Participação dos canais iônicos na hiperreatividade induzida por ovalbumina em traquéias isoladas de ratos

• Ano de defesa: 2004
• Autor(a) principal: Moura, Carlos Tiago Martins
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Canais Iônicos; Broncoconstrição; Inflamação; Ovalbumina
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/2218

In order to verify the interference of the antigenic challenge on traqueal contractility in vitro, male rats (250 -350 g) were ovalbumine (OVA)-sensitized and, 13 to 14 days later, they were challenged through the sensitizing antigen inhalation (OVA, 1 mg/ml, followed by 5 mg/ml). Animals were sacrificed immediately (SD0) or 24 hours (SD24) after the antigenic challenge through chloral hydrate anaesthesia (0,4 g/Kg). Some animals were treated with metilsergide (1 mg/Kg) 40 minutes before the challenge. Control animals (CONT) received only the vehicle (NaCl 0,9 %) by inhalation. Tracheal rings were carefully removed and mounted in a 10 ml isolated bath chamber with modified Krebs-Henseleit solution (at 37±0,5 oC) bubbled with a mixture of 5% of CO2 in 95% of O2. Concentration-effect curves (CCE) were constructed for potassium chloride (KCl), acetycholine (ACh) or serotonin (5-HT). In another experiments, CCE for Ca2+ addition were constructed under Ca2+-free conditions (with 10-5 M EDTA, nifedipine and indomethacin, 10-6 M each) in the presence of KCl, ACh or 5-HT. Sensitization and subsequent antigenic challenge (SD) promoted a significant increase of the maximal response (RM) of the CCE to KCl (force in grams, mean ± S.E.M.: CONT = 0,52 ± 0,01; SD24 = 1,22 ± 0,03; n = 06; p < 0.01), ACh (CONT = 2.11 ± 0,10; SD24 = 3,53 ± 0,03; n = 06; p < 0.01) or to 5-HT (CONT = 0,60 ± 0,03; SD24 = 1,48 ± 0,09; n = 06; p < 0.01). Tracheal rings of sensitized and challenged animals showed a rise in RM for Ca2+ only when they were pre-contracted with KCl (CONT = 0,84 ± 0,08; SD24 = 1,98 ± 0,05; n = 6; p < 0.01) or ACh (CONT = 0,98 ± 0,09; SD24 = 1,54 ± 0,15; n = 6; p < 0,05). When 5-HT was used as agonist this hyperresponsiveness did not occur, being observed only in the nifedipine absence (CONT = 0.81 ± 0,06; SD24 without nifedipine = 1,23 ± 0,08; n = 05; p < 0.01). The sensitized but not challenged animals (SENS) were compared to SD animals in the presence of niflumic acid (AN). AN inhibited the antigenic shock-induced hyperresponsiveness for 5-HT (SENS = 1,28 ± 0,09; SD24 + AN = 1.01 ± 0,08; n = 05), while it was ineffective in inhibit that for the ACh (SENS = 1,44 ± 0,01; SD24 + AN = 1,67 ± 0,03; n = 05; p < 0.01). Therefore, the results show that there is a participation of Ca2+ channels, both voltage- and receptor-operated channels, in the hyperresponsiveness of the respiratory smooth muscle, induced by the representation of the antigen to previously sensitized animals and, in addition, the Cl- channels Ca2+-activated have an important role on 5-HT hyperresponsiveness development.