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[PMID]:22235397
[Au] Autor:Sukoyan GV; Gongadze NV
[Ad] Endereço:Federal Research Center for Molecular Diagnostics and Therapy, Moscow, Russia. galinasukoian@mail.ru
[Ti] Título:Mechanism of cardioprotective effect of adenocine and non-glycoside cardiotonic drugs during experimental chronic cardiac insufficiency.
[So] Source:Bull Exp Biol Med;150(5):610-3, 2011 Mar.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The therapeutic action of adenocine during cardiac insufficiency (heart failure) caused by ischemic (stenosis) or reperfusion (removal of ligature) injury to the myocardium prevents depletion of ATP, the major energy source for myocytes in the right and left ventricles, and a drop in NAD/NADH ratio. The development of energy shortage during heart failure cannot be eliminated by ß-acetyldigoxin, levosimendan, or milrinone: the content of ATP in the right and left ventricular myocardium remained below the normal level by 28 and 29%, 37 and 33%, 32 and 28%, respectively; the NAD/NADH ratio of the energy supply system in cardiomyocytes did not return to normal. Adenocine increased the content of NAD to the normal level in both the right and left ventricles, while it remained below the normal level after administration of ß-acetyldigoxin (by 24 and 19.5%, respectively), levosimendan (by 27 and 29%), and milrinone (by 26 and 24%). In contrast to ß-acetyldigoxin, levosimendan, and milrinone, adenocine inhibited activity of poly(ADP-ribose) polymerase in both ventricles. It is concluded that adenocine directly inhibits the key enzyme triggering apoptosis; we also hypothesized that this drug activates the regulatory and signal mechanisms arresting apoptotic alterations in the myocardium during heart failure.
[Mh] Termos MeSH primário: Adenosina/farmacologia
Cardiotônicos/farmacologia
Insuficiência Cardíaca/tratamento farmacológico
Função Ventricular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetildigoxinas/farmacologia
Trifosfato de Adenosina/metabolismo
Animais
Apoptose/efeitos dos fármacos
Cardiotônicos/uso terapêutico
Constrição Patológica
Feminino
Coração/efeitos dos fármacos
Ventrículos do Coração/metabolismo
Ventrículos do Coração/patologia
Hidrazonas/farmacologia
Masculino
Milrinona/farmacologia
Miocárdio/patologia
Miócitos Cardíacos/efeitos dos fármacos
NAD/análise
NAD/efeitos dos fármacos
Inibidores de Poli(ADP-Ribose) Polimerases
Poli(ADP-Ribose) Polimerases/metabolismo
Piridazinas/farmacologia
Coelhos
Reperfusão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Cardiotonic Agents); 0 (Hydrazones); 0 (Poly(ADP-ribose) Polymerase Inhibitors); 0 (Pyridazines); 0U46U6E8UK (NAD); 349552KRHK (simendan); 8L70Q75FXE (Adenosine Triphosphate); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); JU9YAX04C7 (Milrinone); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120112
[St] Status:MEDLINE


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Fotocópia
[PMID]:21165427
[Au] Autor:Sukoyan GV; Gongadze NV
[Ad] Endereço:All-Russian Research Center for Molecular Diagnostics and Therapy, Moscow, Russia. galinasukoian@mail.ru
[Ti] Título:Comparative therapeutic efficacy of adenocin and non-glycoside cardiotonic drugs in chronic heart failure at rest and under conditions of heart overload.
[So] Source:Bull Exp Biol Med;149(6):714-7, 2010 Nov.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Experiments were performed on the model of chronic heart failure. Functional capacity of myocardial structures under conditions of maximum pressure overload was within the upper limit of normal after treatment with Adenocin. The myocardial functional reserve and potential capacity index were shown to increase to normal under these conditions. Dobutamine, levosimendan, and milrinone increased functional capacity under conditions of maximum pressure overload. Treatment with adenocin restored diastolic function of the heart under conditions of maximum pressure overload. The end-diastolic pressure increased, but remained 1.7 times below the level observed in heart failure. After treatment with dobutamine and milrinone, the end-diastolic pressure (8th episode of ligation) did not differ from the level observed in heart failure, while after administration of levosimendan this parameter decreased by 31%. Contraction-relaxation coupling was completely restored under the influence of Adenocin in all episodes of ligation both before and after removal of the ligature. Nearly all animals with heart failure were resistant to 8 episodes of ligation after treatment with Adenocin (89 vs. 96% under normal conditions). Under these conditions, the survival rate of animals after administration of levosimendan, milrinone, and dobutamine was 65, 60, and 61%, respectively, (the mortality rate of animals with heart failure was 75%). Adenocin, a cardiotonic drug with cardioprotective properties, in contrast to other cardiotonic drugs, has a modulatory effect on the system of cell energy supply, restores myocardial reserves, and improves myocardial function under conditions of overload.
