检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:霍小萍[1] 顾学兰[1] 刘良明[2] 刁有芳[2] 马春艳[1] 陈家慧[1] 李萍[2] 卢是玥 刘建仓[2] 徐强[3]
机构地区:[1]江苏先声药物研究有限公司,江苏南京210042 [2]第三军医大学大坪医院野战外科研究所第二研究室,重庆400042 [3]南京大学生命科学院,江苏南京210093
出 处:《第四军医大学学报》2006年第20期1847-1850,共4页Journal of the Fourth Military Medical University
基 金:江苏省博士后科研资助计划(0401079B)
摘 要:目的:观察氧自由基清除剂依达拉奉(edaravone,ED)对脓毒性休克大鼠心脏功能和心肌损伤的作用.方法:在大鼠脓毒性休克后1h用3个剂量ED(6.0,3.0和1.5mg/kg)治疗,测定休克后4个时相点平均血压(MAP)、左室收缩末期压力(LVESP)、左室舒张末期压力(LVEDP)、左室压力上升及下降最大变化速率(±dp/dtmax)等心功能指标;取心肌组织测超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、乳酸脱氢酶(LDH)活性和乳酸(LD)、丙二醛(MDA)含量,并观察形态学改变.结果:与脓毒性休克组比较,ED可显著升高MAP,LVESP和±dp/dtmax,并使SOD,CAT活性增强以及MDA浓度降低接近对照组;组织学观察可见模型组心肌充血、水肿及炎性细胞浸润等,ED可明显改善以上形态学变化.结论:ED具有抗脓毒性休克心功能不全的作用,其机制与减轻心肌损伤有关.AIM: To investigate the effect of edaravone( ED), a novel free radical scavenger, on cardiac function and myocardial cell injury in rats with septic shock. METHODS : After treatment with three different doses ( 6.0, 3.0 and 1.5 mg/kg ) of ED to rats 1 h after septic shock, changes of MAP, LVESP, LVEDP, + dp/dtmax were determined in 4 different time phases. The activities of SOD, CAT, LDH and the concentrations of MDA, LD in myocardial tissue were measured. The pathologic change of myocardial tissue was observed by HE staining. RESULTS: Compared with septic shock group, MAP,LVESP and + dp/dtmax were increased remarkably in ED treatment groups. The activities of SOD and CAT and the concentration of MDA in ED groups were close to those in normal control group. Histological examination showed congestion, edema and inflammatory cell infiltration in myocardial tissue, while ED treatment attenuated the above pathological changes of myocardium. CONCLUSION: ED has a satisfying therapeutic effect on cardiac dysfunction in rats with septic shock, which may be related to attenuating myocardial injury.
分 类 号:R963[医药卫生—微生物与生化药学]
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.188