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[PMID]:29442035
[Au] Autor:Incecayir T; Ilbasmis-Tamer S; Tirnaksiz F; Degim T
[Ti] Título:Assessment of the potential drug-drug interaction between carvedilol and clopidogrel mediated through intestinal P-glycoprotein.
[So] Source:Pharmazie;71(8):472-477, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The most widely prescribed oral antiplatelet agent, clopidogrel, shows high interindividual variability resulting in an increased risk of cardiovascular events in the patients with reduced platelet inhibition. The purpose of this study was to investigate the role of the P-glycoprotein (P-gp) efflux pump in limiting the intestinal permeability of clopidogrel and the effect of a ß-blocker, namely, carvedilol, on its intestinal transport. Effective permeabilities (Peff) of clopidogrel and carvedilol were investigated in the proximal jejunum and distal ileum of rats using an in situ intestinal perfusion model. Peff values of clopidogrel and carvedilol were found to be concentration dependent with decreased Peff values at the low perfusate concentrations. Coperfusion with the P-gp inhibitors verapamil (100 µM) and carvedilol (10 µM) significantly increased the Peff of clopidogrel in the jejunum (8.31±0.20 x 10-5 and 6.98±0.75 x 10-5 vs. 3.60±0.51 x 10-5, respectively) and ileum (9.08±2.19 x 10-5 and 8.35±1.58 x 10-5 vs. 3.85±0.15 x 10-5, respectively). However, at the highest concentration tested (30 µM), clopidogrel exhibited 3 and 1.4 times higher Peff than those of metoprolol, an FDA high permeability reference standard, in the jejunum and ileum, respectively. Overall, this study indicates that the efflux function appears not to have a significant impact on the in vivo intestinal absorption of clopidogrel due to the saturation of P-gp, suggesting no clinically relevant interaction between carvedilol and clopidogrel mediated through P-gp at intestinal level.
[Mh] Termos MeSH primário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/efeitos dos fármacos
Antagonistas Adrenérgicos beta/farmacologia
Carbazóis/farmacologia
Intestino Delgado/efeitos dos fármacos
Inibidores da Agregação de Plaquetas/farmacologia
Propanolaminas/farmacologia
Ticlopidina/análogos & derivados
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/antagonistas & inibidores
Animais
Interações Medicamentosas
Absorção Intestinal/efeitos dos fármacos
Intestino Delgado/metabolismo
Masculino
Metoprolol/farmacologia
Perfusão
Permeabilidade/efeitos dos fármacos
Ratos
Ratos Wistar
Ticlopidina/farmacologia
Verapamil/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Adrenergic beta-Antagonists); 0 (Carbazoles); 0 (Platelet Aggregation Inhibitors); 0 (Propanolamines); 0K47UL67F2 (carvedilol); A74586SNO7 (clopidogrel); CJ0O37KU29 (Verapamil); GEB06NHM23 (Metoprolol); OM90ZUW7M1 (Ticlopidine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6059


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[PMID]:28469035
[Au] Autor:King KR
[Ad] Endereço:Center for Systems Biology, Massachusetts General Hospital, Boston, MA 02451, USA. Email: King.Kevin@mgh.harvard.edu.
[Ti] Título:Stunning neutrophils changes the forecast: No more showers.
[So] Source:Sci Transl Med;9(388), 2017 May 03.
[Is] ISSN:1946-6242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metoprolol inhibits neutrophil-platelet interactions and reduces microvascular obstructions after acute myocardial infarction.
[Mh] Termos MeSH primário: Infarto do Miocárdio/fisiopatologia
[Mh] Termos MeSH secundário: Plaquetas/efeitos dos fármacos
Seres Humanos
Masculino
Metoprolol/uso terapêutico
Microvasos/efeitos dos fármacos
Infarto do Miocárdio/imunologia
Neutrófilos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
GEB06NHM23 (Metoprolol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28956773
[Au] Autor:Hansson NH; Sörensen J; Harms HJ; Kim WY; Nielsen R; Tolbod LP; Frøkiær J; Bouchelouche K; Dodt KK; Sihm I; Poulsen SH; Wiggers H
[Ad] Endereço:From the Department of Cardiology (N.H.H., W.Y.K., R.N., S.H.P., H.W.) and Department of Nuclear Medicine and PET-Center (J.S., H.J.H., L.P.T., J.F., K.B.), Aarhus University Hospital, Denmark; Department of Cardiology, Horsens Regional Hospital, Denmark (K.K.D.); and Aarhus Hjerteklinik, Denmark (I
[Ti] Título:Metoprolol Reduces Hemodynamic and Metabolic Overload in Asymptomatic Aortic Valve Stenosis Patients: A Randomized Trial.
