntese
Proteínas do Tecido Nervoso/genética
Neuropeptídeos/biossíntese
Neuropeptídeos/genética
Fármacos Neuroprotetores/antagonistas & inibidores
Fármacos Neuroprotetores/uso terapêutico
Neurotoxinas/metabolismo
Oximas/uso terapêutico
Proteínas Proto-Oncogênicas c-akt/biossíntese
Proteínas Proto-Oncogênicas c-akt/genética
Compostos de Piridínio/uso terapêutico
Ratos
Ratos Sprague-Dawley
Receptor trkB/fisiologia
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
Sirolimo/farmacologia
Estado Epiléptico/induzido quimicamente
Estado Epiléptico/complicações
Estado Epiléptico/tratamento farmacológico
Serina-Treonina Quinases TOR/antagonistas & inibidores
Serina-Treonina Quinases TOR/biossíntese
Serina-Treonina Quinases TOR/genética
Ácido alfa-Linolênico/antagonistas & inibidores
Ácido alfa-Linolênico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Antigens, Nuclear); 0 (Atropine Derivatives); 0 (Brain-Derived Neurotrophic Factor); 0 (Microtubule-Associated Proteins); 0 (Multiprotein Complexes); 0 (Nerve Tissue Proteins); 0 (NeuN protein, rat); 0 (Neuropeptides); 0 (Neuroprotective Agents); 0 (Neurotoxins); 0 (Oximes); 0 (Pyridinium Compounds); 0 (doublecortin protein); 0RBV727H71 (alpha-Linolenic Acid); 80719I460H (methylatropine); 96-64-0 (Soman); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.10.1 (Receptor, trkB); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); HUV88P6SJS (asoxime chloride); Q3JTX2Q7TU (Diazepam); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150430
[St] Status:MEDLINE
[do] DOI:10.1007/s12017-015-8353-y


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[PMID]:25870195
[Au] Autor:Mao Y; Tokudome T; Kishimoto I; Otani K; Nishimura H; Yamaguchi O; Otsu K; Miyazato M; Kangawa K
[Ad] Endereço:From the Department of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, Suita, Japan (Y.M., T.T., I.K., H.N., M.M., K.K.); Department of Regenerative Medicine and Tissue Engineering, National Cerebral and Cardiovascular Center Research Institute (K.O.), Department of Car
[Ti] Título:Endogenous ghrelin attenuates pressure overload-induced cardiac hypertrophy via a cholinergic anti-inflammatory pathway.
[So] Source:Hypertension;65(6):1238-44, 2015 Jun.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiac hypertrophy, which is commonly caused by hypertension, is a major risk factor for heart failure and sudden death. Endogenous ghrelin has been shown to exert a beneficial effect on cardiac dysfunction and postinfarction remodeling via modulation of the autonomic nervous system. However, ghrelin's ability to attenuate cardiac hypertrophy and its potential mechanism of action are unknown. In this study, cardiac hypertrophy was induced by transverse aortic constriction in ghrelin knockout mice and their wild-type littermates. After 12 weeks, the ghrelin knockout mice showed significantly increased cardiac hypertrophy compared with wild-type mice, as evidenced by their significantly greater heart weight/tibial length ratios (9.2±1.9 versus 7.9±0.8 mg/mm), left ventricular anterior wall thickness (1.3±0.2 versus 1.0±0.2 mm), and posterior wall thickness (1.1±0.3 versus 0.9±0.1 mm). Furthermore, compared with wild-type mice, ghrelin knockout mice showed suppression of the cholinergic anti-inflammatory pathway, as indicated by reduced parasympathetic nerve activity and higher plasma interleukin-1ß and interleukin-6 levels. The administration of either nicotine or ghrelin activated the cholinergic anti-inflammatory pathway and attenuated cardiac hypertrophy in ghrelin knockout mice. In conclusion, our results show that endogenous ghrelin plays a crucial role in the progression of pressure overload-induced cardiac hypertrophy via a mechanism that involves the activation of the cholinergic anti-inflammatory pathway.
