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[PMID]:28637222
[Au] Autor:Zung A; Bier Palmon R; Golan A; Troitzky M; Eventov-Friedman S; Marom R; Keidar R; Kats N; Almashanu S; Flidel-Rimon O
[Ad] Endereço:Pediatric Endocrinology Unit, Kaplan Medical Center, and the Hebrew University of Jerusalem, Rehovot 76100, Israel.
[Ti] Título:Risk Factors for the Development of Delayed TSH Elevation in Neonatal Intensive Care Unit Newborns.
[So] Source:J Clin Endocrinol Metab;102(8):3050-3055, 2017 Aug 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Delayed thyrotropin (TSH) elevation (dTSH) is defined as elevated TSH at the second neonatal screening (after normal TSH levels at the initial screening) in premature, low-birth-weight, and ill newborns, mostly in the neonatal intensive care unit (NICU) setting. The pathogenesis of dTSH is elusive. Objective: To identify the risk factors for dTSH development among newborns in the NICU. Design, Setting, and Patients: A retrospective medical record review of neonates with dTSH was conducted in eight university-affiliated NICUs. Two controls were selected for each patient, matched for sex and birth weight. The risk factors for dTSH were identified by univariate analysis, followed by multivariate analysis. Main Outcome Measures: Maternal variables, types of NICU treatments and procedures, syndromes, and various medical conditions were compared between dTSH patients and their matched controls. Results: We enrolled 100 dTSH patients and 200 matched controls and 46 variables were compared between the two groups. Twelve risk factors for dTSH were identified on univariate analysis: cesarean section, mechanical ventilation, patent ductus arteriosus (PDA), pneumothorax, and administration of cefotaxime, vancomycin, fluconazole, dopamine, ibuprofen, furosemide, insulin, and packed red blood cells. On multivariate analysis, four risk factors were identified: PDA and vancomycin, insulin, and furosemide administration. In 26 twin pairs, in which one twin had dTSH, all variables presented similarly in both twins. Conclusions: Although some variables had direct effects on pituitary-thyroid axis dysfunction, these variables, altogether, reflect the severity of the clinical conditions in the NICU, which is the common basis for dTSH.
[Mh] Termos MeSH primário: Hipotireoidismo/diagnóstico
Tireotropina/sangue
[Mh] Termos MeSH secundário: Antibacterianos/uso terapêutico
Anti-Inflamatórios não Esteroides/uso terapêutico
Antifúngicos/uso terapêutico
Cefotaxima/uso terapêutico
Cesárea
Diuréticos/uso terapêutico
Dopamina/uso terapêutico
Permeabilidade do Canal Arterial/epidemiologia
Transfusão de Eritrócitos
Feminino
Fluconazol/uso terapêutico
Furosemida/uso terapêutico
Seres Humanos
Hipoglicemiantes/uso terapêutico
Hipotireoidismo/sangue
Ibuprofeno/uso terapêutico
Recém-Nascido de Baixo Peso
Recém-Nascido
Recém-Nascido Prematuro
Insulina/uso terapêutico
Unidades de Terapia Intensiva Neonatal
Masculino
Análise Multivariada
Triagem Neonatal
Pneumotórax/epidemiologia
Respiração Artificial
Estudos Retrospectivos
Fatores de Risco
Simpatomiméticos/uso terapêutico
Fatores de Tempo
Vancomicina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antifungal Agents); 0 (Diuretics); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Sympathomimetics); 6Q205EH1VU (Vancomycin); 7LXU5N7ZO5 (Furosemide); 8VZV102JFY (Fluconazole); 9002-71-5 (Thyrotropin); N2GI8B1GK7 (Cefotaxime); VTD58H1Z2X (Dopamine); WK2XYI10QM (Ibuprofen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00701


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[PMID]:28483802
[Au] Autor:Sassoon DJ; Tune JD; Mather KJ; Noblet JN; Eagleson MA; Conteh AM; Sturek JT; Goodwill AG
[Ad] Endereço:Department of Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN.
