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[PMID]:29235753
[Ti] Título:The influence of heavy metal ions, spermine and sodium nitroprusside on ATP-hydrolases of cell membranes of rat colon smooth muscle.
[So] Source:Ukr Biochem J;88(4):20-8, 2016 Jul-Aug.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The specific features of functional lability of the rat colon smooth muscle (CSM) АТР-hydrolases were studied. Na+,K+-AТРase activity is effectively inhibited by divalent ions of both transition (≥ 0,1 µM) and nontransition (≥ 1 µM) heavy metals in succession by efficiency: Cu2+ > Fe2+ ≥ Cd2+ (10 µM). Polyamine spermine (0,5-1,0 mM) is a weak Na+,K+-AТРase inhibitor at saturation concentrations of ions and substrate. Sodium nitroprusside (1 mM) as nitric oxide-generating compound exhibits weak Na+,K+-AТРase inhibition only after prolonged preincubation with membranes. Mg2+-АТР-hydrolase activity in all cases is much more resistant to studied agents. Considering the example of the CSM Na+,K+-AТРase it is assumed that enzyme has specific biochemical features that contribute to its role as a potential target and redox-sensor, mediating the pathological mechanisms of heavy metal intoxication and cell oxidative damage.
[Mh] Termos MeSH primário: Adenosina Trifosfatases/metabolismo
Membrana Celular/efeitos dos fármacos
Metais Pesados/farmacologia
Nitroprussiato/farmacologia
ATPase Trocadora de Sódio-Potássio/metabolismo
Espermina/farmacologia
[Mh] Termos MeSH secundário: Adenosina Trifosfatases/antagonistas & inibidores
Animais
Cádmio/farmacologia
Cátions Bivalentes
Fracionamento Celular
Membrana Celular/metabolismo
Colo/citologia
Colo/enzimologia
Cobre/farmacologia
Ferro/farmacologia
Cinética
Masculino
Músculo Liso/citologia
Músculo Liso/enzimologia
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/enzimologia
Ratos
Ratos Wistar
ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations, Divalent); 0 (Metals, Heavy); 00BH33GNGH (Cadmium); 169D1260KM (Nitroprusside); 2FZ7Y3VOQX (Spermine); 789U1901C5 (Copper); E1UOL152H7 (Iron); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.1.- (magnesium sodium ATPase); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.04.020


  2 / 11616 MEDLINE  
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[PMID]:29227076
[Au] Autor:Danylovych HV
[Ti] Título:Evaluation of functioning of mitochondrial electron transport chain with NADH and FAD autofluorescence
[So] Source:Ukr Biochem J;88(1):31-43, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:We prove the feasibility of evaluation of mitochondrial electron transport chain function in isolated mitochondria of smooth muscle cells of rats from uterus using fluorescence of NADH and FAD coenzymes. We found the inversely directed changes in FAD and NADH fluorescence intensity under normal functioning of mitochondrial electron transport chain. The targeted effect of inhibitors of complex I, III and IV changed fluorescence of adenine nucleotides. Rotenone (5 µM) induced rapid increase in NADH fluorescence due to inhibition of complex I, without changing in dynamics of FAD fluorescence increase. Antimycin A, a complex III inhibitor, in concentration of 1 µg/ml caused sharp increase in NADH fluorescence and moderate increase in FAD fluorescence in comparison to control. NaN3 (5 mM), a complex IV inhibitor, and CCCP (10 µM), a protonophore, caused decrease in NADH and FAD fluorescence. Moreover, all the inhibitors caused mitochondria swelling. NO donors, e.g. 0.1 mM sodium nitroprusside and sodium nitrite similarly to the effects of sodium azide. Energy-dependent Ca2+ accumulation in mitochondrial matrix (in presence of oxidation substrates and Mg-ATP2- complex) is associated with pronounced drop in NADH and FAD fluorescence followed by increased fluorescence of adenine nucleotides, which may be primarily due to Ca2+- dependent activation of dehydrogenases of citric acid cycle. Therefore, the fluorescent signal of FAD and NADH indicates changes in oxidation state of these nucleotides in isolated mitochondria, which may be used to assay the potential of effectors of electron transport chain.
