小剂量过氧化氢预处理对大鼠心肌缺血/再灌注损伤的保护作用  

Attenuation of cardiac ischemia/reperfusion injury by transient low hydroperoxide pretreatment in rat

作　　者：冯润荷[1] 张金财[2] 李小倩[2] 孙海丽[2] 刘斌[1] 赵蕴珍[1] 唐向东[2] 李静[2] 

机构地区：[1]天津医学高等专科学校,天津300222 [2]南开大学医学院,天津300071

出　　处：《中国应用生理学杂志》2013年第3期247-250,共4页Chinese Journal of Applied Physiology

基　　金：天津市自然科学基金(10JCYBJC14800);国家自然科学基金(81072629);天津市教委科研计划项目(20100115)

摘　　要：目的:探索小剂量过氧化氢预处理与心脏缺血/再灌注损伤之间的关系。方法:SD大鼠随机分为4组,即假手术组、缺血/再灌注组(I/R)、缺血预适应组(IPC)及小剂量过氧化氢预处理组。对各组的心功能与心肌损伤指标进行比较。结果:IPC能够明显保护再灌注损伤,改善心功能。小剂量H2O2预处理能够达到与IPC类似的功效。短暂模拟缺血缺氧导致H2O2产生,小剂量H2O2预处理减少钙超载诱导的细胞色素c释放。结论:IPC导致小剂量H2O2产生,后者通过抑制线粒体通透转换发挥对心肌缺血/再灌注损伤的保护作用。Objective： To investigate how transient low dose of hydroperoxide pretreatment prevents cardiac ischemia/reperfusion injury.Methods： SD rats were divided into 4 groups：sham operation（Sham）,standard ischemia/reperfusion（I/R）,ischemic preconditioning（IPC） and IR preceded by low H2O2 treatment.Cardiac function and injury parameter were compared among groups.Results： IPC protected reperfusion injury and improved cardiac function.Low H2O2 treatment played a role in cardioprotection similar to IPC.Low H2O2 was indeed generated in the early phase of simulated ischemia and attenuated cytochrome c release induced by high Ca2＋ in isolated mitochondria.Conclusion： Low H2O2 plays a critical role in cardioprotection probably by inhibiting mitochondrial permeability transition.

关 键 词：再灌注损伤 缺血预适应 心肌保护 过氧化氢 

分 类 号：R966[医药卫生—药理学] R363[医药卫生—药学]