[Mh] Termos MeSH primário: Acetildigoxinas/uso terapêutico
Cardiotônicos/uso terapêutico
Insuficiência Cardíaca/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Feminino
Insuficiência Cardíaca/fisiopatologia
Masculino
Coelhos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Cardiotonic Agents)
[Em] Mês de entrada:1104
[Cu] Atualização por classe:101217
[Lr] Data última revisão:
101217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:101218
[St] Status:MEDLINE


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Texto completo
[PMID]:18299848
[Au] Autor:Menke T; Neppert B
[Ad] Endereço:Klinik für Augenheilkunde, UK S-H, Campus Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Deutschland. TimMenke@aol.com
[Ti] Título:[Bilateral reduction in vision in the morning, cardiological intensive care in the evening].
[Ti] Título:Morgens beidseitige Visusminderung, abends kardiologische Intensivstation..
[So] Source:Ophthalmologe;105(6):584-7, 2008 Jun.
[Is] ISSN:0941-293X
[Cp] País de publicação:Germany
[La] Idioma:ger
[Mh] Termos MeSH primário: Acetildigoxinas/toxicidade
Antiarrítmicos/toxicidade
Arritmias Cardíacas/tratamento farmacológico
Bloqueio Atrioventricular/induzido quimicamente
Sensibilidades de Contraste
Eletrocardiografia/efeitos dos fármacos
Emergências
Escotoma/induzido quimicamente
Transtornos da Visão/induzido quimicamente
[Mh] Termos MeSH secundário: Acetildigoxinas/administração & dosagem
Antiarrítmicos/administração & dosagem
Bloqueio Atrioventricular/diagnóstico
Bradicardia/induzido quimicamente
Bradicardia/diagnóstico
Diagnóstico Diferencial
Relação Dose-Resposta a Droga
Seres Humanos
Masculino
Erros de Medicação
Meia-Idade
Escotoma/diagnóstico
Transtornos da Visão/diagnóstico
Testes de Campo Visual
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Anti-Arrhythmia Agents)
[Em] Mês de entrada:0809
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080227
[St] Status:MEDLINE
[do] DOI:10.1007/s00347-007-1630-x


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[PMID]:17152361
[Au] Autor:Sukoyan GV; Berberashvili TM; Karsanov NV
[Ad] Endereço:N. V. Karsanov Republican Research Center for Medical Biophysics and Implementation of New Biomedical Technologies, Tbilisi. galinasukoian@mail.ru
[Ti] Título:Submolecular mechanisms underlying in vitro and in vivo effect of cardiac glycosides on contractile activity of myocardial myofibrils during heart failure.
[So] Source:Bull Exp Biol Med;141(4):424-6, 2006 Apr.
[Is] ISSN:0007-4888
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The development of severe heart failure associated with toxicoallergic myocarditis is accompanied by profound structural and conformational changes in the outer domain of actin (major protein in a thin filament of cardiomyocyte sarcomere). These changes were revealed in subdomains 1 (Cys374 and Cys10) and 2 (Lys61 and Tyr69). Structural and conformational changes in the monomer and protomer of the actin thread during heart failure were energetically forbidden. Variations in the distance between amino acid residues exceeded 0.26 nm. They were partly or completely reversible in vivo under the influence of cardiotropic drug refracterin with high antihypoxic activity, as well as in vitro after treatment with digitalis preparations optimizing the concentration of ATP.