[Ti] Título:Glucagon-Like Peptide 1 Receptor Activation Augments Cardiac Output and Improves Cardiac Efficiency in Obese Swine After Myocardial Infarction.
[So] Source:Diabetes;66(8):2230-2240, 2017 Aug.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study tested the hypothesis that glucagon-like peptide 1 (GLP-1) therapies improve cardiac contractile function at rest and in response to adrenergic stimulation in obese swine after myocardial infarction. Obese Ossabaw swine were subjected to gradually developing regional coronary occlusion using an ameroid occluder placed around the left anterior descending coronary artery. Animals received subcutaneous injections of saline or liraglutide (0.005-0.015 mg/kg/day) for 30 days after ameroid placement. Cardiac performance was assessed at rest and in response to sympathomimetic challenge (dobutamine 0.3-10 µg/kg/min) using a left ventricular pressure/volume catheter. Liraglutide increased diastolic relaxation (dP/dt; Tau / ; Tau / ) during dobutamine stimulation ( < 0.01) despite having no influence on the magnitude of myocardial infarction. The slope of the end-systolic pressure volume relationship (i.e., contractility) increased with dobutamine after liraglutide ( < 0.001) but not saline administration ( = 0.63). Liraglutide enhanced the slope of the relationship between cardiac power and pressure volume area (i.e., cardiac efficiency) with dobutamine ( = 0.017). Hearts from animals treated with liraglutide demonstrated decreased ß1-adrenoreceptor expression. These data support that GLP-1 agonism augments cardiac efficiency via attenuation of maladaptive sympathetic signaling in the setting of obesity and myocardial infarction.
[Mh] Termos MeSH primário: Débito Cardíaco/efeitos dos fármacos
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Hipoglicemiantes/administração & dosagem
Liraglutida/administração & dosagem
Infarto do Miocárdio/tratamento farmacológico
Obesidade/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Receptor do Peptídeo Semelhante ao Glucagon 1/fisiologia
Coração/efeitos dos fármacos
Coração/fisiopatologia
Infarto do Miocárdio/etiologia
Infarto do Miocárdio/fisiopatologia
Obesidade/complicações
Obesidade/fisiopatologia
Receptores Adrenérgicos beta 1/efeitos dos fármacos
Suínos
Simpatomiméticos/administração & dosagem
Resultado do Tratamento
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Hypoglycemic Agents); 0 (Receptors, Adrenergic, beta-1); 0 (Sympathomimetics); 839I73S42A (Liraglutide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171029
[Lr] Data última revisão:
171029
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1206


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[PMID]:28480761
[Au] Autor:Dikopf MS; Vajaranant TS; Edward DP
[Ad] Endereço:a Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences , University of Illinois at Chicago , Chicago , IL , USA.
[Ti] Título:Topical treatment of glaucoma: established and emerging pharmacology.
[So] Source:Expert Opin Pharmacother;18(9):885-898, 2017 Jun.
[Is] ISSN:1744-7666
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Glaucoma is a collection of optic neuropathies consisting of retinal ganglion cell death and corresponding visual field loss. Glaucoma is the leading cause of irreversible vision loss worldwide and is forecasted to precipitously increase in prevalence in the coming decades. Current treatment options aim to lower intraocular pressure (IOP) via topical or oral therapy, laser treatment to the trabecular meshwork or ciliary body, and incisional surgery. Despite increasing use of trabecular laser therapy, topical therapy remains first-line in the treatment of most forms of glaucoma. Areas covered: Novel glaucoma therapies are a long-standing focus of investigational study. More than two decades have passed since the last United States Food and Drug Administration (FDA) approval of a topical glaucoma drug. Here, the authors review established topical glaucoma drops as well as those currently in FDA phase 2 and 3 clinical trial, nearing clinical use. Expert opinion: Current investigational glaucoma drugs lower IOP, mainly through enhanced trabecular meshwork outflow. Although few emerging therapies show evidence of retinal ganglion cell and optic nerve neuroprotection in animal models, emerging drugs are focused on lowering IOP, similar to established medicines.
