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作 者:杨天德[1] 杨宗城[2] 罗奇志[2] 黎鳌[2]
机构地区:[1]第三军医大学新桥医院麻醉科,重庆400037 [2]第三军医大学新桥医院烧伤研究所,重庆400037
出 处:《中国药理学通报》1999年第4期316-319,共4页Chinese Pharmacological Bulletin
基 金:全军九五指令性课题
摘 要:目的 观察氯喹、地塞米松对烟雾吸入伤大鼠肺细胞膜损伤的影响。方法 健康 Wistar 大鼠100 只随机分成正常对照组,吸入伤1 h 、3 h 、6 h 、12 h 和24 h 组,氯喹治疗6 h和12 h 组以及地塞米松治疗6 h 和12 h 组。实验毕活杀动物,取肺组织制备细胞膜。提取膜磷脂,并用高效液相色谱仪测定磷脂组份,用荧光偏振法测定膜流动性,用生化比色法测定细胞膜 Na+ , K+ A T P 酶、 Ca2 + A T P 酶和 Mg2 + A T P酶活性。结果 烟雾吸入伤后,细胞膜磷脂酰胆碱( P C) 、磷脂酰乙醇胺( P E) 和磷脂酰肌醇( P I) 明显降低,同时伴有膜荧光偏振度(ρ) 和膜平均微粘度(η) 明显增加及3 种 A T P 酶活性降低( P< 005 ~ P< 001) 。与吸入伤6 h 组相比,氯喹治疗6 h 组动物 P C、 P E 含量明显增加,同时降低ρ和η,并增加 Na + , K+ A T P 酶和 Ca2 + A T P 酶活性( P< 005 ~ P< 001) ,而地塞米松治疗6 h 动物仅增加 P E 含量、降低ρ和η,但对膜上 A T P 酶活性无影响。结论 烟雾吸入可引起肺细胞膜受损,膜流动性及膜 A T P 酶活性降低,而氯?AIM To investigate the effects of chloroquine and dexamethasone on the pulmonary cellular membraneous damages of rats with smoke inhalation injury. METHODS 100 healthy wistar rats were randomised into control group, five injuried groups at 1 h,3 h,6 h,12 h and 24 h following smoke inhalation, and chloroquine treated groups at 6 h,12 h and dexamethasone treated groups at 6 h,12 h following smoke inhalation. After experiment the rats were killed and the lungs were incised for preparing of cellular membrane,membraneous lipids were extracted and the compositions phospholipid were detected with high performance liquid chromatography. The fluidity of cellular membrane was measured by fluorescence polarization, and the activities of Na +,K + ATPase and Mg 2+ ATPase and Ca 2+ ATPase were assayed by biochemical method. RESULTS After smoke inhalation the contents of PC,PE,PI in pul monary cellular membrane were significatly declined and simutaneously accompanying by the increases in fluorescence polarization(ρ)and membraneous microviscosity(η) and the decreases in the activities of three kinds of ATPases ( P <0 05~<0 01),while compared with injuried group at 6 h following smoke inhalation chloroquine markedly increased the contents of PC and PE decreased ρ and η, and enhenced the activities of Na +,K + ATPase and Ca 2+ ATPase in group at 6 h following smoke inhalation, but dexamethasone only increased the content of PE, decreased ρ and η, and had no effect on the activities of ATPases. CONCLUSION Smoke inhalation causes the disruption of pulmonary cellular membrane and the decreases in the fluidity of cellular membrane and the activities of ATPases, both chloroquine and dexamethasone partially improve the function of cellular membrane.
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