RESUMO
1. Miconazole-induced pleurisy was characterized by edema development and leukocyte infiltration. 2. This response was inhibited by chlorpheniramine, methysergide and steroidal and nonsteroidal anti-inflammatory drugs. 3. After miconazole injection, no mast cells were found in the pleural cavity. 4. Our results support the concept that biogenic amines released from mast cells and cyclooxygenase-derived mediators may contribute to the pathogenesis and evolution of miconazole inflammation.
Assuntos
Antifúngicos/farmacologia , Leucócitos/efeitos dos fármacos , Miconazol/farmacologia , Pleurisia/induzido quimicamente , Animais , Anti-Inflamatórios/farmacologia , Antifúngicos/efeitos adversos , Movimento Celular/efeitos dos fármacos , Leucócitos/fisiologia , Masculino , Mastócitos/efeitos dos fármacos , Miconazol/efeitos adversos , Pleurisia/prevenção & controle , Ratos , Ratos Wistar , Fatores de TempoRESUMO
To investigate the significance of mast cells in the popliteal lymph node during the development of an inflammatory response, rats were inoculated with 12 x 10(7) colony-forming units of Staphylococcus aureus in the hind foot pad. Numerical changes in mast cells were then measured in the corresponding popliteal lymph node. Six days after inoculation, despite the enlargement of the responding lymph node, a marked decrease in granulated mast cell number, relative to the contralateral node, was observed in the cortical and medullary compartments. Popliteal lymph nodes from rats treated with compound 48/80 and then inoculated with S. aureus showed a higher cortical and medullary hypertrophic response and a significant increase in degranulated/weakly basophilic mast cell number in the lymph node tissue. The findings suggest that (1) Staphylococcus aureus induces a reduction in granulated mast cell number in the cortical and medullary compartments of regional lymph nodes; (2) pretreatment with compound 48/80 appears to contribute to the lymphoid cell proliferation and the hypertrophic response of lymph nodes induced by S. aureus; and (3) granulated mast cells have a regulatory role on lymphoid cell proliferation.
Assuntos
Linfonodos/patologia , Linfa/citologia , Mastócitos/fisiologia , Infecções Estafilocócicas/patologia , p-Metoxi-N-metilfenetilamina/farmacologia , Animais , Liberação de Histamina/efeitos dos fármacos , Hipertrofia/patologia , Linfa/efeitos dos fármacos , Linfa/metabolismo , Linfonodos/efeitos dos fármacos , Linfonodos/metabolismo , Masculino , Mastócitos/efeitos dos fármacos , Ratos , Ratos Wistar , Serotonina/metabolismoRESUMO
1. Subcutaneous injection of miconazole into the rat paw evoked an acute, circumscribed and long-lasting inflammation. 2. Miconazole edema presented two defined phases of rapid swelling. 3. Miconazole edema was antagonized by chlorpheniramine, dexamethasone and phenylbutazone. 4. This edema was 1.5-2 times more intense than edema due to econazole. 5. It is suggested that miconazole paw edema might be useful in the process of screening anti-inflammatory drugs.
Assuntos
Inflamação/induzido quimicamente , Miconazol/farmacologia , Animais , Edema/induzido quimicamente , Contagem de Leucócitos/efeitos dos fármacos , Masculino , Ratos , Ratos WistarRESUMO
1. Econazole released histamine from rat mast cells in vitro. This response was not affected by the addition of calcium or by prior treatment of mast cells with EDTA or cromoglycate. 2. Rat mast cells treated with econazole were stained by the vital dye trypan blue. 3. The intradermal injection of econazole increased vascular permeability. This response was antagonized by chlorpheniramine and cyproheptadine. 4. Our results demonstrate that econazole releases histamine by the "nonselective" mechanism. It is suggested that econazole inflammatory effects may be due to histamine release from mast cells.
Assuntos
Econazol/farmacologia , Liberação de Histamina/efeitos dos fármacos , Mastócitos/metabolismo , Animais , Cálcio/farmacologia , Bloqueadores dos Canais de Cálcio/farmacologia , Permeabilidade Capilar/efeitos dos fármacos , Clorfeniramina/farmacologia , Cromolina Sódica/farmacologia , Ciproeptadina/farmacologia , Ácido Edético/farmacologia , Feminino , Técnicas In Vitro , Mastócitos/efeitos dos fármacos , Ratos , Ratos Endogâmicos , Azul TripanoRESUMO
In order to study the effects of chronic malnutrition on lung surfactant, adult male Wistar rats reciving a standard diet (SD) were comparaed to animals submitted to food restriction (FR). SD rats given food and water and libitum and FR rats were allowed half (10g) of their usual food comsumption and water ad libitum, for 28 days. the evaluation of the pulmonary surfactant included pressure-volume curve with air inflation, pH and artherial blood gas measurements with rats breathing room air and 100 percent oxygen and determination of phospholipids in the lung washouts. In the pressure-volume curve, the volumes retained at 5 and 10 cmH2O of transpulmonary pressure (Tpt) and the Tpt of 40 percent of total lung capacity (TLC) were not significantly different between the two groups, showing that food restriction did not increase the surface forces. the increase in TLC/lung wet weight ratio in the FR group, probably was secondary to decrease in the elastic recoil forces in the lungs. The PaO2 did not show any significant difference between the groups. The arterial blood pH and PCO2 were also similar in both, SD and FR groups. Total phospholipid content in the lung washouts related to be weight was not signifiantly different in SD as compared with FR rats. Therefore, in this malnutrition model of rats, no alterations in pulmonary surfactant could be shown
Assuntos
Ratos , Animais , Masculino , Distúrbios Nutricionais , Pulmão/metabolismo , Surfactantes Pulmonares/metabolismo , Gasometria , Peso Corporal , Modelos Animais de Doenças , Medidas de Volume Pulmonar , Tamanho do Órgão , Fosfolipídeos/metabolismo , Pulmão/irrigação sanguínea , Ratos WistarRESUMO
Os efeitos toxicos de sudoxicam, N-(2-tiazolil)-4-hidroxi-2-metil-2H-1,2-benzotiazina-3-carboxamida 1,1-dioxido, foram estudados em ratos Wistar, determinando suas toxicidades aguda e subaguda. A DL50, baseada na mortalidade ocorrida no periodo de 6 dias apos administracao oral de dose unica de sudoxicam,foi de 144,0 mg/kg. Doses diarias, por via oral, de 1 mg/kg e 5 mg/kg durante 30 dias foram bem toleradas pelos animais. Quanto ao ganho de peso corporal e consumo de racao, nao houve diferenca significante entre os animais tratados e os do grupo controle, nesse periodo experimental. O exame macroscopico do figado, baco e rins nao revelou nenhuma lesao nos orgaos. A atividade teratogenica de sudoxicam foi testada em embrioes de galinha, injetando-o no saco vitelino de ovos embrionados de galinhas Garrinson, no 8o. dia de incubacao. Observou-se maior letalidade com a utilizacao de doses elevadas. Entretanto, nao foi constatada nenhuma malformacao nas doses de 5 micrograma/ovo e 500 micrograma/ovo