[Mh] Termos MeSH primário: Glicosídeos Cardíacos/química
Cardiopatias/patologia
Músculos/patologia
Miofibrilas/patologia
[Mh] Termos MeSH secundário: Acetildigoxinas/farmacologia
Animais
Cardiopatias/metabolismo
Técnicas In Vitro
Conformação Molecular
Contração Muscular
Contração Miocárdica
Isquemia Miocárdica/patologia
Miocardite/patologia
Miofibrilas/metabolismo
Coelhos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Cardiac Glycosides)
[Em] Mês de entrada:0707
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061213
[St] Status:MEDLINE


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[PMID]:15665959
[Au] Autor:Dzhanashiya PKh; Vladytskaya OV; Salibegashvili NV
[Ad] Endereço:Department of Visceral Diseases, Faculty for Medical Upgrading, Russian State Medical University, Moscow.
[Ti] Título:Efficiency and mechanisms of the antioxidant effect of standard therapy and refracterin in the treatment of chronic heart failure in elderly patients with postinfarction cardiosclerosis.
[So] Source:Bull Exp Biol Med;138(4):412-4, 2004 Oct.
[Is] ISSN:0007-4888
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Refracterin therapy of patients with chronic heart failure caused by coronary heart disease and postinfarction cardiosclerosis markedly promoted improvement in the pulmonary and systemic circulation in comparison with patients receiving traditional therapy. The mean functional class of chronic cardiac failure decreased by 43% under the effect of refracterin vs. 27% decrease in the group receiving traditional therapy. After 1-month refracterin course the end-systolic and end-diastolic sizes of the left ventricle decreased by 12 and 7%, respectively, ejection fraction increased by 7.2% in comparison with the initial level, total oxidant activity and MDA content in the plasma decreased significantly, while total antioxidant activity, catalase and SOD activities, cytochrome C, NADH, and NADPH levels increased. The prooxidant-antioxidant system was shifted towards antioxidants, which attests to activation of the defense and adaptive mechanisms after administration of refracterin, which is especially important in elderly patients with initially decreased reserve potentialities of the antioxidant defense system.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Cardiotônicos/uso terapêutico
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/metabolismo
[Mh] Termos MeSH secundário: Acetildigoxinas/administração & dosagem
Idoso
Idoso de 80 Anos ou mais
Antioxidantes/administração & dosagem
Cardiotônicos/administração & dosagem
Citocromos c/administração & dosagem
Combinação de Medicamentos
Insuficiência Cardíaca/patologia
Seres Humanos
Inosina/administração & dosagem
Infarto do Miocárdio/tratamento farmacológico
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/patologia
NAD/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
Oxifedrina/administração & dosagem
Esclerose
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Antioxidants); 0 (Cardiotonic Agents); 0 (Drug Combinations); 0U46U6E8UK (NAD); 5A614L51CT (Inosine); 9007-43-6 (Cytochromes c); DWL616XF1K (Oxyfedrine)
[Em] Mês de entrada:0507
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050125
[St] Status:MEDLINE


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[PMID]:15514727
[Au] Autor:Kanorskii SG; Galenko-Yaroshevskii PA; Zingilevskii KB
[Ad] Endereço:Krasnodar Research Center, Russian Academy of Medical Sciences, Administration of Krasnodar Krai; Krasnodar City Emergency Hospital.
[Ti] Título:Efficiency of refracterin in patients with chronic cardiac insufficiency caused by coronary heart disease.
[So] Source:Bull Exp Biol Med;138(1):67-9, 2004 Jul.
[Is] ISSN:0007-4888
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Composite preparation refracterin administered in a dose of 300 mg/day for 3 days in addition to routine therapy significantly improved the results of treatment of severe cardiac insufficiency of ischemic genesis compared to placebo. Improvement of clinical status of patients is determined by positive dynamics of systolic and diastolic functions of the left ventricle.
