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作 者:周俊辉[1] 金立达[1] 张圣恭[1] 王良荣[1] 邱晓晓 林丽娜[1]
机构地区:[1]温州医学院附属第一医院麻醉科,325003 [2]温州医学院病理生理学教研室
出 处:《医学研究杂志》2013年第2期84-87,共4页Journal of Medical Research
基 金:浙江省中医药科研基金资助项目(2005C088)
摘 要:目的探讨兔肺缺血/再灌注损伤时脂质过氧化的变化和参麦注射液的影响,为临床防治提供理论依据。方法实验兔70只,随机分为3组:假手术组(C组,n=10)、缺血/再灌注组(I/R1、3、5h组,n=10)和参麦注射液干预组(SM1、3、5h组,n=10)。采用在体兔单侧肺原位缺血/再灌注损伤模型,参麦注射液干预组于缺血前20min经耳缘静脉注射参麦注射液15ml/kg,其余处理同缺血/再灌注组。分别于上述时间点抽取动脉血,检测血清超氧化物歧化酶(SOD)活性及丙二醛(MDA)浓度;提取肺组织,检测肺湿干重比(W/D)以及肺泡损伤数定量评价指标(IQA)。结果与C组比较,I/R3h组和I/R5h组SOD活性下降(P<0.01),MDA浓度、W/D及IQA均升高(P<0.01);与I/R组比较,SM组在相应时间点的SOD活性升高(P<0.01),MDA浓度、W/D和IQA均下降(P<0.01)。结论参麦注射液可通过抑制氧自由基的生成,减轻脂质过氧化对肺缺血/再灌注损伤的肺组织发挥积极的保护作用。Objective To investigate the changes of lipid peroxidatiou in rabbit model of pulmonary ischemia/reperfusion injury and study the effects of Shenmai injection(SM) on it,and provide a theoretical basis for the clinical prevention and treatment. Methods A to- tal of 70 experimental rabbits were randomly divided into three groups: Sham operation group( C group, n = 10) , Ischemia/ Reperfusion group(I/R1h,3h,Sh,n = 10)and Shenmai injection treatment group(SMlh,3h,5h,n = 10). Rabbit model of pulmonary I/R injury in situ was established with unilateral lung in vivo. At the corresponding time points,arterial blood serum was extracted, and then, the activity of superoxide dismutase (SOD) and the concentration of malondialdehyde (MDA) were detected. Lung tissue was extracted, and then, theratio of wet/dry weight (W/D) in lung tissue and alveolar damage several quantitative evaluation index (IQA) were detected. Results Compared with C group, the activity of SOD in I/R 3h group and I/R 5h group declined (P 〈 0.01 ) , while the concentration of MDA, W/D and IQA increased(P 〈0.01 ). Compared with I/R group at the points of corresponding time,the activity of SOD in SM group was higher (P 〈 0.01 ) ,while the concentration of MDA, W/D and IQA decreased ( P 〈 0.01 ). Conclusion Shenmai injection can inhibit oxygen free radical generation, promote oxygen free radical scavenging, and reduce acute lung injury caused by lipid peroxidation, thus play an actively protective role in pulmonary ischemia/reperfusion injury.
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