[Mh] Termos MeSH primário: Cardiomegalia/metabolismo
Colinérgicos
Grelina/farmacologia
Transdução de Sinais/efeitos dos fármacos
Pressão Ventricular/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Derivados da Atropina/farmacologia
Cardiomegalia/fisiopatologia
Modelos Animais de Doenças
Grelina/metabolismo
Camundongos
Camundongos Knockout
Nicotina/farmacologia
Distribuição Aleatória
Valores de Referência
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Atropine Derivatives); 0 (Cholinergic Agents); 0 (Ghrelin); 6M3C89ZY6R (Nicotine); 80719I460H (methylatropine)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:160726
[Lr] Data última revisão:
160726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150415
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.114.04864


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[PMID]:25862588
[Au] Autor:Ferreira CB; Schoorlemmer GH; Rossi MV; Takakura AC; Barna BF; Moreira TS; Cravo SL
[Ad] Endereço:Department of Physiology, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil.
[Ti] Título:Brainstem areas activated by intermittent apnea in awake unrestrained rats.
[So] Source:Neuroscience;297:262-71, 2015 Jun 25.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We investigated the role of the autonomic nervous system to cardiovascular responses to obstructive apnea in awake, unrestrained rats, and measured expression of Fos induced by apnea in the brainstem. We implanted a tracheal balloon contained in a rigid tube to allow the induction of apnea without inducing pain in the trachea. During bouts of 15s of apnea, heart rate fell from 371±8 to 161±11bpm (mean±SEM, n=15, p<0.01) and arterial pressure increased from 115±2 to 131±4mmHg (p<0.01). Bradycardia was due to parasympathetic activity because it was blocked by the muscarinic antagonist, methylatropine. The pressor response was due to vasoconstriction caused by sympathetic activation because it was blocked by the α1 antagonist, prazosin. Apnea induced Fos expression in several brainstem areas involved in cardiorespiratory control such as the nucleus of the solitary tract (NTS), ventrolateral medulla (VLM), and pons. Ligation of the carotid body artery reduced apnea-induced bradycardia, blocked heart rate responses to i.v. injection of cyanide, reduced Fos expression in the caudal NTS, and increased Fos expression in the rostral VLM. In conclusion, apnea activates neurons in regions that process signals from baroreceptors, chemoreceptors, pulmonary receptors, and regions responsible for autonomic and respiratory activity both in the presence and absence of carotid chemoreceptors.
[Mh] Termos MeSH primário: Apneia/patologia
Apneia/fisiopatologia
Tronco Encefálico/fisiopatologia
Vigília
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Derivados da Atropina/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Tronco Encefálico/efeitos dos fármacos
Corpo Carotídeo/citologia
Células Quimiorreceptoras/efeitos dos fármacos
Frequência Cardíaca/efeitos dos fármacos
Masculino
Proteínas Oncogênicas v-fos/metabolismo
Parassimpatolíticos/farmacologia
Prazosina/farmacologia
Ratos
Ratos Wistar
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atropine Derivatives); 0 (Oncogene Proteins v-fos); 0 (Parasympatholytics); 80719I460H (methylatropine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); XM03YJ541D (Prazosin)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150511
[Lr] Data última revisão:
150511
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150412
[St] Status:MEDLINE


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[PMID]:25831206
[Au] Autor:Shimojo GL; Palma RK; Brito JO; Sanches IC; Irigoyen MC; De Angelis K
[Ad] Endereço:Laboratório de Fisiologia Translacional, Programa de Ciências da Reabilitação, Universidade Nove de Julho, São Paulo, SP, Brasil.
[Ti] Título:Dynamic resistance training decreases sympathetic tone in hypertensive ovariectomized rats.