[Mh] Termos MeSH primário: Glaucoma/tratamento farmacológico
Pressão Intraocular/efeitos dos fármacos
Doenças do Nervo Óptico/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Tópica
Antagonistas Adrenérgicos beta/administração & dosagem
Antagonistas Adrenérgicos beta/uso terapêutico
Animais
Inibidores da Anidrase Carbônica/administração & dosagem
Inibidores da Anidrase Carbônica/uso terapêutico
Ensaios Clínicos como Assunto
Glaucoma/metabolismo
Seres Humanos
Agonistas Muscarínicos/administração & dosagem
Agonistas Muscarínicos/uso terapêutico
Nervo Óptico/efeitos dos fármacos
Doenças do Nervo Óptico/metabolismo
Prostaglandinas/administração & dosagem
Prostaglandinas/uso terapêutico
Células Ganglionares da Retina/efeitos dos fármacos
Simpatomiméticos/administração & dosagem
Simpatomiméticos/uso terapêutico
Malha Trabecular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Carbonic Anhydrase Inhibitors); 0 (Muscarinic Agonists); 0 (Prostaglandins); 0 (Sympathomimetics)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1080/14656566.2017.1328498


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[PMID]:28431781
[Au] Autor:Al-Majed AA; Khalil NY; Khbrani I; Abdel-Aziz HA
[Ad] Endereço:College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
[Ti] Título:Clenbuterol Hydrochloride.
[So] Source:Profiles Drug Subst Excip Relat Methodol;42:91-123, 2017.
[Is] ISSN:1871-5125
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Clenbuterol (Broncodil and trade) is a direct-acting sympathomimetic agent with mainly beta-adrenergic activity and a selective action on ß2 receptors (a ß2 agonist). It has properties similar to those of salbutamol. It is used as a bronchodilator in the management of reversible airways obstruction, as in asthma and in certain patients with chronic obstructive pulmonary disease. The uses, applications, and the synthetic pathways of this drug are outlined. Physical characteristics including: ionization constant, solubility, X-ray powder diffraction pattern, thermal methods of analysis, UV spectrum, IR spectrum, mass spectrum are all produced. This profile also includes the monograph of British Pharmacopoeia, together with several reported analytical methods including spectrophotometric, electrochemical, chromatographic, immunochemical methods, and capillary electrophoretic methods. The stability, the pharmacokinetic behavior, and the pharmacology of the drug are also provided.
[Mh] Termos MeSH primário: Clembuterol
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/química
Agonistas Adrenérgicos beta/farmacocinética
Agonistas Adrenérgicos beta/farmacologia
Agonistas Adrenérgicos beta/uso terapêutico
Animais
Asma/tratamento farmacológico
Broncodilatadores/química
Broncodilatadores/farmacocinética
Broncodilatadores/farmacologia
Broncodilatadores/uso terapêutico
Clembuterol/química
Clembuterol/farmacocinética
Clembuterol/farmacologia
Clembuterol/uso terapêutico
Seres Humanos
Estrutura Molecular
Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
Simpatomiméticos/química
Simpatomiméticos/farmacocinética
Simpatomiméticos/farmacologia
Simpatomiméticos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Bronchodilator Agents); 0 (Sympathomimetics); XTZ6AXU7KN (Clenbuterol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE


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[PMID]:28414287
[Au] Autor:Tapbergenov SO; Sovetov BS; Tapbergenov AT; Hahn E
[Ad] Endereço:Department of Biochemistry and Chemical Disciplines, Semey State Medical University, Semey, Kazakhstan.
[Ti] Título:[Metabolic effects of combined introduction of adrenalin and blocker of methanoprolol beta-adrenophyleters].
[Ti] Título:Metabolicheskie éffekty sochetannogo vvedeniia adrenalina i blokatora beta-adrenoretseptorov metoprolola..