[Mh] Termos MeSH primário: Complexo III da Cadeia de Transporte de Elétrons/metabolismo
Complexo IV da Cadeia de Transporte de Elétrons/metabolismo
Complexo I de Transporte de Elétrons/metabolismo
Flavina-Adenina Dinucleotídeo/química
Mitocôndrias/metabolismo
NAD/química
[Mh] Termos MeSH secundário: Animais
Antimicina A/farmacologia
Cálcio/metabolismo
Carbonil Cianeto m-Clorofenil Hidrazona/farmacologia
Fracionamento Celular
Transporte de Elétrons/efeitos dos fármacos
Complexo I de Transporte de Elétrons/antagonistas & inibidores
Complexo III da Cadeia de Transporte de Elétrons/antagonistas & inibidores
Complexo IV da Cadeia de Transporte de Elétrons/antagonistas & inibidores
Inibidores Enzimáticos/farmacologia
Feminino
Flavina-Adenina Dinucleotídeo/metabolismo
Mitocôndrias/efeitos dos fármacos
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Miométrio/efeitos dos fármacos
Miométrio/metabolismo
NAD/metabolismo
Nitroprussiato/farmacologia
Imagem Óptica
Ratos
Rotenona/farmacologia
Azida Sódica/farmacologia
Nitrito de Sódio/farmacologia
Desacopladores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Uncoupling Agents); 03L9OT429T (Rotenone); 0U46U6E8UK (NAD); 146-14-5 (Flavin-Adenine Dinucleotide); 169D1260KM (Nitroprusside); 555-60-2 (Carbonyl Cyanide m-Chlorophenyl Hydrazone); 642-15-9 (Antimycin A); 968JJ8C9DV (Sodium Azide); EC 1.10.2.2 (Electron Transport Complex III); EC 1.6.5.3 (Electron Transport Complex I); EC 1.9.3.1 (Electron Transport Complex IV); M0KG633D4F (Sodium Nitrite); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.031


  3 / 11616 MEDLINE  
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[PMID]:27771299
[Au] Autor:Yannopoulos D; Bartos JA; George SA; Sideris G; Voicu S; Oestreich B; Matsuura T; Shekar K; Rees J; Aufderheide TP
[Ad] Endereço:Division of Cardiology, Department of Medicine, University of Minnesota, Minneapolis, MN, United States. Electronic address: yanno001@umn.edu.
[Ti] Título:Sodium nitroprusside enhanced cardiopulmonary resuscitation improves short term survival in a porcine model of ischemic refractory ventricular fibrillation.
[So] Source:Resuscitation;110:6-11, 2017 Jan.
[Is] ISSN:1873-1570
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Sodium nitroprusside (SNP) enhanced CPR (SNPeCPR) demonstrates increased vital organ blood flow and survival in multiple porcine models. We developed a new, coronary occlusion/ischemia model of prolonged resuscitation, mimicking the majority of out-of-hospital cardiac arrests presenting with shockable rhythms. HYPOTHESIS: SNPeCPR will increase short term (4-h) survival compared to standard 2015 Advanced Cardiac Life Support (ACLS) guidelines in an ischemic refractory ventricular fibrillation (VF), prolonged CPR model. METHODS: Sixteen anesthetized pigs had the ostial left anterior descending artery occluded leading to ischemic VF arrest. VF was untreated for 5min. Basic life support was performed for 10min. At minute 10 (EMS arrival), animals received either SNPeCPR (n=8) or standard ACLS (n=8). Defibrillation (200J) occurred every 3min. CPR continued for a total of 45min, then the balloon was deflated simulating revascularization. CPR continued until return of spontaneous circulation (ROSC) or a total of 60min, if unsuccessful. SNPeCPR animals received 2mg of SNP at minute 10 followed by 1mg every 5min until ROSC. Standard ACLS animals received 0.5mg epinephrine every 5min until ROSC. Primary endpoints were ROSC and 4-h survival. RESULTS: All SNPeCPR animals (8/8) achieved sustained ROSC versus 2/8 standard ACLS animals within one hour of resuscitation (p=0.04). The 4-h survival was significantly improved with SNPeCPR compared to standard ACLS, 7/8 versus 1/8 respectively, p=0.0019. CONCLUSION: SNPeCPR significantly improved ROSC and 4-h survival compared with standard ACLS CPR in a porcine model of prolonged ischemic, refractory VF cardiac arrest.
