Base de dados : MEDLINE
Pesquisa : D02.033.100.291.465.300 [Categoria DeCS]
Referências encontradas : 1724 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 173 ir para página                         

  1 / 1724 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28888956
[Au] Autor:Sytchev VI; Odnoshivkina YG; Ursan RV; Petrov AM
[Ad] Endereço:Department of Normal Physiology, Kazan State Medial University, Kazan 420012, Butlerova st. 49, Russia.
[Ti] Título:Oxysterol, 5α-cholestan-3-one, modulates a contractile response to ß2-adrenoceptor stimulation in the mouse atria: Involvement of NO signaling.
[So] Source:Life Sci;188:131-140, 2017 Nov 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: Atrial ß2-adrenoceptors provide an important mechanism for regulation of cardiac function and changes in their downstream signaling are involved in processes underlying heart disorders. We have investigated the mechanism by which the cholesterol metabolite 5α-cholestan-3-one (5É‘Ch3) modulates inotropic effect of ß2-adrenoceptor agonist fenoterol. MAIN METHODS: Atria from mice were electrically stimulated and changes in contraction amplitude in response to fenoterol were studied in 5É‘Ch3-pretreated samples. Intracellular Ca and NO levels were estimated using fluorescent dyes Fluo-4 and DAF-FM, respectively. KEY FINDINGS: By itself 5αCh3 that appears in the circulation under some pathological conditions had a negligible influence on contraction, Ca -transient and NO production. However, pretreatment with 5αCh3 markedly attenuated the positive inotropic effect of fenoterol which was accompanied by an increase in the NO synthesis. Unexpectedly, the oxysterol also augmented an enhancement of Ca -transient amplitude in response to fenoterol. Under conditions of a pharmacological inhibition of G -protein/Akt/NO synthase/protein kinase G signaling, 5αCh3 augmented the inotropic effect of fenoterol. Herein, Akt antagonist suppressed the increase in NO production, while inhibition of NO synthesis did not modify the increased amplitude of the Ca -transient. Along similar lines, enrichment of plasma membranes with cholesterol reduced the stimulatory effect of 5αCh3 on ß2-adrenoceptor-evoked NO production, but not on the Ca2+-transient amplitude, leading to an elevation of the positive inotropic response to fenoterol. SIGNIFICANCE: These data suggest that 5É‘Ch3 potentiates the effect of pharmacological ß2-adrenoceptor activation on both NO production and Ca transient via independent mechanisms, thereby affecting the positive inotropy.
[Mh] Termos MeSH primário: Função Atrial/efeitos dos fármacos
Fenoterol/antagonistas & inibidores
Átrios do Coração/efeitos dos fármacos
Contração Miocárdica/efeitos dos fármacos
Óxido Nítrico/fisiologia
Oxisteróis/farmacologia
[Mh] Termos MeSH secundário: Agonistas de Receptores Adrenérgicos beta 2/farmacologia
Animais
Função Atrial/fisiologia
Cálcio/metabolismo
Colesterol/farmacologia
Estimulação Elétrica
Fenoterol/agonistas
Fenoterol/farmacologia
Átrios do Coração/metabolismo
Masculino
Camundongos
Contração Miocárdica/fisiologia
Óxido Nítrico/biossíntese
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-2 Receptor Agonists); 0 (Oxysterols); 22M9P70OQ9 (Fenoterol); 31C4KY9ESH (Nitric Oxide); 97C5T2UQ7J (Cholesterol); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170911
[St] Status:MEDLINE


  2 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28254813
[Au] Autor:Desjarlais M; Dussault S; Dhahri W; Mathieu R; Rivard A
[Ad] Endereço:From the Department of Cardiovascular Research, Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada.
[Ti] Título:MicroRNA-150 Modulates Ischemia-Induced Neovascularization in Atherosclerotic Conditions.