[So] Source:Biomed Khim;63(2):154-158, 2017 Mar.
[Is] ISSN:2310-6972
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The effect of combined administration of adrenaline (0.4 mg/kg, i.p.) and b1-blocker metoprolol (25 mg/kg) on the activity of glutathione peroxidase (GPO), glutathione reductase (GR), catalase, adenosine deaminase (AD), AMP deaminase (AMPD), 5¢-nucleotidase (5¢N), on the level ofmalonic dialdehyde (MDA) and conjugated dienes (CD) was investigated. In blood adrenaline administration to animals caused an increase in the activity of AMPD, AD, 5¢N and GPO, and the increase the level of CD in the blood increases. Metoprolol caused a more pronounced increase in the activity of blood AMPD, AD, 5'N and the amount of CD. In contrast to adrenaline, metoprolol decreased the MDA level of, and decreased the activity of GPO and catalase. Combined administration of metoprolol and adrenaline to animals was accompanied by an increase in the activity of AD, AMPD, 5¢N, a decrease in the activity of GR, GPO, catalase, and a decrease in MDA in the blood. In the heart, adrenaline injection was accompanied by an increase in the MDA level, a decrease in 5¢N activity and an increase in the ratio of the activities of the enzymes AD+AMPD/5¢N. Metoprolol injection reduced MDA and CD levels and the activity of GR and GPO. The combined administration of metoprolol and adrenaline in the heart was accompanied by activation of AD, AMPD and 5¢N, and a decrease in the amount of MDA and CD, and a decrease in the activity of GR, GPO, and catalase. In the liver adrenaline caused an increase in MDA and DC levels, activation of catalase, AD, AMPD, and 5¢N. Metoprolol caused a decrease in MDA and CD levels and activity of catalase and GPO, an increase in the activity of AD and AMPD in the liver. Combined administration of adrenaline and metoprolol reduced manifestations of the heart and liver oxidative stress response as compared with administration of adrenaline alone.
[Mh] Termos MeSH primário: Antagonistas de Receptores Adrenérgicos beta 1/farmacologia
Epinefrina/farmacologia
Coração/efeitos dos fármacos
Fígado/efeitos dos fármacos
Metoprolol/farmacologia
Simpatomiméticos/farmacologia
[Mh] Termos MeSH secundário: 5'-Nucleotidase/metabolismo
AMP Desaminase/metabolismo
Adenosina Desaminase/metabolismo
Animais
Animais não Endogâmicos
Antioxidantes/metabolismo
Catalase/metabolismo
Combinação de Medicamentos
Glutationa Peroxidase/metabolismo
Glutationa Redutase/metabolismo
Injeções Intraperitoneais
Fígado/metabolismo
Malondialdeído/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-1 Receptor Antagonists); 0 (Antioxidants); 0 (Drug Combinations); 0 (Sympathomimetics); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.8.1.7 (Glutathione Reductase); EC 3.1.3.5 (5'-Nucleotidase); EC 3.5.4.4 (Adenosine Deaminase); EC 3.5.4.6 (AMP Deaminase); GEB06NHM23 (Metoprolol); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.18097/PBMC20176302154


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Quevedo, Joäo
Texto completo
[PMID]:28284339
[Au] Autor:Comim CM; Freiberger V; Ventura L; Mina F; Ferreira GK; Michels M; Generoso JS; Streck EL; Quevedo J; Barichello T; Dal-Pizzol F
[Ad] Endereço:Research Group of Experimental Neuropathology, Laboratory of Experimental Neuroscience, Postgraduate Program in Health Sciences, University of South Santa Catarina, Palhoça, SC, Brazil. Electronic address: clarissamc@gmail.com.
[Ti] Título:Inhibition of indoleamine 2,3-dioxygenase 1/2 prevented cognitive impairment and energetic metabolism changes in the hippocampus of adult rats subjected to polymicrobial sepsis.
