急性超容性血液稀释对缺血／再灌注损伤在体兔心肌细胞凋亡的影响  

Effcts of acute hypervolemic hemodilution on cardiomyocyte apoptosis during ischemic/reperfusion injury in rabbits

作　　者：程明华[1] 方雄水[1] 林拥华[1] 杨普春[1] 

机构地区：[1]汕头大学医学院第一附属医院,广东汕头515041

出　　处：《现代保健（医学创新研究）》2006年第11X期1-2,共2页

摘　　要：目的 探讨急性超容性血液稀释（AHH）对缺血／再灌注（I／R）损伤在体兔心肌细胞凋亡的影响。方法 36只兔随机分为三组，每组12只，Ⅰ组为对照组；Ⅱ组为急性等容性血液稀释组（ANH）；Ⅲ组为AHH。观察心肌缺血45min及再灌注180min时SOD、MDA含量变化、心肌超微结构改变、心肌细胞凋亡和Bcl-2及Bax表达。结果与Ⅰ组比较，Ⅱ、Ⅲ组再灌后SOD活性增加，凋亡指数和Bax含量减少，Bcl-2含量增加（P〈0.05）。心肌细胞超微结构表现为损伤减轻。Ⅱ、Ⅲ组间比较，各参数无明显差异。结论 AHH能通过抗氧化作用和调节Bcl-2及Bax表达来减轻I／R损伤后的心肌细胞凋亡。Objective To observe the effcts of acute hypervolemic hemodilution （AHH） on cardiomyocyte apoptosis during ischemic/reperfusion（I/R） injury in rabbits. Methods 36 rabbits were randomly divided into 3 groups with 12 in each one ： group Ⅰ （control） , group Ⅱ（ acute normovolemic hemodilution , ANH） and group Ⅲ （AHH）. The activities of SOD, the content of MDA and the expressions of Fas, Bcl - 2 protein in myocardium were measured , the uhrastructure were observed after 45 min of ischemia and 180 min of reperfusion. Apoptosis was identified by TUNEL and apoptosis index（AI） was obtained. Results Compared with the group Ⅰ , group Ⅱ and Ⅲ rabbits showed protection against I/R injury as evidenced by marked decrease of AI and the content of Fas protein, significantly increased the content of Bci - 2 protein and activity of SOD （ P 〈 0.05）. The uhrastructure of myocardium showed attenuated injury. Conclusion AHH can reduce rabbit myocardial apoptosis induced by I/R injury through regulating the expressions of Bcl -2 and Bax gene.

关 键 词：急性超容性血液稀释 I/R 心肌凋亡 兔 

分 类 号：R331[医药卫生—人体生理学]