[So] Source:Circ Cardiovasc Imaging;10(10), 2017 Oct.
[Is] ISSN:1942-0080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Currently, no pharmacological treatment can modify the natural history of aortic valve stenosis (AS). This underlines the critical need to explore novel treatment strategies, which could postpone or prevent the need for aortic valve replacement in patients with asymptomatic AS. The objectives of this study were to investigate whether metoprolol reduce the hemodynamic and metabolic burden imposed by AS. METHODS AND RESULTS: In a double-blinded design, 40 patients with moderate-severe asymptomatic AS (aortic valve area, 0.5±0.1 cm /m ; peak gradient, 53±19 mm Hg) were randomized to placebo or metoprolol treatment for 22 weeks. Patients were evaluated by echocardiography, cardiovascular magnetic resonance, and C-acetate positron emission tomography. Compared with placebo, metoprolol (100±53 mg/d) decreased heart rate; mean difference (95% confidence interval) -8 minute (-13, -3; =0.003) and increased ejection time 26 ms (2, 50; =0.03). Furthermore, metoprolol reduced aortic valve peak -7 mm Hg (-13, 0; =0.05) and mean -4 mm Hg (-7, -1; =0.03) gradients, without affecting stroke volume 3 mL/m (-2, 8; =0.16). Valvuloarterial impedance (ie, global afterload) and myocardial oxygen consumption were reduced by -11% and -12% ( =0.03 and 0.01), respectively; and decreased heart rate correlated with lower valvuloarterial impedance, myocardial oxygen consumption, and improved myocardial efficiency defined as stroke work/myocardial oxygen consumption ( =0.63-0.65; all <0.01). There were 2 adverse cardiovascular events in the metoprolol group and none in the placebo group. CONCLUSIONS: In patients with asymptomatic AS, metoprolol increases systolic ejection time and reduces aortic valve gradients, global afterload, and myocardial oxygen requirements. Thus, metoprolol displays favorable hemodynamic and metabolic effects and could improve outcome in patients with asymptomatic AS. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT02076711.
[Mh] Termos MeSH primário: Antagonistas de Receptores Adrenérgicos beta 1/uso terapêutico
Estenose da Valva Aórtica/tratamento farmacológico
Valva Aórtica/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Hemodinâmica/efeitos dos fármacos
Metoprolol/uso terapêutico
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos beta 1/efeitos adversos
Idoso
Valva Aórtica/diagnóstico por imagem
Valva Aórtica/metabolismo
Valva Aórtica/fisiopatologia
Estenose da Valva Aórtica/diagnóstico por imagem
Estenose da Valva Aórtica/metabolismo
Estenose da Valva Aórtica/fisiopatologia
Doenças Assintomáticas
Dinamarca
Método Duplo-Cego
Ecocardiografia Doppler
Feminino
Seres Humanos
Imagem Cinética por Ressonância Magnética
Masculino
Metoprolol/efeitos adversos
Meia-Idade
Consumo de Oxigênio/efeitos dos fármacos
Tomografia por Emissão de Pósitrons
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Adrenergic beta-1 Receptor Antagonists); GEB06NHM23 (Metoprolol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE


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[PMID]:28882337
[Au] Autor:Li J; Chen Z; Gao X; Zhang H; Xiong W; Ju J; Xu H
[Ad] Endereço:Graduate School, Beijing University of Chinese Medicine, Beijing, China.
[Ti] Título:Meta-Analysis Comparing Metoprolol and Carvedilol on Mortality Benefits in Patients With Acute Myocardial Infarction.