[So] Source:J Neuroimmunol;305:167-171, 2017 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection that may affect the brain. We investigated the role of indoleamine 2,3-dioxygenase (IDO-1/2) inhibition on long-term memory and energetic metabolism after experimental sepsis by caecal ligation and perforation (CLP). Experimental sepsis increased the activity of complexes I, II-III and IV at 24h after CLP, and IDO-1/2 inhibition normalized the activity of these complexes in the hippocampus. Wistar rats presented impairment of habituation and aversive memories 10days after CLP. Adjuvant treatment with the IDO inhibitor prevented long-term cognitive impairment triggered by sepsis.
[Mh] Termos MeSH primário: Transtornos Cognitivos/etiologia
Transtornos Cognitivos/metabolismo
Transtornos Cognitivos/prevenção & controle
Metabolismo Energético/fisiologia
Hipocampo/metabolismo
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Sepse/complicações
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Modelos Animais de Doenças
Metabolismo Energético/efeitos dos fármacos
Comportamento Exploratório/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Antígenos de Histocompatibilidade/metabolismo
Inibição (Psicologia)
Injeções Intra-Articulares
Masculino
Ratos
Ratos Wistar
Sepse/etiologia
Sepse/microbiologia
Estatísticas não Paramétricas
Simpatomiméticos/farmacologia
Simpatomiméticos/uso terapêutico
p-Hidroxianfetamina/farmacologia
p-Hidroxianfetamina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histocompatibility Antigens); 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (Sympathomimetics); FQR280JW2N (p-Hydroxyamphetamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


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[PMID]:28209155
[Au] Autor:Sack M; Spieler D; Wizelman L; Epple G; Stich J; Zaba M; Schmidt U
[Ad] Endereço:Technische Universität München, Klinikum rechts der Isar, Department of Psychosomatic Medicine and Psychotherapy, Langerstr. 3, 81675, München, Germany.
[Ti] Título:Intranasal oxytocin reduces provoked symptoms in female patients with posttraumatic stress disorder despite exerting sympathomimetic and positive chronotropic effects in a randomized controlled trial.
[So] Source:BMC Med;15(1):40, 2017 Feb 17.
[Is] ISSN:1741-7015
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Posttraumatic stress disorder (PTSD) is a severe psychiatric disease accompanied by neuroendocrine changes such as adrenergic overdrive and hence an elevated cardiovascular morbidity. Current pharmacotherapeutic options for PTSD are less than suboptimal, necessitating the development of PTSD-specific drugs. Although the neuropeptide oxytocin has been repeatedly suggested to be effective in PTSD treatment, there are, to our knowledge, only three studies that have assessed its efficacy on the intensity of PTSD symptoms in PTSD patients - among them one symptom provocation study in male veterans. METHODS: To evaluate for the first time how oxytocin influences the intensity of provoked PTSD symptoms and, furthermore, cardiac control in female PTSD patients, we assessed their psychic and cardiac response to trauma-script exposure with and without oxytocin pretreatment in a double-blind randomized placebo-controlled study. We used a within-subject design to study 35 female PTSD patients who received oxytocin and placebo in a 2-week interval. Furthermore, we performed a small pilot study to get an idea of the relation of the stress-modulated endogenous oxytocin levels and heart rate - we correlated oxytocin serum levels with the heart rate of 10 healthy individuals before and after exposure to the Trier Social Stress Test (TSST). RESULTS: Intranasal oxytocin treatment was followed by a reduction of provoked total PTSD symptoms, in particular of avoidance, and by an elevation in baseline and maximum heart rate together with a drop in the pre-ejection period, a marker for sympathetic cardiac control. Furthermore, we found a positive correlation between endogenous oxytocin levels and heart rate both before and after TSST challenge in healthy control subjects. CONCLUSIONS: This study provides the first evidence that oxytocin treatment reduces the intensity of provoked PTSD symptoms in female PTSD patients. The small size of both samples and the heterogeneity of the patient sample restrict the generalizability of our findings. Future studies have to explore the gender dependency and the tolerability of the oxytocin-mediated increase in heart rate. This randomized controlled trial was retrospectively registered at the German Trials Register (DRKS00009399) on the 02 October 2015.
