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作 者:曹钰[1] 董玉龙[2] 姚尧[3] 胡海[1] 周毅武[1] 余海放[1]
机构地区:[1]四川大学华西医院急诊科,四川成都610041 [2]四川省第三人民医院急诊科 [3]四川大学华西药学院药理教研室
出 处:《中国呼吸与危重监护杂志》2005年第4期303-305,i001,共4页Chinese Journal of Respiratory and Critical Care Medicine
摘 要:目的从病理学改变、酶学指标、肺组织细胞内钙离子浓度变化等方面,探讨急性百草枯中毒的损伤机制.方法取SD大鼠36只,随机分为2组,实验组大鼠腹腔内注射百草枯20 mg/kg,用无菌生理盐水配成5 mg/mL的溶液,一次性染毒.对照组大鼠腹腔内注入等体积无菌生理盐水.在6个不同时间点观察其肺组织病理学改变,测量肺组织匀浆内的丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力及肺组织细胞内钙离子浓度变化.结果百草枯中毒可引起弥漫性毛细血管内皮细胞和肺泡上皮细胞损害,主要表现为肺泡水肿、出血、透明膜形成和程度不等的肺泡炎,炎症细胞浸润;肺组织匀浆内MDA含量显著高于对照组(P<0.01);SOD活力下降(P<0.01);肺组织细胞浆内钙离子浓度明显升高,与对照组比较差异有统计学意义(P<0.01),以第2~4 d明显,钙离子荧光强度分别为82.91±28.68和55.42±29.61.结论急性百草枯中毒的损伤机制可能与联吡啶阳离子产生反应态氧、胞内钙稳态失衡有关,最终导致不可逆的肺间质纤维化.Objective To investigate the enzymatic levels of MDA and SOD in lung tissue and the intracellular concentration of Ca~ to explore the pathogenesis of acute paraquat(PQ)intoxication induced lung injury.Methods 36 SD rats were divided into PQ intoxication group and control group.Animals in intoxication group were given PQ at the dose of 20 mg/kg.The ultrastructural changes of lung tissue were observed while the MDA and SOD concentrations in the lung homogenate and intracellular Ca~ concentrations were measured. Results Pathological study revealed diffuse capillary endothelium and alveolar epithelium damage which resulted in alveolar edema,bleeding,hyaline membrane formation and alveolitis with intensive inflammatory cell infiltration.The level of MDA in the lung homogenate increased significantly and the level of SOD decreased significantly in intoxication group compared with control group (P<0.01).The intracellular concentration of Ca~ was increased significantly compared with control (fluorescence intensity:82.91±28.68 vs 55.42±29.61,P<0.01) which was most obvious on the second to the fourth day.Conclusion The pathogenesis of PQ intoxication is related to oxygen free radical overload and intracellular Ca~ homeostasis disequilibrium.
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