[Mh] Termos MeSH primário: Acetildigoxinas/uso terapêutico
Baixo Débito Cardíaco/tratamento farmacológico
Cardiotônicos/uso terapêutico
Doença das Coronárias/tratamento farmacológico
Citocromos c/uso terapêutico
Inosina/uso terapêutico
NAD/uso terapêutico
Oxifedrina/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Baixo Débito Cardíaco/etiologia
Doença Crônica
Doença das Coronárias/complicações
Combinação de Medicamentos
Ecocardiografia/efeitos dos fármacos
Feminino
Seres Humanos
Masculino
Meia-Idade
Sístole/efeitos dos fármacos
Resultado do Tratamento
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:CLINICAL TRIAL; COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Cardiotonic Agents); 0 (Drug Combinations); 0U46U6E8UK (NAD); 5A614L51CT (Inosine); 9007-43-6 (Cytochromes c); DWL616XF1K (Oxyfedrine)
[Em] Mês de entrada:0505
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:041030
[St] Status:MEDLINE


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[PMID]:14579055
[Au] Autor:Schrickel J; Bielik H; Yang A; Schwab JO; Shlevkov N; Schimpf R; Lüderitz B; Lewalter T
[Ad] Endereço:Medizinische Klinik und Poliklinik II, Universitätsklinikum Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. Jan.Schrickel@ukb.uni-bonn.de
[Ti] Título:Amiodarone-associated "torsade de pointes". Relevance of concomitant cardiovascular medication in a patient with atrial fibrillation and structural heart disease.
[So] Source:Z Kardiol;92(10):889-92, 2003 Oct.
[Is] ISSN:0300-5860
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A 69 year old female with history of coronary heart disease, myocardial infarction and paroxysmal atrial fibrillation suffered from occipital apoplexy. Under treatment with amiodarone 600 mg daily and concomitant medication with beta-acetyldigoxine (0.1 mg daily) and bisoprolole (1.25 mg daily), significant QT-prolongation (max. 700 ms; QTc: 614 ms) could be documented. Out of normofrequent sinus rhythm but as well out of bradycardia, the patient developed repetitive short-lasting "torsade de pointes" tachycardias (320 bpm) which terminated spontaneously. Serum electrolytes, plasma levels of digoxine (1.76 ng/ml) and amiodarone (1.9 mcg/ml) were within therapeutic range. This case report is the first to describe induction of amiodarone-associated "torsade de pointes" tachycardia during concomitant beta-blocker and digitalis medication in a patient with atrial fibrillation and structural heart disease. This points towards an elevated risk for proarrhythmia under this triple therapy.
[Mh] Termos MeSH primário: Amiodarona/efeitos adversos
Antiarrítmicos/efeitos adversos
Fibrilação Atrial/tratamento farmacológico
Insuficiência Cardíaca/tratamento farmacológico
Torsades de Pointes/induzido quimicamente
[Mh] Termos MeSH secundário: Acetildigoxinas/efeitos adversos
Acetildigoxinas/uso terapêutico
Antagonistas Adrenérgicos beta/efeitos adversos
Antagonistas Adrenérgicos beta/uso terapêutico
Idoso
Amiodarona/uso terapêutico
Antiarrítmicos/uso terapêutico
Bisoprolol/efeitos adversos
Bisoprolol/uso terapêutico
Interações Medicamentosas
Quimioterapia Combinada
Eletrocardiografia/efeitos dos fármacos
Feminino
Seres Humanos
Torsades de Pointes/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Adrenergic beta-Antagonists); 0 (Anti-Arrhythmia Agents); N3RQ532IUT (Amiodarone); Y41JS2NL6U (Bisoprolol)
[Em] Mês de entrada:0405
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:031028
[St] Status:MEDLINE


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[PMID]:11854275
[Au] Autor:Short MK; Krykbaev RA; Jeffrey PD; Margolies MN
[Ad] Endereço:Antibody Engineering Laboratory, Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
[Ti] Título:Complementary combining site contact residue mutations of the anti-digoxin Fab 26-10 permit high affinity wild-type binding.
[So] Source:J Biol Chem;277(19):16365-70, 2002 May 10.