[Mh] Termos MeSH primário: Ocitocina/uso terapêutico
Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Intranasal
Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
Simpatomiméticos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Sympathomimetics); 50-56-6 (Oxytocin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170218
[St] Status:MEDLINE
[do] DOI:10.1186/s12916-017-0801-0


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[PMID]:28202248
[Au] Autor:Okada S; Yamaguchi N
[Ad] Endereço:Department of Pharmacology, Graduate School of Medicine, Aichi Medical University, 1-1 Yazakokarimata, Nagakute, Aichi 480-1195, Japan. Electronic address: okadas@aichi-med-u.ac.jp.
[Ti] Título:Possible role of adrenoceptors in the hypothalamic paraventricular nucleus in corticotropin-releasing factor-induced sympatho-adrenomedullary outflow in rats.
[So] Source:Auton Neurosci;203:74-80, 2017 Mar.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: A functional interaction between the corticotropin-releasing factor (CRF) system and noradrenergic neurons in the brain has been suggested. In the present study, we investigated the interrelationship between the central CRF-induced elevation of plasma catecholamines and adrenoceptor activation in the paraventricular nucleus of the hypothalamus (PVN) using urethane-anesthetized rats. MAIN METHODS: In rats under urethane anesthesia, a femoral venous line was inserted for infusion of saline, and a femoral arterial line was inserted for collecting blood samples. Next, animals were placed in a stereotaxic apparatus for the application of test agents. Catecholamines in the plasma were extracted by alumina absorption and were assayed with high-performance liquid chromatography with electrochemical detection. Quantification of noradrenaline in rat PVN microdialysates was performed with high-performance liquid chromatography with electrochemical detection. KEY FINDINGS: We showed that centrally administered CRF elevated noradrenaline release in the PVN. Furthermore, we demonstrated that microinjection of phenylephrine into the PVN induced elevation of plasma levels of adrenaline, but not of noradrenaline, whereas microinjection of isoproterenol into the PVN induced elevation of plasma levels of noradrenaline, but not of adrenaline. Bilateral blockade of adrenoceptors in the PVN revealed that phentolamine significantly suppressed the CRF-induced elevation of plasma adrenaline level, while propranolol significantly CRF-induced elevation of plasma noradrenaline level. SIGNIFICANCE: Our results suggest that centrally administered CRF-induced elevation of plasma levels of adrenaline and noradrenaline can be mediated via activation of α-adrenoceptors and ß-adrenoceptors, respectively, in the rat PVN.
[Mh] Termos MeSH primário: Medula Suprarrenal/efeitos dos fármacos
Hormônio Liberador da Corticotropina/administração & dosagem
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Receptores Adrenérgicos alfa/metabolismo
Receptores Adrenérgicos beta/metabolismo
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Medula Suprarrenal/metabolismo
Adrenérgicos/farmacologia
Anestésicos Intravenosos/farmacologia
Animais
Hormônio Liberador da Corticotropina/metabolismo
Epinefrina/sangue
Isoproterenol/farmacologia
Masculino
Norepinefrina/sangue
Núcleo Hipotalâmico Paraventricular/metabolismo
Fentolamina/farmacologia
Fenilefrina/farmacologia
Propranolol/farmacologia
Ratos Wistar
Sistema Nervoso Simpático/metabolismo
Simpatomiméticos/farmacologia
Uretana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Anesthetics, Intravenous); 0 (Receptors, Adrenergic, alpha); 0 (Receptors, Adrenergic, beta); 0 (Sympathomimetics); 1WS297W6MV (Phenylephrine); 3IN71E75Z5 (Urethane); 9015-71-8 (Corticotropin-Releasing Hormone); 9Y8NXQ24VQ (Propranolol); L628TT009W (Isoproterenol); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE


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[PMID]:28114580
[Au] Autor:Turnbull PR; Irani N; Lim N; Phillips JR
[Ad] Endereço:School of Optometry and Vision Science, The University of Auckland, Auckland, New Zealand.