[So] Source:Am J Cardiol;120(9):1479-1486, 2017 Nov 01.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although carvedilol, a nonselective beta-blocker with alpha-adrenergic blocking and multiple ancillary activities, has been demonstrated to be superior to metoprolol in chronic heart failure, it remains unclear whether the superiority of carvedilol still exists in myocardial infarction (MI). Therefore, we performed a network meta-analysis of randomized controlled trials (RCTs) to compare the 2 drugs in patients with MI. All RCTs that compared either 2 of the following interventions, carvedilol, metoprolol, and placebo, for the treatment of MI were included. The Cochrane Collaboration Central Register of Controlled Trials, Embase, and PubMed were searched thoroughly for potential eligible studies. Finally, 12 RCTs involving 61,081 patients were included. Pooled results showed that compared with placebo, carvedilol and metoprolol significantly reduced composite cardiovascular events (risk ratio [RR] 0.63; 95% credible interval [CrI] 0.41, 0.85 for carvedilol; RR 0.78; 95% CrI 0.65, 0.93 for metoprolol) and re-infarction (RR 0.57; 95% CrI 0.37, 0.84 for carvedilol; RR 0.77; 95% CrI 0.62, 0.91 for metoprolol) in patients with MI. However, neither carvedilol nor metoprolol showed significant benefits on all-cause death, cardiovascular death, revascularization, and rehospitalization. Also, no obvious difference was found when comparing carvedilol and metoprolol on primary or secondary outcomes. In conclusion, there is insufficient evidence supporting the superiority of carvedilol over metoprolol for the treatment of MI. Further studies are needed to confirm our findings.
[Mh] Termos MeSH primário: Antagonistas de Receptores Adrenérgicos alfa 1/uso terapêutico
Antagonistas de Receptores Adrenérgicos beta 1/uso terapêutico
Carbazóis/uso terapêutico
Metoprolol/uso terapêutico
Infarto do Miocárdio/mortalidade
Propanolaminas/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Masculino
Meia-Idade
Infarto do Miocárdio/tratamento farmacológico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Adrenergic alpha-1 Receptor Antagonists); 0 (Adrenergic beta-1 Receptor Antagonists); 0 (Carbazoles); 0 (Propanolamines); 0K47UL67F2 (carvedilol); GEB06NHM23 (Metoprolol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28705745
[Au] Autor:Chenoweth JA; Colby DK; Sutter ME; Radke JB; Ford JB; Nilas Young J; Richards JR
[Ad] Endereço:Department of Emergency Medicine, Division of Cardiothoracic Surgery, University of California Davis Medical Center, Sacramento, CA, United States; Division of Toxicology, Division of Cardiothoracic Surgery, University of California Davis Medical Center, Sacramento, CA, United States. Electronic add
[Ti] Título:Massive diltiazem and metoprolol overdose rescued with extracorporeal life support.
[So] Source:Am J Emerg Med;35(10):1581.e3-1581.e5, 2017 Oct.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The management of overdoses of cardioactive medications in the emergency department can be challenging. The reversal of severe toxicity from one or more types of cardioactive medication may fail maximal medical therapies and require extreme invasive measures such as transvenous cardiac pacing and extracorporeal life support. We present a case of massive diltiazem and metoprolol overdose refractory to maximal medical therapy, including intravenous calcium, glucagon, vasopressors, high dose insulin, and lipid emulsion. The patient experienced refractory bradydysrhythmia that responded only to transvenous pacing. Extracorporeal life support was initiated and resulted in successful organ perfusion and complete recovery of the patient. This case highlights the potential utility of extracorporeal life support in cases of severe toxicity due to multiple cardioactive medications.
[Mh] Termos MeSH primário: Diltiazem/envenenamento
Overdose de Drogas/terapia
Metoprolol/envenenamento
[Mh] Termos MeSH secundário: Adulto
Antiarrítmicos/envenenamento
Relação Dose-Resposta a Droga
Oxigenação por Membrana Extracorpórea/métodos
Feminino
Seguimentos
Seres Humanos
Vasodilatadores/envenenamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Vasodilator Agents); EE92BBP03H (Diltiazem); GEB06NHM23 (Metoprolol)
[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:170715
[St] Status:MEDLINE


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Brandão, Marcos Antonio Fernandes
[PMID]:28557789
[Au] Autor:Ferreira AO; Polonini HC; Loures da Silva S; Cerqueira de Melo VA; de Andrade L; Brandão MAF
[Ad] Endereço:Ortofarma-Quality Control Laboratories, Matias Barbosa, MG, Brazil. anderson@ortofarma.
