Participação dos hormônios tireoideanos no desenvolvimento de hiperreatividade induzida pelo desafio antigênico com ovalbumina em traquèias isoladas de ratos sensibilizados

• Ano de defesa: 2005
• Autor(a) principal: Bezerra, Fernanda Carvalho
• Orientador(a): Magalhães , Pedro Jorge Caldas
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Hormônios Tireóideos; Ovalbumina; Metimazol
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/2346

In other to verify the influence of thyroid hormones on the tracheal hyperreactivity development, euthyroid, hypothyroid (propiltiouracil [PTU] - p.o. 0.05% w/v, 4 weeks) or hyperthyroid (L-tiroxine [T4] – 0.5 mg/kg s.c.,7 or 9 days) male rats (200 - 250 g) were sensitized to ovalbumine (OVA) and, 14 days later, challenged with OVA inhalation, (1 mg/ml, followed by 5 mg/ml, 15 min each). Animals sacrifice was carried out 24 later by means of anaesthesia with chloral hydrate (400 mg/Kg). Isolated trachea was mounted in 10 ml bath chamber filled with modified Krebs-Henseleit (37 oC, 5% de CO2 em O2). Concentration-effect curves (CEC) were carried out for potassium chloride (KCl), carbachol (CCh) or serotonin (5-HT). CEC to Ca2+ added in tissues maintained in Ca2+-free medium stimulated with KCl, CCh or 5-HT also were carried out. Antigenic challenge produced significant increase (p < 0.05, two-way ANOVA) of the maximal response (Emax) of the CCE for KCl from 0.96 ± 0.10 gF to 1.53 ± 0.11 gF (n = 7), for CCh from 1.98 ± 0.06 gF to 2.92 ± 0.07 gF (n = 7) and for 5-HT from 1.64 ± 0.14 gF to 2.41 ± 0.15 (n = 6) in tissues obtained from sensitized or challenged animals, respectively. Tracheae also showed increase on the Emax to Ca2+ (p < 0.05, two-way ANOVA) when stimulated with KCl from 0.54 ± 0.06 gF to 0.86 ± 0.07 gF (n = 6), with CCh from 1.20 ± 0.14 gF to 1.77 ± 0.14 gF (n = 6) or with 5-HT from 0.59 ± 0.10 gF to 1.15 ± 0.05 gF (n = 6) on sensitized or challenged tissues, respectively. The hypothyroidism did not modify significantly the KCl- or CCh-induced Emax, while the 5-HT-induced contractile effect was reduced from 1.64 ± 0.14 gF in euthyroid tissues to 0.34 ± 0.07 gF in hypothyroid tissues (p < 0.001, two-way ANOVA). After challenge, 5-HT produced in hypothyroid tissues a contraction corresponding to 0.56 ± 0.11 gF (n = 7, p < 0.001, two-way ANOVA). Hypothyroidism prevented hyperreactivity development for KCl and CCh. It was observed an increased EC50 value in CCE for CCh from 0.49 x 10-6M to 4.65 x 10-6 M (p < 0,05, two-way ANOVA). After challenge, CE50 value was reduced to 1.53 x 10-6 M (n = 6, p < 0,05, two-way ANOVA). Tracheae from challenged hypothyroid animals showed decreased Emax to Ca2+ when they were stimulated with KCl, CCh and 5-HT. It was observed an increased EC50 value in CCE to Ca2+ in challenged tissues stimulated with CCh from 5.77 x 10-4 M to 22.50 x 10-4 M (n = 6, p < 0.01, two-way ANOVA). Hyperthyroidism significantly increased Emax of the KCl-induced CCE (0.96 ± 0,10 gF in control versus 1.58 ± 0.15 on hyperthyroid tissue). Hyperreactivity was not showed after antigenic challenge (Emax = 1.87 ± 0.14 gF). It was observed a reduction of the EC50 value to CCh from 0.67 x 10-4 M in control to 0.14 x 10-4 M after T4 treatment. Our results show that there is a putative thyroid hormones involvement in hyperreactivity development on rat trachea, after an antigenic challenge.