[Mh] Termos MeSH primário: Parada Cardíaca
Isquemia Miocárdica
Nitroprussiato/administração & dosagem
Fluxo Sanguíneo Regional/efeitos dos fármacos
Fibrilação Ventricular/complicações
[Mh] Termos MeSH secundário: Suporte Vital Cardíaco Avançado/métodos
Suporte Vital Cardíaco Avançado/mortalidade
Animais
Reanimação Cardiopulmonar/métodos
Modelos Animais de Doenças
Esquema de Medicação
Monitoramento de Medicamentos/métodos
Cardioversão Elétrica/métodos
Parada Cardíaca/etiologia
Parada Cardíaca/terapia
Isquemia Miocárdica/tratamento farmacológico
Isquemia Miocárdica/etiologia
Isquemia Miocárdica/fisiopatologia
Análise de Sobrevida
Suínos
Fatores de Tempo
Resultado do Tratamento
Vasodilatadores/administração & dosagem
Fibrilação Ventricular/fisiopatologia
Fibrilação Ventricular/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vasodilator Agents); 169D1260KM (Nitroprusside)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


  4 / 11616 MEDLINE  
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[PMID]:28973370
[Au] Autor:Song M; Wu J; Lei Y; Sun X
[Ad] Endereço:Department of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
[Ti] Título:Genetic Deletion of the NOS3 Gene in CAV1-/- Mice Restores Aqueous Humor Outflow Function.
[So] Source:Invest Ophthalmol Vis Sci;58(12):4976-4987, 2017 Oct 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The purpose of this study was to investigate the impact of genetic deletion of NOS3 in CAV1-/- mice on aqueous humor outflow function using a mouse genetic double knockout model (DKO, NOS3-/- CAV1-/-). Methods: IOP was measured in DKO, NOS3 KO, CAV1 KO, and wild-type (WT) mice by rebound tonometry. Outflow facility was measured by perfusing enucleated mouse eyes at multiple pressure steps. Sodium nitroprusside (SNP) and L-NG-nitroarginine methyl ester (L-NAME) was administered topically, whereas the contralateral eyes served as vehicle controls. IOP was measured in both eyes before drug treatment and 1 hour after the last drug treatment. Mock aqueous humor ± the nitric oxide (NO) donor SNP or NOS inhibitor L-NAME was perfused into enucleated eyes. Results: IOP was 11 ± 0.23 mm Hg in DKO mice, which was similar to WT mice and significantly lower than CAV1 KO mice (n = 18, P > 0.05). NOS3 deletion in CAV1-/- mice resulted in a 1.9-fold increase in conventional outflow facility (Ccon) compared with CAV1 KO mice (n = 7, P < 0.05). Topical application of NO donor SNP did not significantly change IOP (n = 18, P > 0.05) or Ccon in DKO mice (SNP, n = 20; vehicle, n = 11, P > 0.05). Topical application of L-NAME significantly increased IOP in WT, DKO, and CAV1 mice by reducing Ccon. Nitrotyrosine and PKG levels of DKO mice were similar to, whereas sGC was lower than, WT mice (P < 0.05). Conclusions: Genetic deletion of NOS3 in CAV1-deficient mice restored IOP and conventional aqueous humor drainage to WT level. NOS3 and CAV1 interaction is important to IOP regulation.