[Ti] Título:Stability of Alprazolam, Atropine Sulfate, Glutamine, Levofloxacin, Metoprolol Tartrate, Nitrofurantoin, Ondansetron Hydrochloride, Oxandrolone, Pregabaline, and Riboflavin in SyrSpend SF pH4 Oral Suspensions.
[So] Source:Int J Pharm Compd;21(3):255-263, 2017 May-Jun.
[Is] ISSN:1092-4221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to evaluate the stability of 10 commonly used active pharmaceutical ingredients compounded in oral suspensions using an internationally used suspending vehicle (SyrSpend SF PH4): alprazolam 1.0 mg/mL, atropine sulfate 0.1 mg/mL, glutamine 250.0 mg/mL, levofloxacin 50.0 mg/mL, metoprolol tartrate 10.0 mg/mL, nitrofurantoin 2.0 mg/mL, ondansetron hydrochloride 0.8 mg/mL, oxandrolone 3.0 mg/mL, pregabaline 20.0 mg/mL, riboflavin 10.0 mg/mL. All suspensions were stored at both controlled refrigeration (2°C to 8°C) and controlled room temperature (20°C to 25°C). Stability was assessed by measuring the percent recovery at varying time points throughout a 90-day period. Active pharmaceutical ingredients quantification was performed by high-performance liquid chromatography via a stability-indicating method. Given the percentage of recovery of the active pharmaceutical ingredients within the suspensions, the beyond-use date of the final products (active pharmaceutical ingredients + vehicle) was at least 90 days for all suspensions with regard to both temperatures. This suggests that the vehicle is stable for compounding active pharmaceutical ingredients from different pharmacological classes.
[Mh] Termos MeSH primário: Preparações Farmacêuticas/química
Suspensões/química
[Mh] Termos MeSH secundário: Alprazolam/química
Atropina/química
Composição de Medicamentos/métodos
Estabilidade de Medicamentos
Armazenamento de Medicamentos/métodos
Glutamina/química
Levofloxacino/química
Metoprolol/química
Nitrofurantoína/química
Ondansetron/química
Oxandrolona/química
Pregabalina/química
Refrigeração/métodos
Riboflavina/química
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pharmaceutical Preparations); 0 (Suspensions); 0RH81L854J (Glutamine); 4AF302ESOS (Ondansetron); 55JG375S6M (Pregabalin); 6GNT3Y5LMF (Levofloxacin); 7C0697DR9I (Atropine); 7H6TM3CT4L (Oxandrolone); 927AH8112L (Nitrofurantoin); GEB06NHM23 (Metoprolol); TLM2976OFR (Riboflavin); YU55MQ3IZY (Alprazolam)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE


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[PMID]:28545280
[Au] Autor:Zhou M; Lu Q; Jiang JQ; Chen ZN; Gong ZG; Li ZG; Fu WW; Ding SF
[Ad] Endereço:Graduate School of Southern Medical University, Wuhan 430070, China.
[Ti] Título:[Impacts of early metoprolol intervention on connexin 43 and phosphorylated connexin 43 expression in rabbits with experimental myocardial infarction].
[So] Source:Zhonghua Xin Xue Guan Bing Za Zhi;45(4):294-298, 2017 Apr 24.