[So] Source:Braz J Med Biol Res;48(6):523-7, 2015 Jun.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate the effects of resistance exercise training on hemodynamics and cardiac autonomic control in ovariectomized spontaneously hypertensive rats. Female rats were divided into 4 groups: sedentary control (SC), sedentary hypertensive (SH), sedentary hypertensive ovariectomized (SHO), and resistance-trained hypertensive ovariectomized (RTHO). Resistance exercise training was performed on a vertical ladder (5 days/week, 8 weeks) at 40-60% maximal load. Direct arterial pressure was recorded. Vagal and sympathetic tones were measured by heart rate (HR) responses to methylatropine (3 mg/kg, iv) and propranolol (4 mg/kg, iv). Ovariectomy resulted in additional increases in blood pressure in hypertensive rats and was associated with decreased vagal tone. Resistance exercise trained rats had lower mean arterial pressure than untrained rats (RTHO: 159±2.2 vs SHO: 177±3.4 mmHg), as well as resting bradycardia (RTHO: 332±9.0 vs SHO: 356±5 bpm). Sympathetic tone was also lower in the trained group. Moreover, sympathetic tone was positively correlated with resting HR (r=0.7, P<0.05). The additional arterial pressure increase in hypertensive rats caused by ovarian hormone deprivation was attenuated by moderate-intensity dynamic resistance training. This benefit may be associated with resting bradycardia and reduced cardiac sympathetic tone after training, which suggests potential benefits of resistance exercise for the management of hypertension after ovarian hormone deprivation.
[Mh] Termos MeSH primário: Sistema Nervoso Autônomo/fisiologia
Hemodinâmica/fisiologia
Hipertensão/fisiopatologia
Ovariectomia
Condicionamento Físico Animal/fisiologia
Treinamento de Resistência/métodos
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/farmacologia
Derivados da Atropina/farmacologia
Sistema Nervoso Autônomo/efeitos dos fármacos
Peso Corporal
Bradicardia/fisiopatologia
Bradicardia/prevenção & controle
Feminino
Hemodinâmica/efeitos dos fármacos
Hipertensão/tratamento farmacológico
Menopausa/fisiologia
Parassimpatolíticos/farmacologia
Propranolol/farmacologia
Ratos Endogâmicos SHR
Ratos Wistar
Reprodutibilidade dos Testes
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Atropine Derivatives); 0 (Parasympatholytics); 80719I460H (methylatropine); 9Y8NXQ24VQ (Propranolol)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:161018
[Lr] Data última revisão:
161018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150402
[St] Status:MEDLINE


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[PMID]:25673780
[Au] Autor:Rodrigues FL; Silva LE; Hott SC; Bomfim GF; da Silva CA; Fazan R; Resstel LB; Tostes RC; Carneiro FS
[Ad] Endereço:Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, São Paulo, Brazil;
[Ti] Título:Toll-like receptor 9 plays a key role in the autonomic cardiac and baroreflex control of arterial pressure.
[So] Source:Am J Physiol Regul Integr Comp Physiol;308(8):R714-23, 2015 Apr 15.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The crosstalk between the immune and the autonomic nervous system may impact the cardiovascular function. Toll-like receptors are components of the innate immune system and play developmental and physiological roles. Toll-like receptor 9 (TLR9) is involved in the pathogenesis of cardiovascular diseases, such as hypertension and heart failure. Since such diseases are commonly accompanied by autonomic imbalance and lower baroreflex sensitivity, we hypothesized that TLR9 modulates cardiac autonomic and baroreflex control of arterial pressure (AP). Toll-like receptor 9 knockout (TLR9 KO) and wild-type (WT) mice were implanted with catheters into carotid artery and jugular vein and allowed to recover for 3 days. After basal recording of AP, mice received methyl-atropine or propranolol. AP and pulse interval (PI) variability were evaluated in the time and frequency domain (spectral analysis), as well as by multiscale entropy. Spontaneous baroreflex was studied by sequence technique. Behavioral and cardiovascular responses to fear-conditioning stress were also evaluated. AP was similar between groups, but TLR9 KO mice exhibited lower basal heart rate (HR). AP variability was not different, but PI variability was increased in TLR9 KO mice. The total entropy was higher in TLR9 KO mice. Moreover, baroreflex function was found higher in TLR9 KO mice. Atropine-induced tachycardia was increased in TLR9 KO mice, whereas the propranolol-induced bradycardia was similar to WT mice. TLR9 KO mice exhibit increased behavioral and decreased tachycardia responses to fear-conditioning stress. In conclusion, our findings suggest that TLR9 may negatively modulate cardiac vagal tone and baroreflex in mice.