[Mh] Termos MeSH primário: Humor Aquoso/fisiologia
Caveolina 1/deficiência
Deleção de Genes
Óxido Nítrico Sintase Tipo III/fisiologia
[Mh] Termos MeSH secundário: Animais
Humor Aquoso/efeitos dos fármacos
Modelos Animais de Doenças
Inibidores Enzimáticos/farmacologia
Pressão Intraocular/efeitos dos fármacos
Camundongos
Camundongos Knockout
NG-Nitroarginina Metil Éster/farmacologia
Doadores de Óxido Nítrico/farmacologia
Óxido Nítrico Sintase Tipo III/genética
Nitroprussiato/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caveolin 1); 0 (Enzyme Inhibitors); 0 (Nitric Oxide Donors); 169D1260KM (Nitroprusside); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21072


  5 / 11616 MEDLINE  
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[PMID]:28966136
[Au] Autor:Raheja R; Gupta H; Pandey U; Deshpande SB
[Ad] Endereço:Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.
[Ti] Título:Lignocaine augments the in-vitro uterine contractions involving NO-guanylyl cyclase dependent mechanisms.
[So] Source:Life Sci;190:52-57, 2017 Dec 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Lignocaine is used during intrapartum and postpartum period but there are conflicting reports regarding the effect of lignocaine on uterine contractility. Therefore, this study was undertaken to delineate the effect of lignocaine on uterine contractility and the underlying mechanisms. MAIN METHODS: The in vitro contractions were recorded from the uterine segments obtained from adult rats (in estrous phase) and also from human myometrial tissue. Effect of lignocaine on spontaneous uterine contractions was recorded in the absence or presence of antagonists. Effect of sodium nitroprusside (SNP, NO donor) on uterine contractility was assessed. The NO was assayed (indicator of NO activity) from the supernatant after exposing the myometrial tissue to lignocaine in the absence or the presence of L-NAME or hemoglobin. KEY FINDINGS: Lignocaine (100µM) increased the amplitude of uterine contractions by 75% with no alterations in frequency. Similar magnitude of increase was seen with human myometrial tissue also. The spontaneous activities were absent in Ca -free or in nifedipine (10µM) containing medium. Heparin (IP blocker, 10IU/ml), but not the indomethacin (10µM) blocked the lignocaine-induced augmentation. L-NAME (NOS inhibitor, 10µM) or methylene blue (guanylyl cyclase inhibitor, 100µM) partially blocked the lignocaine-induced augmentation. SNP (30µM) increased the amplitude of spontaneous uterine contractions. Lignocaine increased the NO content (indicator of NO activity) of uterine tissue and the increase was blocked by L-NAME or hemoglobin. SIGNIFICANCE: Present observations indicate that lignocaine augments the amplitude of uterine contractions via Ca -dependent mechanisms involving NO-G cyclase-dependent mechanisms.
[Mh] Termos MeSH primário: Anestésicos Locais/farmacologia
Guanilato Ciclase/metabolismo
Lidocaína/farmacologia
Óxido Nítrico/metabolismo
Contração Uterina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Feminino
Hemoglobinas/metabolismo
Seres Humanos
NG-Nitroarginina Metil Éster/farmacologia
Nifedipino/farmacologia
Nitroprussiato/farmacologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anesthetics, Local); 0 (Hemoglobins); 169D1260KM (Nitroprusside); 31C4KY9ESH (Nitric Oxide); 98PI200987 (Lidocaine); EC 4.6.1.2 (Guanylate Cyclase); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE


  6 / 11616 MEDLINE  
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[PMID]:28882231
[Au] Autor:Lloyd JW; Nishimura RA; Borlaug BA; Eleid MF
[Ad] Endereço:Department of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota.
[Ti] Título:Hemodynamic Response to Nitroprusside in Patients With Low-Gradient Severe Aortic Stenosis and Preserved Ejection Fraction.