[Is] ISSN:0253-3758
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the early intervention effects of metoprolol on connexin 43(Cx43) and phosphorylated Cx43 (p-Cx43) expression in rabbits with post myocardial infarction. A total of 24 adult male New Zealand white rabbits were divided into sham group ( =6), early treatment group( =6), routine treatment group( =6), and myocardial infarction group( =6) with a randomized block design blocked by weight. Myocardial infarction was induced by left anterior descending coronary artery (LAD) ligation. Rabbits in sham group received similar surgical procedure without LAD ligation. Metoprolol (12.5 mg/kg dissolved in 2 ml distilled water) was applied to rabbits in early treatment group and routine treatment group per gavage immediately after recovery from anesthesia and at 24 hours after myocardial infarction, respectively, then treated daily for 40 days. Rabbits in sham group and myocardial infarction group received 2 ml distilled water per gavage daily for 40 days. Plasma lactate dehydrogenase (LDH) and creatine kinase (CK) level were detected by automatic biochemistry analyzer after 6 hours in all rabbits. Ventricular fibrillation threshold (VFT) was measured in vivo by bipolar pacing electrodes at 40 days. Cx43 and p-Cx43 distribution in ventricular tissue was detected by immunofluorescence analyses. Cx43 and p-Cx43 protein level in ventricular tissue was determined by Western blot. (1) Plasma LDH ((851.7±85.9)U/L vs. (332.3±39.6)U/L, <0.01) and CK ((1 192.7±105.3)U/L vs. (462.3±65.6)U/L, <0.01) were significantly higher in myocardial infarction group than in sham group (both <0.01). (2) VFT was significantly lower in myocardial infarction group than that in sham group ((470.0±91.0) beats per minute vs. (683.3±60.9) beats per minute, <0.05), and VFT was significantly higher in early treatment group ((633.3±43.2) beats per minute) and routine treatment group ((645.0±30.8) beats per minute) than in the myocardial infarction group (both <0.05). (3) Immunofluorescence analyses showed that Cx43 was mainly localized in the intercalated disk, which was perpendicular to the cell long axis with linear arrangement, and less lateral distribution in sham group, early treatment group and routine treatment group, which was significantly different as the case in the myocardial infarction group. The expression of p-Cx43 in myocardial infarction group was less than in sham group, which was significantly upregulated in in early treatment group and routine treatment group when compared with myocardial infarction group, and expression of p-Cx43 was significantly higher in early treatment group than in routine treatment group. (4)The p-Cx43/Cx43 ratio of protein was significantly lower in myocardial infarction group than in sham group (0.165±0.011 vs. 0.363±0.046, <0.05), and significantly higher in early treatment group (0.720±0.063) and routine treatment group (0.364±0.030) than in myocardial infarction group (both <0.05), and this ratio was significantly higher in early treatment group than in routine treatment group ( <0.05). Metoprolol treatment, especially the early metoprolol treatment (within 24 hours after LAD ligation), could significantly improve VFT by ameliorating the distribution and dephosphorylation of myocardial Cx43 in rabbits with experimental myocardial infarction.
[Mh] Termos MeSH primário: Conexina 43
Metoprolol/uso terapêutico
Infarto do Miocárdio
Simpatolíticos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Vasos Coronários
Ventrículos do Coração
Masculino
Miocárdio
Fosforilação
Coelhos
Fibrilação Ventricular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Sympatholytics); GEB06NHM23 (Metoprolol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3758.2017.04.008


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[PMID]:28526593
[Au] Autor:Li W; Frohwein T; Ong K
[Ad] Endereço:Internal Medicine, SUNY Upstate Medical University, United States. Electronic address: liwi@upstate.edu.
[Ti] Título:Cardiac tamponade as an initial presentation for systemic lupus erythematosus.
[So] Source:Am J Emerg Med;35(8):1213.e1-1213.e4, 2017 Aug.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease which follows a relapsing and remitting course that can manifest in any organ system. While classic manifestations consist of arthralgia, myalgia, frank arthritis, a malar rash and renal failure to name a few, cardiac tamponade, however, is a far less common and far more dangerous presentation. We highlight the case of a 61year-old male with complaints of acute onset shortness of breath and generalized body aches associated with a fever and chills in the ER. A bedside echocardiogram revealed a significant pericardial effusion concerning for pericardial tamponade. An emergent pericardiocentesis performed drained 800mL of serosanguinous fluid. While denying a history of any rash, photosensitivity, oral ulcers, or seizures, his physical examination did reveal metacarpal phalangeal joint swelling along with noted pulsus paradoxus of 15-200mmHg. Subsequent lab work revealed ANA titer of 1:630 and anti-DS DNA antibody level of 256IU/mL consistent with SLE. This case highlights cardiac tamponade as a rare but life-threatening presentation for SLE and raises the need to keep it in the differential when assessing patients presenting with pertinent exam findings.