[So] Source:Arterioscler Thromb Vasc Biol;37(5):900-908, 2017 May.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Hypercholesterolemia is an atherosclerotic condition that is associated with impaired neovascularization in response to ischemia. This study sought to define the role of microRNAs in that pathophysiology. APPROACH AND RESULTS: Next-generation sequencing and quantitative reverse transcription polymerase chain reaction analyses identified miR-150 as a proangiogenic microRNA, which expression is significantly reduced in the ischemic muscles of hypercholesterolemic apolipoprotein E-deficient (ApoE ) mice, and in human umbilical vein endothelial cells exposed to oxidized low-density lipoprotein. Forced expression of miR-150 using a miR mimic could rescue oxidized low-density lipoprotein-mediated impairment of endothelial cell migration and tubule formation in vitro. In a mouse model of hindlimb ischemia, intramuscular injection of miR-150 mimic restored blood flow recuperation, vascular densities in ischemic muscles, and functional mobility in ApoE mice. Treatment of ApoE mice with miR-150 also increased the number and the activities of proangiogenic cells. miR-150 targets SRC kinase signaling inhibitor 1, an important regulator of Src (proto-oncogene tyrosine-protein kinase Src) activity. Here we found that hypercholesterolemia and oxidized low-density lipoprotein exposure are associated with increased SRC kinase signaling inhibitor 1 expression and decreased Src activity. However, treatment with miR-150 mimic reduces SRC kinase signaling inhibitor 1 expression and restores Src and downstream endothelial nitric oxide synthase and Akt (protein kinase B) activities both in vitro and in vivo. We also demonstrate the interrelation between miR-150 and SRC kinase signaling inhibitor 1 and their importance for endothelial cell angiogenic activities. CONCLUSIONS: Hypercholesterolemia is associated with reduced expression of miR-150, impaired Src signaling, and inefficient neovascularization in response to ischemia. Forced expression of miR-150 using a miR mimic could constitute a novel therapeutic strategy to improve ischemia-induced neovascularization in atherosclerotic conditions.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Isquemia/metabolismo
MicroRNAs/metabolismo
Músculo Esquelético/irrigação sanguínea
Neovascularização Fisiológica
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Animais
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Aterosclerose/genética
Aterosclerose/fisiopatologia
Células Cultivadas
Modelos Animais de Doenças
Feminino
Fenoterol
Predisposição Genética para Doença
Membro Posterior
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Seres Humanos
Hipercolesterolemia/genética
Hipercolesterolemia/metabolismo
Isquemia/genética
Isquemia/fisiopatologia
Lipoproteínas LDL/farmacologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
MicroRNAs/genética
Óxido Nítrico Sintase Tipo III/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Interferência de RNA
Transdução de Sinais
Transfecção
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Apolipoproteins E); 0 (Lipoproteins, LDL); 0 (MIRN150 microRNA, human); 0 (MicroRNAs); 0 (Mirn150 microRNA, mouse); 0 (SNIP protein, human); 0 (oxidized low density lipoprotein); 22M9P70OQ9 (Fenoterol); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, mouse); EC 2.7.10.2 (src-Family Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309189


  3 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28126898
[Au] Autor:Velzel J; Vlemmix F; Opmeer BC; Molkenboer JF; Verhoeven CJ; van Pampus MG; Papatsonis DN; Bais JM; Vollebregt KC; van der Esch L; Van der Post JA; Mol BW; Kok M
[Ad] Endereço:Department of Obstetrics and Gynaecology, Academic Medical Centre, Amsterdam, Netherlands j.velzel@amc.nl.
[Ti] Título:Atosiban versus fenoterol as a uterine relaxant for external cephalic version: randomised controlled trial.