[So] Source:J Am Coll Cardiol;70(11):1339-1348, 2017 Sep 12.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Low-gradient severe aortic stenosis (LGSAS) with preserved ejection fraction (EF) is incompletely understood. The influence of arterial afterload and diastolic dysfunction on the hemodynamic presentation of LGSAS remains unknown. OBJECTIVES: The authors sought to determine the acute hemodynamic response to sodium nitroprusside in LGSAS with preserved EF. METHODS: Symptomatic patients with LGSAS and preserved EF underwent cardiac catheterization with comparison of hemodynamic measurements before and after nitroprusside. RESULTS: Forty-one subjects (25 with low flow [LF], stroke volume index [SVI] ≤35 ml/m , 16 with normal flow [NF]) were included. At baseline, LF patients had lower total arterial compliance (0.36 ± 0.12 ml/m /mm Hg vs. 0.48 ± 0.16 ml/m /mm Hg; p = 0.01) and greater effective arterial elastance (2.77 ± 0.84 mm Hg · m /ml vs. 1.89 ± 0.82 mm Hg · m /ml; p = 0.002). In all patients, nitroprusside reduced elastance, left ventricular filling pressures, and pulmonary artery pressures and improved compliance (p < 0.05). Aortic valve area increased to ≥1.0 cm in 6 LF (24%) and 4 NF (25%) subjects. Change in SVI with nitroprusside varied inversely to baseline SVI and demonstrated improvement in LF only (3 ± 6 ml/m ; p = 0.02). CONCLUSIONS: Nitroprusside reduces afterload and left ventricular filling pressures in patients with LGSAS and preserved EF, enabling reclassification to moderate stenosis in 25% of patients. An inverse relationship between baseline SVI and change in SVI with afterload reduction was observed, suggesting that heightened sensitivity to afterload is a significant contributor to LF-LGSAS pathophysiology. These data highlight the utility of afterload reduction in the diagnostic assessment of LGSAS.
[Mh] Termos MeSH primário: Estenose da Valva Aórtica/fisiopatologia
Hemodinâmica/efeitos dos fármacos
Nitroprussiato/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Estenose da Valva Aórtica/diagnóstico
Cateterismo Cardíaco
Relação Dose-Resposta a Droga
Ecocardiografia
Feminino
Seguimentos
Seres Humanos
Infusões Intravenosas
Masculino
Estudos Retrospectivos
Índice de Gravidade de Doença
Volume Sistólico
Vasodilatadores/administração & dosagem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vasodilator Agents); 169D1260KM (Nitroprusside)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  7 / 11616 MEDLINE  
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[PMID]:28796814
[Au] Autor:Smit B; Smulders YM; de Waard MC; Oudemans-van Straaten HM; Girbes ARJ; Eringa EC; Spoelstra-de Man AME
[Ad] Endereço:Department of Intensive Care, VU University Medical Center, Amsterdam, the Netherlands.
[Ti] Título:Hyperoxia does not directly affect vascular tone in isolated arteries from mice.
[So] Source:PLoS One;12(8):e0182637, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hospitalized patients often receive oxygen supplementation, which can lead to a supraphysiological oxygen tension (hyperoxia). Hyperoxia can have hemodynamic effects, including an increase in systemic vascular resistance. This increase suggests hyperoxia-induced vasoconstriction, yet reported direct effects of hyperoxia on vessel tone have been inconsistent. Furthermore, hyperoxia-induced changes in vessel diameter have not been studied in mice, currently the most used mammal model of disease. In this study we set out to develop a pressure-myograph model using isolated vessels from mice for investigation of pathways involved in hyperoxic vasoconstriction. Isolated conduit and resistance arteries (femoral artery and gracilis arteriole, respectively) from C57BL/6 mice were exposed to normoxia (PO2 of 80 mmHg) and three levels of hyperoxia (PO2 of 215, 375 and 665 mmHg) in a no-flow pressure myograph setup. Under the different PO2 levels, dose-response agonist induced endothelium-dependent vasodilation (acetylcholine, arachidonic acid), endothelium-independent vasodilation (s-nitroprusside), as well as vasoconstriction (norepinephrine, prostaglandin F2α) were examined. The investigated arteries did not respond to oxygen by a change in vascular tone. In the dose-response studies, maximal responses and EC50 values to any of the aforementioned agonists were not affected by hyperoxia either. We conclude that arteries and arterioles from healthy mice are not intrinsically sensitive to hyperoxic conditions. The present ex-vivo model is therefore not suitable for further research into mechanisms of hyperoxic vasoconstriction.
