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作 者:景友玲[1] 王艳蕾[1] 段国贤[1] 赵春秀[1] 崔国金[1] 张硕森[1] 王志鹏[1]
机构地区:[1]河北联合大学基础医学部生理教研室,唐山063000
出 处:《中国应用生理学杂志》2011年第1期19-22,共4页Chinese Journal of Applied Physiology
基 金:华北煤炭医学院科研基金资助(3099)
摘 要:目的:观察肢体缺血/再灌注(LI/R)时肺损伤的变化并探讨缺血预处理(IPC)对其保护作用。方法:复制家兔LI/R损伤模型,观察肢体缺血4 h再灌注4 h肺损伤的变化以及采用肢体IPC干预后对肺损伤的影响。从右颈外静脉和左颈总动脉采血,分别代表入肺血和出肺血,检测入、出肺血及肺组织超氧化物歧化酶(SOD)的活性、脂质过氧化物的代谢产物丙二醛(MDA)和一氧化氮(NO)的含量;同时测定肺组织总一氧化氮合酶(tNOS)和诱导型一氧化氮合酶(iNOS)的活性以及肢体IPC对上述指标的影响。结果:与对照组和缺血前比较,LI/R组松夹再灌注4 h入、出肺血及肺组织SOD活性明显降低,MDA和NO含量增高(P<0.05,P<0.01);肺组织tNOS和iNOS活性亦升高,与对照组比较,有统计学意义(P<0.01)。在缺血前给予IPC组,SOD活性升高,而MDA、NO含量降低,tNOS、iNOS活性也降低(P<0.01)。相关分析显示MDA与SOD间存在明显负相关(P<0.01),而MDA与NO及iNOS呈显著正相关(P<0.01)。结论:LI/R时并发的急性肺损伤与组织氧化代谢紊乱有关,IPC通过改善LI/R时肺组织氧化与抗氧化之间的平衡,进而增强肺组织的抗氧化能力,对LI/R肺损伤具有保护作用。Objective: To explore the protective effects of ischemic preconditioning(IPC) on the lung injury following with limbs ischemia/reperfusion(LI/R).Methods: The models of LI/R injury were constructed in rabbits.The blood from right external jugular vein and left common carotid artery,into and out-flowing pulmonary blood(IPB,OPB) respectively.Superoxide dismutase(SOD),malondialdehyde(MDA),nitric oxide(NO) in IPB and OPB and lung tissues were measured,as well as total nitric oxide synthase(tNOS) and inducible nitric oxide synthase(iNOS) in lung tissues were detected in different groups.The effects of IPC on the lung injury were observed.Results: Compared with sham and before ischemic,the activity of SOD decreased and the content of MDA and NO increased after 4 h ischemia followed by 4 h reperfusion in IPB,OPB and lung tissues.The activity of tNOS and iNOS in lung tissues increased remarkably as well,there was statistical significance(P0.05,P0.01).SOD increased and MDA, NO,tNOS,iNOS decreased significantly by IPC before ischemia/reperfusion.The correlation analysis indicated that MDA was negatively correlated with SOD and was positively correlated with MDA,NO,iNOS(P0.01).Conclusion: Oxygen free radicals metabolic confusion of lung occurred in the course of LI/R,IPC could strengthen the resistance of peroxidation in lung and had protective effects on the lung injury following with LI/R.
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