[Mh] Termos MeSH primário: Tamponamento Cardíaco/diagnóstico
Ecocardiografia
Lúpus Eritematoso Sistêmico/diagnóstico
Derrame Pericárdico/diagnóstico
Pericardiocentese/métodos
[Mh] Termos MeSH secundário: Anti-Hipertensivos/uso terapêutico
Tamponamento Cardíaco/tratamento farmacológico
Tamponamento Cardíaco/imunologia
Fármacos Cardiovasculares/uso terapêutico
Calafrios
Diltiazem/uso terapêutico
Dispneia
Febre
Seres Humanos
Lúpus Eritematoso Sistêmico/complicações
Lúpus Eritematoso Sistêmico/tratamento farmacológico
Masculino
Metoprolol/uso terapêutico
Meia-Idade
Derrame Pericárdico/tratamento farmacológico
Derrame Pericárdico/imunologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Cardiovascular Agents); EE92BBP03H (Diltiazem); GEB06NHM23 (Metoprolol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170521
[St] Status:MEDLINE


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[PMID]:28487342
[Au] Autor:Dewenter M; Neef S; Vettel C; Lämmle S; Beushausen C; Zelarayan LC; Katz S; von der Lieth A; Meyer-Roxlau S; Weber S; Wieland T; Sossalla S; Backs J; Brown JH; Maier LS; El-Armouche A
[Ad] Endereço:From the Institute of Pharmacology (M.D., C.B., L.C.Z.) and Department of Cardiology and Pneumology (S.S.), University Medical Center Göttingen (UMG) Heart Center, Georg August University Medical School Göttingen, Germany; Department Molecular Cardiology and Epigenetics, Heidelberg University, Germa
[Ti] Título:Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic ß-Adrenoceptor Blockade in Experimental and Human Heart Failure.
[So] Source:Circ Heart Fail;10(5):e003840, 2017 May.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Considerable evidence suggests that calcium/calmodulin-dependent protein kinase II (CaMKII) overactivity plays a crucial role in the pathophysiology of heart failure (HF), a condition characterized by excessive ß-adrenoceptor (ß-AR) stimulation. Recent studies indicate a significant cross talk between ß-AR signaling and CaMKII activation presenting CaMKII as a possible downstream mediator of detrimental ß-AR signaling in HF. In this study, we investigated the effect of chronic ß-AR blocker treatment on CaMKII activity in human and experimental HF. METHODS AND RESULTS: Immunoblot analysis of myocardium from end-stage HF patients (n=12) and non-HF subjects undergoing cardiac surgery (n=12) treated with ß-AR blockers revealed no difference in CaMKII activity when compared with non-ß-AR blocker-treated patients. CaMKII activity was judged by analysis of CaMKII expression, autophosphorylation, and oxidation and by investigating the phosphorylation status of CaMKII downstream targets. To further evaluate these findings, CaMKIIδ transgenic mice were treated with the ß -AR blocker metoprolol (270 mg/kg*d). Metoprolol significantly reduced transgene-associated mortality (n≥29; <0.001), attenuated the development of cardiac hypertrophy (-14±6% heart weight/tibia length; <0.05), and strongly reduced ventricular arrhythmias (-70±22% premature ventricular contractions; <0.05). On a molecular level, metoprolol expectedly decreased protein kinase A-dependent phospholamban and ryanodine receptor 2 phosphorylation (-42±9% for P-phospholamban-S16 and -22±7% for P-ryanodine receptor 2-S2808; <0.05). However, this was paralled neither by a reduction in CaMKII autophosphorylation, oxidation, and substrate binding nor a change in the phosphorylation of CaMKII downstream target proteins (n≥11). The lack of CaMKII modulation by ß-AR blocker treatment was confirmed in healthy wild-type mice receiving metoprolol. CONCLUSIONS: Chronic ß-AR blocker therapy in patients and in a mouse model of CaMKII-induced HF is not associated with a change in CaMKII activity. Thus, our data suggest that the molecular effects of ß-AR blockers are not based on a modulation of CaMKII. Directly targeting CaMKII may, therefore, further improve HF therapy in addition to ß-AR blockade.
[Mh] Termos MeSH primário: Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo
Insuficiência Cardíaca/metabolismo
Metoprolol/farmacologia
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos beta/farmacologia
Animais
Modelos Animais de Doenças
Ecocardiografia
Insuficiência Cardíaca/diagnóstico
Insuficiência Cardíaca/tratamento farmacológico
Seres Humanos
Immunoblotting
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2); GEB06NHM23 (Metoprolol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCHEARTFAILURE.117.003840


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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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