[Mh] Termos MeSH primário: Artéria Femoral/fisiopatologia
Hiperóxia/fisiopatologia
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Animais
Ácido Araquidônico/farmacologia
Avaliação Pré-Clínica de Medicamentos
Artéria Femoral/efeitos dos fármacos
Masculino
Camundongos Endogâmicos C57BL
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/fisiopatologia
Nitroprussiato/farmacologia
Norepinefrina/farmacologia
Oxigênio/farmacologia
Vasoconstrição
Vasoconstritores/farmacologia
Vasodilatação
Vasodilatadores/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vasoconstrictor Agents); 0 (Vasodilator Agents); 169D1260KM (Nitroprusside); 27YG812J1I (Arachidonic Acid); N9YNS0M02X (Acetylcholine); S88TT14065 (Oxygen); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182637


  8 / 11616 MEDLINE  
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[PMID]:28792879
[Au] Autor:Khot UN; Vogan ED; Militello MA
[Ad] Endereço:Cleveland Clinic, Cleveland, OH khotu@ccf.org.
[Ti] Título:Nitroprusside and Isoproterenol Use after Major Price Increases.
[So] Source:N Engl J Med;377(6):594-595, 2017 08 10.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Uso de Medicamentos/estatística & dados numéricos
Isoproterenol/uso terapêutico
Nitroprussiato/uso terapêutico
[Mh] Termos MeSH secundário: Uso de Medicamentos/economia
Hospitais
Seres Humanos
Isoproterenol/economia
Nitroprussiato/economia
Estados Unidos
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
169D1260KM (Nitroprusside); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1700244


  9 / 11616 MEDLINE  
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[PMID]:28692698
[Au] Autor:Sarkar O; Li Y; Anand-Srivastava MB
[Ad] Endereço:Department of Pharmacology and Physiology, Faculty of Medicine, University of Montréal, Montréal, Canada.
[Ti] Título:Nitric oxide attenuates overexpression of Giα proteins in vascular smooth muscle cells from SHR: Role of ROS and ROS-mediated signaling.
[So] Source:PLoS One;12(7):e0179301, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) exhibit decreased levels of nitric oxide (NO) that may be responsible for the overexpression of Giα proteins that has been shown as a contributing factor for the pathogenesis of hypertension in SHR. The present study was undertaken to investigate if increasing the intracellular levels of NO by NO donor S-Nitroso-N-acetyl-DL-penicillamine (SNAP) could attenuate the enhanced expression of Giα proteins in VSMC from SHR and explore the underlying mechanisms responsible for this response. The expression of Giα proteins and phosphorylation of ERK1/2, growth factor receptors and c-Src was determined by Western blotting using specific antibodies. Treatment of VSMC from SHR with SNAP for 24 hrs decreased the enhanced expression of Giα-2 and Giα-3 proteins and hyperproliferation that was not reversed by 1H (1, 2, 4) oxadiazole (4, 3-a) quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, however, PD98059, a MEK inhibitor restored the SNAP-induced decreased expression of Giα proteins towards control levels. In addition, the increased production of superoxide anion, NAD(P)H oxidase activity, overexpression of AT1 receptor, Nox4, p22phox and p47phox proteins, enhanced levels of TBARS and protein carbonyl, increased phosphorylation of PDGF-R, EGF-R, c-Src and ERK1/2 in VSMC from SHR were all decreased to control levels by SNAP treatment. These results suggest that NO decreased the enhanced expression of Giα-2/3 proteins and hyperproliferation of VSMC from SHR by cGMP-independent mechanism and involves ROS and ROS-mediated transactivation of EGF-R/PDGF-R and MAP kinase signaling pathways.