[So] Source:BMJ;356:i6773, 2017 Jan 26.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE:  To compare the effectiveness of the oxytocin receptor antagonist atosiban with the beta mimetic fenoterol as uterine relaxants in women undergoing external cephalic version (ECV) for breech presentation. DESIGN:  Multicentre, open label, randomised controlled trial. SETTING:  Eight hospitals in the Netherlands, August 2009 to May 2014. PARTICIPANTS:  830 women with a singleton fetus in breech presentation and a gestational age of more than 34 weeks were randomly allocated in a 1:1 ratio to either 6.75 mg atosiban (n=416) or 40 µg fenoterol (n=414) intravenously for uterine relaxation before ECV. MAIN OUTCOME MEASURES:  The primary outcome measures were a fetus in cephalic position 30 minutes after the procedure and cephalic presentation at delivery. Secondary outcome measures were mode of delivery, incidence of fetal and maternal complications, and drug related adverse events. All analyses were done on an intention-to-treat basis. RESULTS:  Cephalic position 30 minutes after ECV occurred significantly less in the atosiban group than in the fenoterol group (34% v 40%, relative risk 0.73, 95% confidence interval 0.55 to 0.93). Presentation at birth was cephalic in 35% (n=139) of the atosiban group and 40% (n=166) of the fenoterol group (0.86, 0.72 to 1.03), and caesarean delivery was performed in 60% (n=240) of women in the atosiban group and 55% (n=218) in the fenoterol group (1.09, 0.96 to 1.20). No significant differences were found in neonatal outcomes or drug related adverse events. CONCLUSIONS:  In women undergoing ECV for breech presentation, uterine relaxation with fenoterol increases the rate of cephalic presentation 30 minutes after the procedure. No statistically significant difference was found for cephalic presentation at delivery. TRIAL REGISTRATION:  Dutch Trial Register, NTR 1877.
[Mh] Termos MeSH primário: Apresentação Pélvica
Fenoterol/uso terapêutico
Tocolíticos/uso terapêutico
Vasotocina/análogos & derivados
Versão Fetal/métodos
[Mh] Termos MeSH secundário: Adulto
Cesárea
Feminino
Seres Humanos
Países Baixos
Gravidez
Resultado da Gravidez
Vasotocina/uso terapêutico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Tocolytic Agents); 081D12SI0Z (atosiban); 22M9P70OQ9 (Fenoterol); W6S6URY8OF (Vasotocin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170128
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.i6773


  4 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28126642
[Au] Autor:Sliwinski L; Cegiela U; Pytlik M; Folwarczna J; Janas A; Zbrojkiewicz M
[Ad] Endereço:Department of Pharmacology, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Poland. Electronic address: lsliw@o2.pl.
[Ti] Título:Effects of fenoterol on the skeletal system depend on the androgen level.
[So] Source:Pharmacol Rep;69(2):260-267, 2017 Apr.
[Is] ISSN:1734-1140
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The role of sympathetic nervous system in the osseous tissue remodeling is not clear enough. METHODS: The effects of fenoterol, a selective ß -adrenomimetic drug, on the skeletal system of normal and androgen deficient (orchidectomized) rats were studied in vivo. Osteoclastogenesis and mRNA expression in osteoblasts were investigated in vitro in mouse cell cultures. RESULTS: Fenoterol administered to animals with physiological androgen level unfavorably affected the skeletal system, damaging the bone microarchitecture. Androgen deficiency induced osteoporotic changes, and fenoterol protected the osseous tissue from consequences of androgen deficiency. The results of in vitro studies correlated with the in vivo observations. A significantly increased number of osteoclasts in bone marrow cell cultures to which testosterone and fenoterol were added simultaneously was demonstrated. In cultures without the addition of testosterone, fenoterol significantly inhibited osteoclastogenesis in comparison with control cultures. CONCLUSIONS: The results indicate the favorable action of fenoterol in conditions of testosterone deficiency, and its destructive influence upon the skeleton in the presence of androgens. The results confirm the key role of sympathetic nervous system in the regulation of bone remodeling.
