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1.
Inflamm Res ; 50(12): 585-91, 2001 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-11822783

RESUMO

OBJECTIVE AND DESIGN: The present study was designed to investigate the role of sex steroids in burn-induced remote organ injury. MATERIAL OR SUBJECTS: Male Wistar albino rats were given burn trauma (n=39), and underwent castration or sham operation at 2 h following the burn injury. TREATMENT: Rats were injected sc with either 17beta estradiol benzoate (E2, 10 mg/kg) or an androgen receptor blocker cyproterone acetate (CPA, 25 mg/kg) or vehicle, immediately after burn and at 12 h. METHODS: At 24 h of burn insult, rats were decapitated. Blood samples for RIA of testosterone, estradiol and tumor necrosis factor (TNF)-alpha and the tissue samples for myeloperoxidase activitiy (MPO) were taken. ANOVA student's t test was used for statistical analysis. RESULTS: Castration, antiandrogen and E2 treatments increased plasma estradiol levels and depressed burn-induced elevation in serum TNF-alpha levels. In the liver and lung, burn-induced increase in MPO was reduced by E2 and castration, while CPA was effective in reducing neutrophil infiltration only in the liver. CONCLUSION: We propose that treatment with estrogens or antiandrogens might be applicable in clinical situations to ameliorate systemic inflammation induced by burn.


Assuntos
Anti-Inflamatórios , Queimaduras/patologia , Estrogênios/farmacologia , Inflamação/tratamento farmacológico , Inflamação/patologia , Animais , Queimaduras/complicações , Estrogênios/sangue , Inflamação/etiologia , Masculino , Peroxidase/metabolismo , Radioimunoensaio , Ratos , Ratos Wistar , Testosterona/sangue , Testosterona/farmacologia , Fator de Necrose Tumoral alfa/metabolismo
2.
Intensive Care Med ; 25(10): 1155-9, 1999 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-10551975

RESUMO

OBJECTIVE: To assess whether hyperthermic (HT) preconditioning prevents the lethal effects of peritonitis by acting on the immune system. DESIGN: Prospective, controlled, experimental study. SETTING: Laboratory and animal facility of the university. MATERIALS: Adult male Sprague-Dawley rats. INTERVENTIONS: In the HT groups animals were subjected to hyperthermia (42 degrees C, 15 min) and 8 h later peritonitis (P) (n = 14) was induced. In the normothermic (NT) groups, animals were subjected to normothermia (38 degrees C, 15 min) and 8 h later peritonitis (n = 14) was induced. Each group had a corresponding sham laparotomy group (n = 14). Six rats from each group were allowed to live 7 days for survival. In the control group (n = 4), rats were not anesthetized or heat treated. MEASUREMENTS AND RESULTS: Sixteen hours after peritonitis and laparotomy, rats were killed. Blood was taken to measure the percentage of CD(4)(+), CD(8)(+), CD(4)(+)CD(56)(+), CD(8)(+) CD(11 b)(+), NK(+), B cells and the level of tumor necrosis factor. Grading of peritonitis and the measurement of free oxygen radicals in the peritoneal fluid were undertaken. All rats in the HT + P and sham laparotomy groups survived for 7 days, while in the NT + P group two rats died in 7 days. HT decreased the severity of peritonitis and increased the free oxygen radicals in the peritoneal fluid; however, the difference did not reach statistical significance. HT prevented the decrease in CD(4)(+) and B cells and the increase in CD(11 b)(+). CONCLUSIONS: HT may have a protective role in sepsis by reducing the severity of peritonitis. A causal relation between hyperthermia and an improved immune system seems possible.


Assuntos
Modelos Animais de Doenças , Hipertermia Induzida/métodos , Precondicionamento Isquêmico/métodos , Peritonite/imunologia , Peritonite/prevenção & controle , Animais , Líquido Ascítico/química , Linfócitos B/metabolismo , Antígenos CD4/sangue , Antígeno CD56/sangue , Antígenos CD8/sangue , Radicais Livres/análise , Imunofenotipagem , Células Matadoras Naturais/metabolismo , Antígeno de Macrófago 1/sangue , Masculino , Peritonite/sangue , Estudos Prospectivos , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Índice de Gravidade de Doença , Fator de Necrose Tumoral alfa/metabolismo
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