[Is] ISSN:0021-9258
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antibody 26-10, obtained in a secondary immune response, binds digoxin with high affinity (K(a) = 1.3 x 10(10) M(-1)) because of extensive shape complementarity. We demonstrated previously that mutations of the hapten contact residue HTrp-100 to Arg (where H refers to the heavy chain) resulted in increased specificity for digoxin analogs substituted at the cardenolide 16 position. However, mutagenesis of H:CDR1 did not result in such a specificity change despite the proximity of the H:CDR1 hapten contact residue Asn-35 to the cardenolide 16 position. Here we constructed a bacteriophage-displayed library containing randomized mutations at H chain residues 30-35 in a 26-10 mutant containing Arg-100 (26-10-RRALD). Phage were selected by panning against digoxin, gitoxin (16-OH), and 16-acetylgitoxin coupled to bovine serum albumin. Clones that retained wild-type Asn at position 35 showed preferred binding to gitoxin, like the 26-10-RRALD parent. In contrast, clones containing Val-35 selected mainly on digoxin-bovine serum albumin demonstrated a shift back to wild-type specificity. Several clones containing Val-35 bound digoxin with increased affinity, approaching that of the wild type in a few instances, in contrast to the mutation Val-35 in the wild-type 26-10 background, which reduces affinity for digoxin 90-fold. It has therefore proven possible to reorder the 26-10 binding site by mutations including two major contact residues on opposite sides of the site and yet to retain high affinity for binding for digoxin. Thus, even among antibodies that have undergone affinity maturation in vivo, different structural solutions to high affinity binding may be revealed.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/química
Digoxina/análogos & derivados
Digoxina/química
Mutação
[Mh] Termos MeSH secundário: Acetildigoxinas/química
Animais
Anticorpos Monoclonais/imunologia
Arginina/química
Sítios de Ligação
Cristalografia por Raios X
Digoxina/imunologia
Digoxina/farmacologia
Ensaio de Imunoadsorção Enzimática
Vetores Genéticos
Haptenos/química
Cinética
Camundongos
Modelos Químicos
Mutagênese Sítio-Dirigida
Ligação Proteica
Albumina Sérica/química
Valina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Antibodies, Monoclonal); 0 (Haptens); 0 (Serum Albumin); 7242-07-1 (16-acetylgitoxin); 73K4184T59 (Digoxin); 94ZLA3W45F (Arginine); HG18B9YRS7 (Valine); VOR2TD6SO4 (gitoxin)
[Em] Mês de entrada:0206
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020221
[St] Status:MEDLINE


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[PMID]:11284449
[Au] Autor:Pauli-Magnus C; Mürdter T; Godel A; Mettang T; Eichelbaum M; Klotz U; Fromm MF
[Ad] Endereço:Dr. Margarete Fischer-Bosch-Institut für Klinische Pharmakologie, Stuttgart, Germany. chrispm@itsa.ucsf.edu
[Ti] Título:P-glycoprotein-mediated transport of digitoxin, alpha-methyldigoxin and beta-acetyldigoxin.
[So] Source:Naunyn Schmiedebergs Arch Pharmacol;363(3):337-43, 2001 Mar.
[Is] ISSN:0028-1298
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Digoxin is a drug with a narrow therapeutic index, which is substrate of the ATP-dependent efflux pump P-glycoprotein. Increased or decreased digoxin plasma concentrations occur in humans due to inhibition or induction of this drug transporter in organs with excretory function such as small intestine, liver and kidneys. Whereas particle size, dissolution rate and lipophilic properties have been identified as determinants for absorption of digitalis glycosides, little is known about P-glycoprotein transport characteristics of digitalis glycosides such as digitoxin, alpha-methyldigoxin, beta-acetyldigoxin and ouabain. Using polarized P-glycoprotein-expressing cell lines we therefore studied whether these compounds are substrates of P-glycoprotein. Polarized transport of digitalis glycosides was assessed in P-glycoprotein-expressing Caco-2 and L-MDR1 cells (LLC-PK1 cells stably transfected with the human MDR1 P-glycoprotein). Inhibition of P-glycoprotein-mediated transport of these compounds in Caco-2 cells was determined using the cyclosporine analogue PSC-833 (valspodar) as inhibitor of P-glycoprotein. No polarized transport was observed for ouabain. However, basal-to-apical transport of digitoxin, alpha-methyldigoxin and beta-acetyldigoxin was greater than apical-to-basal transport in Caco-2 and L-MDR1 cells. In Caco-2 cells net transport rates of these compounds were similar to those of digoxin (digoxin: 16.0+/-4.4%, digitoxin: 15.0+/-3.3%, beta-acetyldigoxin: 16.2+/-1.6%, alpha-methyldigoxin: 13.5+/-4.8%). Furthermore, polarized transport of these compounds could be completely inhibited by 1 microM PSC-833. In summary, these data provide evidence that not only digoxin, but also digitoxin, alpha-methyldigoxin and beta-acetyldigoxin are substrates of P-glycoprotein.