[Mh] Termos MeSH primário: Androgênios/metabolismo
Osso e Ossos/efeitos dos fármacos
Fenoterol/farmacologia
[Mh] Termos MeSH secundário: Animais
Reabsorção Óssea/tratamento farmacológico
Reabsorção Óssea/metabolismo
Osso e Ossos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Orquiectomia/métodos
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Osteoclastos/efeitos dos fármacos
Osteoclastos/metabolismo
Osteogênese/efeitos dos fármacos
RNA Mensageiro/metabolismo
Ratos
Ratos Wistar
Testosterona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (RNA, Messenger); 22M9P70OQ9 (Fenoterol); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170128
[St] Status:MEDLINE


  5 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27657826
[Au] Autor:Wang W; Chen J; Li XG; Xu J
[Ad] Endereço:Department of Infectious Diseases, Peking University Third Hospital, Hua-Yuan North Road 49, Haidian District, Beijing 100191, China.
[Ti] Título:Anti-inflammatory activities of fenoterol through ß-arrestin-2 and inhibition of AMPK and NF-κB activation in AICAR-induced THP-1 cells.
[So] Source:Biomed Pharmacother;84:185-190, 2016 Dec.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The AMP-activated protein kinase (AMPK) pathway has been shown to be able to regulate inflammation in several cell lines. We reported that fenoterol, a ß -adrenergic receptor (ß -AR) agonist, inhibited lipopolysaccharide (LPS)-induced AMPK activation and inflammatory cytokine production in THP-1 cells, a monocytic cell line in previous studies. 5-amino-1-ß-d-ribofuranosyl-imidazole-4-carboxamide (AICAR) is an agonist of AMPK. Whether AICAR induced AMPK activation and inflammatory cytokine production in THP-1 cells can be inhibited by fenoterol is unknown. In this study, we explored the mechanism of ß -AR stimulation with fenoterol in AICAR-induced inflammatory cytokine secretion in THP-1 cells. We studied AMPK activation using p-AMPK and AMPK antibodies, nuclear factor-kappa B (NF-κB) activation and inflammatory cytokine secretion in THP-1 cells stimulated by ß -AR in the presence or absence of AICAR and small interfering RNA (siRNA)-mediated knockdown of ß-arrestin-2 or AMPKα1 subunit. AICAR-induced AMPK activation, NF-κB activation and tumor necrosis factor (TNF)-α release were reduced by fenoterol. In addition, siRNA-mediated knockdown of ß-arrestin-2 abolished fenoterol's inhibition of AICAR-induced AMPK activation and TNF-α release, thus ß-arrestin-2 mediated the anti-inflammatory effects of fenoterol in AICAR-treated THP-1 cells. Furthermore, siRNA-mediated knockdown of AMPKα1 significantly attenuated AICAR-induced NF-κB activation and TNF-α release, so AMPKα1 was a key signaling molecule involved in AICAR-induced inflammatory cytokine production. These data suggested that fenoterol inhibited AICAR-induced AMPK activation and TNF-α release through ß-arrestin-2 in THP-1 cells. Management especially inhibition of AMPK signaling may provide new approaches and strategies for the treatments of immune diseases including inflammatory diseases and other critical illness.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/antagonistas & inibidores
Agonistas de Receptores Adrenérgicos beta 2/farmacologia
Aminoimidazol Carboxamida/análogos & derivados
Anti-Inflamatórios/farmacologia
Fenoterol/farmacologia
Mediadores da Inflamação/antagonistas & inibidores
Inflamação/prevenção & controle
Monócitos/efeitos dos fármacos
NF-kappa B/antagonistas & inibidores
Inibidores de Proteínas Quinases/farmacologia
Ribonucleotídeos/farmacologia
beta-Arrestina 2/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Proteínas Quinases Ativadas por AMP/metabolismo
Aminoimidazol Carboxamida/farmacologia
Linhagem Celular Tumoral
Ativação Enzimática
Seres Humanos
Inflamação/enzimologia
Inflamação/imunologia
Mediadores da Inflamação/metabolismo
Monócitos/enzimologia
Monócitos/imunologia
NF-kappa B/metabolismo
Fosforilação
Interferência de RNA
Transdução de Sinais/efeitos dos fármacos
Transfecção
Fator de Necrose Tumoral alfa/metabolismo
beta-Arrestina 2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ARRB2 protein, human); 0 (Adrenergic beta-2 Receptor Agonists); 0 (Anti-Inflammatory Agents); 0 (Inflammation Mediators); 0 (NF-kappa B); 0 (Protein Kinase Inhibitors); 0 (Ribonucleotides); 0 (Tumor Necrosis Factor-alpha); 0 (beta-Arrestin 2); 22M9P70OQ9 (Fenoterol); 360-97-4 (Aminoimidazole Carboxamide); EC 2.7.11.1 (PRKAA1 protein, human); EC 2.7.11.31 (AMP-Activated Protein Kinases); F0X88YW0YK (AICA ribonucleotide)
[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:160923
[St] Status:MEDLINE


  6 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27186619
[Ti] Título:COMMON STEM--(-)terol.
