TY - T1的反复过敏原接触提高兴奋性nonadrenergic noncholinergic nerve-mediated在敏化因为豚鼠支气管收缩JF -欧洲呼吸杂志》乔和J SP - 1439 LP - 1444欧元六世- 9 - 7盟Kageyama N盟——Ichinose M AU - Igarashi),非盟——三浦,M盟,山内H盟——佐佐木,Y盟—石川,J盟——Tomaki M盟——Shirato K Y1 - 1996/07/01 UR - //www.qdcxjkg.com/content/9/7/1439.abstract N2 -反复过敏原吸入对呼吸道的影响兴奋nonadrenergic noncholinergic (e-NANC) nerve-mediated支气管收缩的反应,研究了在卵白蛋白(OA)敏化因为豚鼠。三周后敏感、OA吸入0.03% 3分钟(挑战组),或吸入生理盐水(对照组)4周每天重复。e-NANC神经功能检查在体外通过等距张力测量主支气管。与阿托品预处理后(10 (6)M)和普萘洛尔(10(6)米),我们进行了电场刺激(EFS)或外源性神经激肽A (NKA)管理。In the challenged group, EFS-induced main bronchial contraction was significantly greater than that of the control group (p < 0.05 or p < 0.01), but exogenous NKA-mediated responses were almost the same in both groups. The e-NANC-induced main bronchial contractions after EFS were enhanced by pretreatment with the neutral endopeptidase inhibitor, phosphoramidon, to the same degree in the control and challenged groups, indicating that the peptide degradation mechanisms were not impaired even in the challenged group. Substance P immunoreactivities in the lung of the challenged group were significantly higher than those of the control group. These results suggest that chronic airway inflammation after repeated allergen challenge increases excitatory nonadrenergic noncholinergic nerve function, possibly by enhancing sensory neuropeptide production and/or release. ER -