Minoguchi K, Kobayashi H, Sunouchi K, Hoshino H, Konno S, Okazawa A, Kokubu F, Mita S, Adachi M, Takahashi T
Department of First Internal Medicine, Showa University School of Medicine.
Arerugi. 1991 Feb;40(2):164-7.
We have previously demonstrated that airway responsiveness was enhanced following a late bronchial response (LBR) after an allergen challenge in ovalbumin (OA)-sensitized guinea pigs. The purpose of the present studies was to evaluate whether airway responsiveness to methacholine increased after an immediate bronchial response (IBR) and the possible involvement of the beta-adrenoceptor dysfunction in OA-sensitized guinea pigs. Guinea pigs were actively sensitized by aerosolized OA. Following OA exposure, IBR appeared. After IBR when specific airway resistance returned to the base line value, airway responsiveness to methacholine increased significantly. Before OA exposure, propranolol induced bronchoconstriction (PIB) was not provoked, however, after IBR, PIB was provoked and the guinea pigs died because of severe bronchoconstriction. These results suggest that airway responsiveness to methacholine increases significantly after IBR. Furthermore, the dysfunction of the beta-adrenoceptor may be a mechanism of this hyperresponsiveness in OA-sensitized guinea pigs.
我们之前已经证明，在卵清蛋白（OA）致敏的豚鼠中，变应原激发后出现迟发性支气管反应（LBR），气道反应性会增强。本研究的目的是评估在即刻支气管反应（IBR）后，OA致敏豚鼠对乙酰甲胆碱的气道反应性是否增加，以及β-肾上腺素能受体功能障碍是否可能参与其中。豚鼠通过雾化OA进行主动致敏。暴露于OA后，出现IBR。IBR后，当特异性气道阻力恢复到基线值时，对乙酰甲胆碱的气道反应性显著增加。在暴露于OA之前，普萘洛尔诱发的支气管收缩（PIB）未被激发，然而，IBR后，PIB被激发，豚鼠因严重支气管收缩而死亡。这些结果表明，IBR后对乙酰甲胆碱的气道反应性显著增加。此外，β-肾上腺素能受体功能障碍可能是OA致敏豚鼠这种高反应性的一种机制。
