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1.
J Am Coll Cardiol ; 37(3): 719-25, 2001 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-11693742

RESUMO

OBJECTIVES: We examined whether patients with ischemic heart disease (IHD) should be treated with nicorandil, an adenosine triphosphate-sensitive potassium channel opener, in addition to the regular use of nitrates. BACKGROUND: It has been reported that nicorandil possibly has additive effects on nitroglycerin (NTG) treatment for angina, but the mechanism is not clear. METHODS: We directly measured anterograde coronary blood flow (CBF) with a Doppler guide wire to examine the effects of intravenous administration of NTG (0.3 mg) and nicorandil (6 mg) during continuous administration of NTG at a sufficient dose (25 microg/min) in subjects with normal and stenotic coronary arteries. RESULTS: Additional systemic administration of NTG decreased anterograde CBF (normal -19.7%; stenotic -21.2%). In contrast, nicorandil increased anterograde CBF in both normal (54.6%) and stenotic (89.6%) coronary arteries, without the coronary steal phenomenon. There was a tendency toward nicorandil-dilated diameters in the patients with stenotic arteries (p = 0.06). There were no effects of additional administration on pulmonary artery wedge pressure. There was no difference in changes in heart rate and mean aortic blood pressure between NTG and nicorandil therapy. CONCLUSIONS: These results suggest that in patients treated with nitrates, additional administration of nicorandil is more useful, in terms of increasing CBF, than additional administration of nitrates. Adjunctive use of nicorandil with nitrates may provide the further benefit of myocardial protection and may improve the prognosis of patients with IHD.


Assuntos
Circulação Coronária/efeitos dos fármacos , Estenose Coronária/tratamento farmacológico , Nicorandil/farmacologia , Vasodilatadores/farmacologia , Idoso , Velocidade do Fluxo Sanguíneo/efeitos dos fármacos , Estenose Coronária/fisiopatologia , Vasos Coronários/efeitos dos fármacos , Vasos Coronários/fisiologia , Relação Dose-Resposta a Droga , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Nicorandil/uso terapêutico , Nitroglicerina/farmacologia , Fluxo Sanguíneo Regional/efeitos dos fármacos , Vasodilatadores/uso terapêutico
2.
FEBS Lett ; 373(3): 189-92, 1995 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-7589463

RESUMO

We compared the phagocytosis of immune complexes (IC) and iC3b-opsonized derivatives (iC3b-IC) by human neutrophils. The phagocytosis of iC3b-IC via Fc gamma R and CR3 was much greater than that of IC via Fc gamma R alone. Adding ethanol to the cells decreased iC3b-IC phagocytosis to that of IC, which was not affected by these reagents, suggesting that the enhanced phagocytosis is attributable to CR3-mediated phospholipase D activation. The IC phagocytosis was inhibited more effectively by anti-Fc gamma IIIB, whereas the iC3b-IC phagocytosis was partly inhibited only by anti-Fc gamma RII. The main Fc gamma R might differ in IC and iC3b-IC phagocytosis.


Assuntos
Complexo Antígeno-Anticorpo/metabolismo , Complemento C3b/metabolismo , Antígeno de Macrófago 1/imunologia , Neutrófilos/imunologia , Fagocitose , Receptores de IgG/imunologia , Complexo Antígeno-Anticorpo/imunologia , Complemento C3b/imunologia , Eletroforese em Gel de Poliacrilamida , Ativação Enzimática , Etanol/farmacologia , Humanos , Proteínas Opsonizantes/imunologia , Fagocitose/efeitos dos fármacos , Fosfolipase D/metabolismo , Propranolol/farmacologia
3.
Immunology ; 83(3): 507-11, 1994 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-7835978

RESUMO

We prepared immune complexes (IC) composed of human anti-tetanus toxoid IgG and tetanus toxoid, and examined the effect of C1q on the processing of IC by human neutrophils. Treating IC with increasing amounts of C1q enhanced the binding and phagocytosis of IC by neutrophils, unless the amounts of C1q added were less than those required to saturate the C1q binding sites of IC. With the increase of unbound excess C1q, the IC processing by neutrophils decreased. Superoxide anions generated during the processing of IC-C1q were entrapped in phagosomes and were not released from neutrophils. The C1q-dependent inhibition of IC processing by neutrophils was not observed when C1q-treated neutrophils were washed and allowed to react with IC, suggesting that the inhibition by excess C1q is due to the hindrance of IC-C1q binding to neutrophils by loosely bound C1q on neutrophils. The C1q-treated, washed neutrophils still showed enhanced responses to IC, suggesting that free C1q as well as the IC-C1q complex can prime neutrophils to enhance Fc receptor (FcR)-mediated cellular responses. Thus, C1q may have two effects on the processing of IC by neutrophils; firstly, it enhances FcR-mediated cellular responses, and secondly, it prevents superoxide anion-induced tissue damage by trapping superoxide anions in phagosomes.


Assuntos
Complexo Antígeno-Anticorpo/imunologia , Complemento C1q/imunologia , Neutrófilos/imunologia , Humanos , Imunoglobulina G/imunologia , Neutrófilos/metabolismo , Fagocitose/imunologia , Superóxidos/metabolismo , Toxoide Tetânico/imunologia
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