[So] Source:Prescrire Int;25(170):92, 2016 Apr.
[Is] ISSN:1167-7422
[Cp] País de publicação:France
[La] Idioma:eng
[Mh] Termos MeSH primário: Broncodilatadores
Terminologia como Assunto
[Mh] Termos MeSH secundário: Álcoois Benzílicos
Clorobenzenos
Fenoterol
Fumarato de Formoterol
Seres Humanos
Indanos
Quinolonas
Xinafoato de Salmeterol
Terbutalina/análogos & derivados
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzyl Alcohols); 0 (Bronchodilator Agents); 0 (Chlorobenzenes); 0 (Indans); 0 (Quinolones); 028LZY775B (vilanterol); 22M9P70OQ9 (Fenoterol); 6EW8Q962A5 (Salmeterol Xinafoate); 8OR09251MQ (indacaterol); N8ONU3L3PG (Terbutaline); W34SHF8J2K (Formoterol Fumarate); Y1850G1OVC (bambuterol)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160517
[Lr] Data última revisão:
160517
[Sb] Subgrupo de revista:T
[Da] Data de entrada para processamento:160518
[St] Status:MEDLINE


  7 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26935825
[Au] Autor:Alves E; Lukoyanov N; Serrão P; Moura D; Moreira-Rodrigues M
[Ad] Endereço:Laboratory of General Physiology, Institute of Biomedical Sciences Abel Salazar, University of Porto (ICBAS/UP), Porto, Portugal.
[Ti] Título:Epinephrine increases contextual learning through activation of peripheral ß2-adrenoceptors.
[So] Source:Psychopharmacology (Berl);233(11):2099-108, 2016 06.
[Is] ISSN:1432-2072
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Phenylethanolamine-N-methyltransferase knockout (Pnmt-KO) mice are unable to synthesize epinephrine and display reduced contextual fear. However, the precise mechanism responsible for impaired contextual fear learning in these mice is unknown. OBJECTIVES: Our aim was to study the mechanism of epinephrine-dependent contextual learning. METHODS: Wild-type (WT) or Pnmt-KO (129x1/SvJ) mice were submitted to a fear conditioning test either in the absence or in the presence of epinephrine, isoprenaline (non-selective ß-adrenoceptor agonist), fenoterol (selective ß2-adrenoceptor agonist), epinephrine plus sotalol (non-selective ß-adrenoceptor antagonist), and dobutamine (selective ß1-adrenoceptor agonist). Catecholamines were separated by reverse-phase HPLC and quantified by electrochemical detection. Blood glucose was measured by coulometry. RESULTS: Re-exposure to shock context induced higher freezing in WT and Pnmt-KO mice treated with epinephrine and fenoterol than in mice treated with vehicle. In addition, freezing response in Pnmt-KO mice was much lower than in WT mice. Freezing induced by epinephrine was blocked by sotalol in Pnmt-KO mice. Epinephrine and fenoterol treatment restored glycemic response in Pnmt-KO mice. Re-exposure to shock context did not induce a significant difference in freezing in Pnmt-KO mice treated with dobutamine and vehicle. CONCLUSIONS: Aversive memories are best retained if moderately high plasma epinephrine concentrations occur at the same moment as the aversive stimulus. In addition, epinephrine increases context fear learning by acting on peripheral ß2-adrenoceptors, which may induce high levels of blood glucose. Since glucose crosses the blood-brain barrier, it may enhance hippocampal-dependent contextual learning.
