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机构地区:[1]第三军医大学附二院呼吸科,军事医学科学院基础医学研究所
出 处:《中国药理学通报》1996年第4期342-344,共3页Chinese Pharmacological Bulletin
摘 要:用放射性配基结合分析法,检测大鼠内毒素性肺损伤中肺α1肾上腺素受体(α1受体)的变化,并观察山莨菪碱对肺α1受体和磷脂酶A2(PLA2)的影响。结果表明,(1)iv内毒素(ET)后4h,大鼠肺α1受体的最大结合容量明显降低,较对照组减少34%,同时肺组织PLA2激活及膜磷脂含量减少。(2)山莨菪碱能减轻ET诱导的大鼠急性肺损伤,其作用机制与阻滞α1受体,抑制PLA2、防止膜磷脂降解、减少花生四烯酸的释放等有关。Change of α1-adrenergic receptor(α1AR) in lung tissues during endotoxin-induced rat acute lung injury was measured with radioligand binding assay.The effects of anisodamine on pulmonary α1-AR and phospholipase A2(PLA2) were observed.The results showed that:(1) 4 hours after the endotoxin injection,there was a significant decrease in the maximal binding capacity of α1-AR by 34% as compared with the control group,meanwhile elevated activity of PLA2 in rat lung and reduction of the phospholipids content of cell membrane was found.(2)Anisodamine could attenuate endotoxin induced acute lung injury in rats.This effect might be related to anisodamine's blockage of α1-AR and suppression of PLA2,prevention of membranous phospholipids from degradation,and the reduction of arachidonic acid release.
关 键 词:山莨菪碱 肺损伤 内毒素 α1 受体 磷 脂酶A2
分 类 号:R285.5[医药卫生—中药学] R282.710.5[医药卫生—中医学]
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