[Mh] Termos MeSH primário: Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/metabolismo
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/metabolismo
Óxido Nítrico/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
GMP Cíclico/análogos & derivados
GMP Cíclico/farmacologia
DNA/biossíntese
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Flavonoides/farmacologia
Masculino
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/enzimologia
NADPH Oxidases/metabolismo
Doadores de Óxido Nítrico/farmacologia
Nitroprussiato/farmacologia
Oxidiazóis/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Carbonilação Proteica/efeitos dos fármacos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Receptor Tipo 1 de Angiotensina/metabolismo
S-Nitroso-N-Acetilpenicilamina/farmacologia
Superóxidos/metabolismo
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Flavonoids); 0 (Nitric Oxide Donors); 0 (Oxadiazoles); 0 (Reactive Oxygen Species); 0 (Receptor, Angiotensin, Type 1); 0 (Thiobarbituric Acid Reactive Substances); 11062-77-4 (Superoxides); 169D1260KM (Nitroprusside); 31356-94-2 (8-bromocyclic GMP); 31C4KY9ESH (Nitric Oxide); 79032-48-7 (S-Nitroso-N-Acetylpenicillamine); 9007-49-2 (DNA); EC 1.6.3.- (NADPH Oxidases); EC 2.7.10.2 (src-Family Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gi-Go); H2D2X058MU (Cyclic GMP)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179301


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[PMID]:28669696
[Au] Autor:Ulici A; Jancik J; Lam TS; Reidt S; Calcaterra D; Cole JB
[Ad] Endereço:Department of Pharmacy, Hennepin County Medical Center, 701 Park Avenue, Minneapolis, MN 55415, United States. Electronic address: Alexandru.Ulici@hcmed.org.
[Ti] Título:Clevidipine versus sodium nitroprusside in acute aortic dissection: A retrospective chart review.
[So] Source:Am J Emerg Med;35(10):1514-1518, 2017 Oct.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: Intravenous vasodilators are often added to beta-blocking agents to reach blood pressure (BP) goals in aortic dissection. Control of BP using clevidipine has been described in hypertensive emergencies and cardiac surgery but not in aortic dissection. The aim of this study was to compare clevidipine versus sodium nitroprusside (SNP) as adjunct agents to esmolol for BP management in aortic dissection. METHODS: A single-center retrospective chart review evaluated patients diagnosed with aortic dissection. The primary outcome measure was time to reach patient specific systolic blood pressure (SBP ) goals after initiation of esmolol infusion. Efficacy of clevidipine and SNP was assessed using area under the curve analysis of positive and negative excursions outside of SBP goals (AUC ). Cost data was calculated using average wholesale price in U.S. dollars. RESULTS: Fourteen patients were included in final analyses. Median systolic BP immediately prior to initiation of esmolol was 162mm Hg vs 161mm Hg for clevidipine and SNP groups, respectively (p=0.99). Median time to reach SBP goal was similar between clevidipine and SNP (1.68 versus 1.03h [p=0.99]). Median AUC was similar for clevidipine and SNP (206.9 versus 538.9 mm Hg∗min∗hr [p=0.11]). Cost was significantly reduced using clevidipine versus SNP ($1223.28/day versus $7674.24/day [p<0.001]). CONCLUSIONS: Clevidipine administration during initial medical management of aortic dissection showed similar efficacy compared to SNP when used as adjunct therapy to esmolol. These data suggest clevidipine is a less costly, reasonable alternative to SNP in acute aortic dissection as adjunct therapy to esmolol. Further studies are needed to validate these results.
[Mh] Termos MeSH primário: Aneurisma Dissecante/tratamento farmacológico
Aneurisma da Aorta Torácica/tratamento farmacológico
Pressão Sanguínea/efeitos dos fármacos
Nitroprussiato/administração & dosagem
Piridinas/administração & dosagem
[Mh] Termos MeSH secundário: Doença Aguda
Idoso
Aneurisma Dissecante/fisiopatologia
Aneurisma da Aorta Torácica/fisiopatologia
Bloqueadores dos Canais de Cálcio/administração & dosagem
Relação Dose-Resposta a Droga
Feminino
Seguimentos
Seres Humanos
Injeções Intravenosas
Masculino
Meia-Idade
Estudos Retrospectivos
Resultado do Tratamento
Vasodilatadores/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Pyridines); 0 (Vasodilator Agents); 169D1260KM (Nitroprusside); 19O2GP3B7Q (clevidipine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE



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