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos beta 2/farmacologia
Epinefrina/farmacologia
Aprendizagem/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos beta 2/farmacologia
Agonistas Adrenérgicos beta/farmacologia
Antagonistas Adrenérgicos beta/farmacologia
Animais
Dobutamina/farmacologia
Medo/psicologia
Fenoterol/farmacologia
Glucose/metabolismo
Isoproterenol/farmacologia
Camundongos
Camundongos Knockout
Feniletanolamina N-Metiltransferase/genética
Feniletanolamina N-Metiltransferase/fisiologia
Sotalol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic beta-2 Receptor Agonists); 0 (Adrenergic beta-2 Receptor Antagonists); 0 (Adrenergic beta-Agonists); 0 (Adrenergic beta-Antagonists); 22M9P70OQ9 (Fenoterol); 3S12J47372 (Dobutamine); A6D97U294I (Sotalol); EC 2.1.1.28 (Phenylethanolamine N-Methyltransferase); IY9XDZ35W2 (Glucose); L628TT009W (Isoproterenol); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160304
[St] Status:MEDLINE
[do] DOI:10.1007/s00213-016-4254-5


  8 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
Texto completo
[PMID]:26645888
[Au] Autor:Yamasmit W; Chaithongwongwatthana S; Tolosa JE; Limpongsanurak S; Pereira L; Lumbiganon P
[Ad] Endereço:Department of Obstetrics and Gynecology, Faculty of Medicine Vajira Hospital, Navamindradhiraj University, Samsen Road, Dusit, Bangkok, Thailand, 10300.
[Ti] Título:Prophylactic oral betamimetics for reducing preterm birth in women with a twin pregnancy.
[So] Source:Cochrane Database Syst Rev;(12):CD004733, 2015 Dec 08.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Twin pregnancies are associated with a high risk of neonatal mortality and morbidity due to an increased rate of preterm birth. Betamimetics can decrease contraction frequency or delay preterm birth in singleton pregnancies by 24 to 48 hours. The efficacy of oral betamimetics in women with a twin pregnancy is unproven. OBJECTIVES: To assess the effectiveness of prophylactic oral betamimetics for the prevention of preterm labour and birth for women with twin pregnancies. SEARCH METHODS: We searched the Cochrane Pregnancy and Childbirth Group Trials Register (21 September 2015), MEDLINE (January 1966 to 31 July 2015), EMBASE (January 1985 to 31 July 2015) and reference lists of retrieved studies. SELECTION CRITERIA: Randomised controlled trials in twin pregnancies comparing oral betamimetics with placebo or any intervention with the specific aim of preventing preterm birth. Quasi-randomised controlled trials, cluster-randomised trials and cross-over trials were not eligible for inclusion. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trials for inclusion and risk of bias, extracted data and checked them for accuracy. Two authors assessed the quality of the evidence using the GRADE approach. MAIN RESULTS: Overall, the quality of evidence is low for the primary outcomes. All of the included trials had small numbers of participants and few events. Preterm birth, the most important primary outcome, had wide confidence intervals crossing the line of no effect.Six trials (374 twin pregnancies) were included, but only five trials (344 twin pregnancies) contributed data. All trials compared oral betamimetics with placebo.Betamimetics reduced the incidence of preterm labour (two trials, 194 twin pregnancies, risk ratio (RR) 0.37; 95% confidence interval (CI) 0.17 to 0.78; low quality evidence). However, betamimetics did not reduce prelabour rupture of membranes (one trial, 144 twin pregnancies, RR 1.42; 95% CI 0.42 to 4.82; low quality evidence), preterm birth less than 37 weeks' gestation (four trials, 276 twin pregnancies, RR 0.85; 95% CI 0.65 to 1.10; low quality evidence), or less than 34 weeks' gestation (one trial, 144 twin pregnancies, RR 0.47; 95% CI 0.15 to 1.50; low quality evidence). Mean neonatal birthweight in the betamimetic group was significantly higher than in the placebo group (three trials, 478 neonates, mean difference 111.22 g; 95% CI 22.21 to 200.24). Nevertheless, there