[Mh] Termos MeSH primário: Pressão Arterial
Barorreflexo
Bradicardia/metabolismo
Sistema Cardiovascular/inervação
Imunidade Inata
Taquicardia/metabolismo
Receptor Toll-Like 9/metabolismo
Nervo Vago/metabolismo
[Mh] Termos MeSH secundário: Animais
Derivados da Atropina
Comportamento Animal
Bradicardia/induzido quimicamente
Bradicardia/genética
Bradicardia/imunologia
Bradicardia/fisiopatologia
Sistema Cardiovascular/imunologia
Condicionamento (Psicologia)
Modelos Animais de Doenças
Medo
Frequência Cardíaca
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Propranolol
Transdução de Sinais
Taquicardia/induzido quimicamente
Taquicardia/genética
Taquicardia/imunologia
Taquicardia/fisiopatologia
Fatores de Tempo
Receptor Toll-Like 9/deficiência
Receptor Toll-Like 9/genética
Nervo Vago/imunologia
Nervo Vago/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Atropine Derivatives); 0 (Tlr9 protein, mouse); 0 (Toll-Like Receptor 9); 80719I460H (methylatropine); 9Y8NXQ24VQ (Propranolol)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150416
[Lr] Data última revisão:
150416
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150213
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00150.2014


  10 / 1157 MEDLINE  
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[PMID]:25416192
[Au] Autor:Santos-Almeida FM; Girão H; da Silva CA; Salgado HC; Fazan R
[Ad] Endereço:Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil; and.
[Ti] Título:Cholinergic stimulation with pyridostigmine protects myocardial infarcted rats against ischemic-induced arrhythmias and preserves connexin43 protein.
[So] Source:Am J Physiol Heart Circ Physiol;308(2):H101-7, 2015 Jan 15.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We investigated the effects of acute pyridostigmine (PYR) treatment, an acetylcholinesterase inhibitor, on arterial pressure (AP), heart rate (HR), cardiac sympathovagal balance, and the incidence of arrhythmias during the first 4 h after myocardial infarction (MI) in anesthetized rats. Male Wistar rats were implanted with catheters into the femoral artery and vein for AP recordings and drug administration. Rats received the autonomic receptor blockers methyl-atropine (1 mg/kg iv) and propranolol (2 mg/kg iv) at intervals of 15 min, 1 h after saline (n=16) or PYR (0.25 mg/kg iv, n=18), to indirectly assess sympathovagal balance. Acute treatment with PYR increased cardiac vagal (86±7 vs. 44±5 beats/min) and decreased sympathetic tone (-31±8 vs. -69±7 beats/min). Different animals were implanted with ECG electrodes and catheters. A large MI was induced via left coronary artery ligation after basal recordings. Rats received PYR (n=14) or saline (n=14) 10-15 min after MI, and the recordings lasted up to 4 h. In part of the animals, hearts were removed for connexin43 quantification after all procedures. MI elicited a fall in AP (-45±5 mmHg), a progressive rise in HR (26±14 beats/min), and an increase in corrected QT interval (33±13 ms). PYR elicited a prompt bradycardia (-50±14 beats/min) that returned to basal levels over time, and it prevented the lengthening of the corrected QT interval. Treatment with PYR increased by ∼20% the occurrence of rats free of arrhythmias after MI. MI markedly decreased connexin43 in left ventricles, and PYR treatment partially prevented this decrease.
[Mh] Termos MeSH primário: Arritmias Cardíacas/tratamento farmacológico
Inibidores da Colinesterase/uso terapêutico
Conexina 43/metabolismo
Frequência Cardíaca/efeitos dos fármacos
Infarto do Miocárdio/tratamento farmacológico
Brometo de Piridostigmina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Arritmias Cardíacas/prevenção & controle
Derivados da Atropina/farmacologia
Pressão Sanguínea
Inibidores da Colinesterase/farmacologia
Masculino
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/fisiopatologia
Propranolol/farmacologia
Brometo de Piridostigmina/farmacologia
Ratos
Ratos Wistar
Nervo Vago/efeitos dos fármacos
Nervo Vago/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Atropine Derivatives); 0 (Cholinesterase Inhibitors); 0 (Connexin 43); 80719I460H (methylatropine); 9Y8NXQ24VQ (Propranolol); KVI301NA53 (Pyridostigmine Bromide)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:150101
[Lr] Data última revisão:
150101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141123
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00591.2014



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