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目的 观察氯胺酮雾化吸入对哮喘大鼠气道炎症的影响及其机制。方法 雄性SD大鼠40只,随机分成对照组(N组)、哮喘模型组(A组)和不同浓度氯胺酮预处理组(K1组、K2组和K3组),每组8只。A组用卵蛋白(OA)辅以百日咳杆菌菌苗和氢氧化铝为佐剂注射致敏,两周后雾化吸入OA激发。K1、K2、K3组大鼠以同样方法致敏,但在激发前分别雾化吸入氯胺酮12.5、25、50mg／ml。N组注射和吸入生理盐水。取血分离淋巴细胞,检测胞浆和胞膜内蛋白激酶C(PKC)的活性,并作肺组织病理学检查。结果 A组肺组织切片显示为急性气道炎症性病理改变。K1组气道壁上皮细胞脱落、结构破坏、炎性细胞浸润等改变多见。K2组支气管壁、肺泡间隔仅见少量的炎症细胞。K3组气道黏膜上皮水肿脱落、黏膜下炎症细胞浸润等程度减轻。与N组比较,A、K1、K3组淋巴细胞PKC总活性(PKCT)、胞浆PKC活性(PKCC)、胞膜PKC活性(PKCM)及PKCM％(PKCM占PKCT的百分比)均增高(P<0.01),K2组PKCT、PKCC、PKCM增高(P<0.01)、PKCM％差异无显著性(P>0.05)。与A组比较,K2、K3组PKCT、PKCC、PKCM及PKCM％均减低(P<0.05或0.01),K1组PKCT、PKCC、PKCM均降低(P<0.01)、PKCM％差异无显著性(P>0.05)。结论 雾化吸入氯胺酮25 mg／ml或50 mg/ml通过PKC途径而发挥抗炎效应,对致敏原所激发的气
Objective To observe the effect of ketamine inhalation on airway inflammation in asthmatic rats and its mechanism. Methods Forty male Sprague-Dawley rats were randomly divided into control group (N group), asthma model group (A group) and ketamine pretreatment group (K1 group, K2 group and K3 group) with 8 rats in each group. A group with ovalbumin (OA) supplemented with Bordetella pertussis vaccine and aluminum hydroxide as an adjuvant injection sensitized, two weeks after inhalation of OA inspired by atomization. Rats in K1, K2 and K3 groups were sensitized in the same way but were inhaled with ketamine 12.5, 25 and 50 mg / ml respectively before challenge. Group N was injected and inhaled saline. Blood was collected to separate lymphocytes, and the activities of protein kinase C (PKC) in cytoplasm and cytoplasm were detected, and lung histopathological examination was performed. Results A group of lung tissue sections showed acute airway inflammatory pathological changes. K1 group of airway wall epithelial cells shedding, structural damage, inflammatory cell infiltration and other changes more common. K2 group bronchial wall, alveolar septum only a small amount of inflammatory cells. K3 group mucosal epithelial edema loss, submucosal inflammatory cell infiltration extent reduced. Compared with N group, PKC, PKC, PKCM and PKCM% of lymphocytes in groups A, K1 and K3 were significantly increased (P < 0.01). The levels of PKCT, PKCC and PKCM in group K2 were increased (P <0.01), while there was no significant difference in PKCM% (P> 0.05). Compared with group A, the levels of PKCT, PKCC, PKCM and PKCM in group K2 and K3 were decreased (P <0.05 or 0.01), but PKCK, PKCM and PKCM in group K1 were decreased (P <0.01) > 0.05). Conclusion Inhalation of ketamine 25 mg / ml or 50 mg / ml through the PKC pathway to play an anti-inflammatory effect, the sensitivity of the allergen-induced gas