was no evidence of an effect of betamimetics in reduction of low birthweight (two trials, 366 neonates, average RR 1.19; 95% CI 0.77 to 1.85, random-effects), or small-for-gestational age neonates (two trials, 178 neonates, average RR 0.90; 95% CI 0.41 to 1.99, random-effects). Two trials showed that betamimetics significantly reduced the incidence of respiratory distress syndrome (388 neonates, RR 0.30; 95% CI 0.12 to 0.77), but the difference was not significant when the analysis was adjusted to account for the non-independence of twins (194 twins, RR 0.35; 95% CI 0.11 to 1.16). Three trials showed no evidence of an effect of betamimetics in reducing neonatal mortality, either with the unadjusted analysis, assuming twins are completely independent of each other (452 neonates, average RR 0.90; 95% CI 0.15 to 5.37, random-effects), or in the adjusted analysis, assuming non-independence of twins (226 twins, average RR 0.74; 95% CI 0.23 to 2.38, random-effects). A maternal death was reported in one trial without a significant difference between the groups (144 women, RR 2.84; 95% CI 0.12 to 68.57). AUTHORS' CONCLUSIONS: There is insufficient evidence to support or refute the use of prophylactic oral betamimetics for preventing preterm birth in women with a twin pregnancy.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos beta/administração & dosagem
Gravidez de Gêmeos
Nascimento Prematuro/prevenção & controle
Tocolíticos/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Adulto
Albuterol/administração & dosagem
Feminino
Fenoterol/administração & dosagem
Ruptura Prematura de Membranas Fetais/prevenção & controle
Idade Gestacional
Seres Humanos
Isoxsuprina/administração & dosagem
Gravidez
Ensaios Clínicos Controlados Aleatórios como Assunto
Ritodrina/administração & dosagem
Terbutalina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Tocolytic Agents); 22M9P70OQ9 (Fenoterol); I0Q6O6740J (Ritodrine); N8ONU3L3PG (Terbutaline); QF8SVZ843E (Albuterol); R15UI3245N (Isoxsuprine)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:160602
[Lr] Data última revisão:
160602
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151210
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD004733.pub4


  9 / 1724 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:26376527
[Au] Autor:Tomczyk K; Rzymski P; Wilczak M
[Ti] Título:Have we achieved progress in tocolytic treatment?--results of a retrospective cohort study in a tertiary university hospital.
[So] Source:Ginekol Pol;86(7):504-8, 2015 Jul.
[Is] ISSN:0017-0011
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Beta-agonists play an important role in tocolytic treatment. In light of recent changes in the Polish medical care system, we decided to assess the effectiveness of oral continuous treatment (in 2012) and compare it with a 3-day intravenous administration of fenoterol (in 2013). The aim of our study was to contrast cost and effectiveness of fenoterol therapy in pregnant women at risk of preterm labor during two consecutive years: 2012 - when fenoterol had been widely used (group A), and 2013 when its extensive use had been withdrawn (group B). MATERIAL AND METHODS: Retrospective cohort study of 129 pregnant women: 76 treated with intravenous fenoterol, followed by continuous oral administration (November 2012; group A), and 53 treated with intravenous fenoterol only for 48-72 hours (November 2013; group B). RESULTS: Perinatal outcomes (based on the Apgar score and neonatal weight) were comparable in both groups. Continuous oral application of fenoterol resulted in earlier gestational age at delivery and lower cost of hospitalization among women from group A as compared to group B. Regardless, the difference was not statistically significant (37 hbd vs. 35 hbd, p = 0.626; 4334,700PLN vs. 5232,470PLN, p = 0.533). CONCLUSIONS: A 3-day intravenous application of fenoterol is as effective as oral continuous therapy and is characterized by reduced risk of negative side effects.