[Ti] Título:Origins of Pupillary Hippus in the Autonomic Nervous System.
[So] Source:Invest Ophthalmol Vis Sci;58(1):197-203, 2017 Jan 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The purpose of this study was to determine the relative roles of the sympathetic (SNS) and parasympathetic nervous system (PNS) in pupillary hippus. Methods: We used a paired-eye control study design with three cohorts receiving either 1.0% tropicamide (PNS antagonist) in light (TL), 1.0% tropicamide in dark (TD), or 10% phenylephrine (SNS) in light (PL), n = 12 in each. Each subject received one drop to the randomly determined treatment eye, while the other eye served as control. Bilateral measures of pupil size and dynamics were made over 2.6 seconds using an infrared eye-tracker sampling at 500 Hz. Measures were taken at baseline, then every 5 minutes for 40 minutes. Hippus, analyzed in both time and frequency domains, was compared between eyes and cohorts. Results: Pupillary hippus with a distinct dominant frequency was present in all measures at baseline (mean: 0.62 Hz, SD: 0.213 Hz), and that frequency did not change in any group (P = 0.971). Hippus magnitude (treatment eye relative to control eye) decreased in the TL (-72.8 ± 4.7%, P < 0.0001) and TD (-71.3 ± 2.6%, P < 0.0001) groups, but did not change in the PL (+5.4 ± 13.7%, P = 0.173) group, despite PL pupils dilating to a proportion similar to TD. Conclusions: Pupillary hippus can be extinguished by antagonizing the PNS, whereas agonizing the SNS dilates the pupil without affecting hippus. This suggests that hippus originates from central PNS activity, and not from SNS activity, or oscillations in the balance between PNS and SNS at the pupil.
[Mh] Termos MeSH primário: Adaptação Ocular/fisiologia
Sistema Nervoso Autônomo/fisiopatologia
Fenilefrina/farmacologia
Distúrbios Pupilares/etiologia
Pupila/fisiologia
Reflexo Pupilar/fisiologia
Tropicamida/farmacologia
[Mh] Termos MeSH secundário: Adulto
Sistema Nervoso Autônomo/efeitos dos fármacos
Feminino
Seres Humanos
Luz
Masculino
Midriáticos/farmacologia
Soluções Oftálmicas
Estimulação Luminosa
Distúrbios Pupilares/diagnóstico
Distúrbios Pupilares/fisiopatologia
Reflexo Pupilar/efeitos dos fármacos
Simpatomiméticos/farmacologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mydriatics); 0 (Ophthalmic Solutions); 0 (Sympathomimetics); 1WS297W6MV (Phenylephrine); N0A3Z5XTC6 (Tropicamide)
[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:170124
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-20785


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[PMID]:28076873
[Au] Autor:Eberhart LH; Bein B
[Ti] Título:Intraoperative Hypotonie: Therapie..
[So] Source:Anasthesiol Intensivmed Notfallmed Schmerzther;52(1):45-54, 2017 Jan.
[Is] ISSN:1439-1074
[Cp] País de publicação:Germany
[La] Idioma:ger
[Mh] Termos MeSH primário: Hipotensão/diagnóstico
Hipotensão/tratamento farmacológico
Hipotensão/prevenção & controle
Complicações Intraoperatórias/tratamento farmacológico
Complicações Intraoperatórias/prevenção & controle
Simpatomiméticos/administração & dosagem
[Mh] Termos MeSH secundário: Anestesia/efeitos adversos
Determinação da Pressão Arterial/métodos
Seres Humanos
Complicações Intraoperatórias/diagnóstico
Monitorização Intraoperatória/métodos
Oximetria/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Sympathomimetics)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170126
[Lr] Data última revisão:
170126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.1055/s-0042-106074



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