[Mh] Termos MeSH primário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Acetildigoxinas/farmacocinética
Cardiotônicos/farmacocinética
Digitoxina/farmacocinética
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/antagonistas & inibidores
Transporte Biológico
Células CACO-2/efeitos dos fármacos
Células CACO-2/metabolismo
Ciclosporinas/farmacologia
Seres Humanos
Medigoxina/farmacocinética
[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 (Acetyldigoxins); 0 (Cardiotonic Agents); 0 (Cyclosporins); E90NZP2L9U (Digitoxin); I7GG1YUC5V (Medigoxin); Q7ZP55KF3X (valspodar)
[Em] Mês de entrada:0105
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:010404
[St] Status:MEDLINE


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[PMID]:10498985
[Au] Autor:Karsanov NV; Sukoian GV; Dzhibgashvili IK; Tatulashvili DR; Gorelishvili II; Guchua EI
[Ti] Título:[The subcellular pathophysiology of heart failure due to toxic-allergic myocarditis and the action of refracterin on intracardiac hemodynamics and the functional state of the 3 subcellular cardiomyocyte systems responsible for the act of contraction-relaxation].
[Ti] Título:Subkletochnaia patofiziologiia nedostatochnosti serdtsa, obuslovennoi toksiko-allergicheskim miokarditom, i deistvie refrakterina na vnutriserdechnuiu gemodinamiku i funktsional'noe sostoianie trekh subkletochnykh sistem kardiomiotsita otvetstvennykh za akt sokrashchenie--rasslablenie..
[So] Source:Patol Fiziol Eksp Ter;(3):3-8, 1999 Jul-Sep.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:It is shown that cardiotropic drug refracterin promotes recovery of cardiac contraction and relaxation, their coordination destroyed in cardiac failure (CF) caused by 10-day toxico-allergic myocarditis (TAM). Pumping capacity of the heart returns to normal after normalization of functional activity of three systems of cardiomyocyte responsible for contraction-relaxation: contractile proteins, energy supply and calcium transport. The key process is refracterin-related reestablishment of normal content and proportion of adenyl nucleotides and creatininephosphate and regulation role of phosphorylation and energy of metabolic processes in the cells and their interaction. Thus, refracterin effectiveness lies in its ability to interfere in intracellular metabolic processes in the myocardium, to reestablish normal homeostasis of the systems responsible for contraction-relaxation function and eventually to remove left ventricular cardiac dysfunction.
[Mh] Termos MeSH primário: Acetildigoxinas/farmacologia
Fármacos Cardiovasculares/farmacologia
Grupo dos Citocromos c/farmacologia
Insuficiência Cardíaca/fisiopatologia
Coração/efeitos dos fármacos
Contração Miocárdica/efeitos dos fármacos
Miocardite/fisiopatologia
Miocárdio/ultraestrutura
Oxifedrina/farmacologia
[Mh] Termos MeSH secundário: Acetildigoxinas/uso terapêutico
Animais
Transporte Biológico/efeitos dos fármacos
Cálcio/metabolismo
Fármacos Cardiovasculares/uso terapêutico
Grupo dos Citocromos c/uso terapêutico
Combinação de Medicamentos
Avaliação Pré-Clínica de Medicamentos
Coração/fisiopatologia
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/etiologia
Hemodinâmica/efeitos dos fármacos
Proteínas Musculares/efeitos dos fármacos
Proteínas Musculares/fisiologia
Contração Miocárdica/fisiologia
Miocardite/complicações
Miocardite/tratamento farmacológico
Miocárdio/metabolismo
Oxifedrina/uso terapêutico
Coelhos
Fatores de Tempo
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetyldigoxins); 0 (Cardiovascular Agents); 0 (Cytochrome c Group); 0 (Drug Combinations); 0 (Muscle Proteins); DWL616XF1K (Oxyfedrine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:9910
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:990928
[St] Status:MEDLINE



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