Putative involvement of the thyroid hormones in hyperreactivity development induced by antigenic challenge with ovalbumin on ovalbumin-sensitized rat isolated tracheae. / Participação dos hormônios tireoideanos no desenvolvimento de hiperreatividade induzida pelo desafio antigênico com ovalbumina em traquèias isoladas de ratos sensibilizados

Fernanda Carvalho Bezerra

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.

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