[Mh] Termos MeSH primário: Fenoterol/uso terapêutico
Trabalho de Parto Prematuro/tratamento farmacológico
Resultado da Gravidez
Tocólise/métodos
Tocolíticos/uso terapêutico
[Mh] Termos MeSH secundário: Centros Médicos Acadêmicos
Adulto
Estudos de Coortes
Quimioterapia Combinada
Feminino
Seres Humanos
Recém-Nascido
Trabalho de Parto Prematuro/prevenção & controle
Polônia
Gravidez
Estudos Retrospectivos
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tocolytic Agents); 22M9P70OQ9 (Fenoterol)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:170303
[Lr] Data última revisão:
170303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150918
[St] Status:MEDLINE


  10 / 1724 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26073741
[Au] Autor:Soon E; Crosby A; Southwood M; Yang P; Tajsic T; Toshner M; Appleby S; Shanahan CM; Bloch KD; Pepke-Zaba J; Upton P; Morrell NW
[Ad] Endereço:1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
[Ti] Título:Bone morphogenetic protein receptor type II deficiency and increased inflammatory cytokine production. A gateway to pulmonary arterial hypertension.
[So] Source:Am J Respir Crit Care Med;192(7):859-72, 2015 Oct 01.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Mutations in bone morphogenetic protein receptor type II (BMPR-II) underlie most cases of heritable pulmonary arterial hypertension (PAH). However, disease penetrance is only 20-30%, suggesting a requirement for additional triggers. Inflammation is emerging as a key disease-related factor in PAH, but to date there is no clear mechanism linking BMPR-II deficiency and inflammation. OBJECTIVES: To establish a direct link between BMPR-II deficiency, a consequentially heightened inflammatory response, and development of PAH. METHODS: We used pulmonary artery smooth muscle cells from Bmpr2(+/-) mice and patients with BMPR2 mutations and compared them with wild-type controls. For the in vivo model, we used mice heterozygous for a null allele in Bmpr2 (Bmpr2(+/-)) and wild-type littermates. MEASUREMENTS AND MAIN RESULTS: Acute exposure to LPS increased lung and circulating IL-6 and KC (IL-8 analog) levels in Bmpr2(+/-) mice to a greater extent than in wild-type controls. Similarly, pulmonary artery smooth muscle cells from Bmpr2(+/-) mice and patients with BMPR2 mutations produced higher levels of IL-6 and KC/IL-8 after lipopolysaccharide stimulation compared with controls. BMPR-II deficiency in mouse and human pulmonary artery smooth muscle cells was associated with increased phospho-STAT3 and loss of extracellular superoxide dismutase. Chronic lipopolysaccharide administration caused pulmonary hypertension in Bmpr2(+/-) mice but not in wild-type littermates. Coadministration of tempol, a superoxide dismutase mimetic, ameliorated the exaggerated inflammatory response and prevented development of PAH. CONCLUSIONS: This study demonstrates that BMPR-II deficiency promotes an exaggerated inflammatory response in vitro and in vivo, which can instigate development of pulmonary hypertension.
[Mh] Termos MeSH primário: Receptores de Proteínas Morfogenéticas Ósseas Tipo II/deficiência
Citocinas/biossíntese
Hipertensão Pulmonar/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/uso terapêutico
Receptores de Proteínas Morfogenéticas Ósseas Tipo II/metabolismo
Óxidos N-Cíclicos/uso terapêutico
Fenoterol
Predisposição Genética para Doença
Seres Humanos
Hipertensão Pulmonar/genética
Imuno-Histoquímica
Camundongos Endogâmicos
Marcadores de Spin
Superóxido Dismutase/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cyclic N-Oxides); 0 (Cytokines); 0 (Spin Labels); 22M9P70OQ9 (Fenoterol); EC 1.15.1.1 (SOD3 protein, human); EC 1.15.1.1 (Superoxide Dismutase); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type II); U78ZX2F65X (tempol)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150616
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201408-1509OC



página 1 de 173 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde