摘要
目的探讨诱导金属硫蛋白(MT)在未成熟心肌中的表达对缺血/再灌注未成熟心肌细胞功能的影响。方法采用Langendorff离体灌注模型 ,大白兔分为4组 :对照组(C ,n=9) ,腹腔注射蒸馏水0.3ml,按注射后时间12、24、和48h取离体心脏 ,灌注KH液15min转为工作心15min,全心停灌45min,恢复灌注15min改为工作心30min ;E12h组 (n=6)、E24h组 (n=6)、E48h组 (n=6)各组分别按腹腔注射3.6 %ZnSO4(1.5ml/kg)后12、24和48h取离体心脏 ,常规建立Langendorff灌注模型。方法同C组。以心肌细胞中MT含量、CK和LDH漏出率、ATP含量、心肌细胞内Ca2 +含量、心肌线粒体Ca2 +-ATPase活性及其Ca2 +含量、心肌线粒体合成ATP能力[ATP]m作为观察指标。结果腹腔注射ZnSO4 后12hMT开始表达 ,24h达高峰 ,48h仍在高表达水平。MT含量在E24h、E48h组与C、E12h组比较明显增高 ;E24h、E48h组ATP含量优于C组和E12h 组 (P<0.05) ,CK、LDH漏出率均低于C组和E12h组(P<0.05) ,心肌线粒体Ca2 +-ATPase活性、[ATP]m均优于C组和E12h组(P<0.01) ,心肌细胞内Ca2 +含量、心肌线粒体Ca2 +含量低于C组和E12h组(P<0.01)。结论腹腔注射ZnSO4 可诱导心肌MT长时间表达 ,MT可减轻未成熟心肌细胞缺血/再灌注损伤。
Objective To investigate the protective effects of metallothionein(MT)for immature myocar-dial cell.Methods Isolated working rabbit heart model was used in this study.27rabbits(aged14~21days)were divided into4groups.Distilled water in controll group(n=9)was injected intraperitoneally.3.6%ZnSO 4 was injected intraperitoneally in E 12h group(n=6)、E 24h group(n=6)、E 48h group(n=6)according to the time when ZnSO 4 postintraperitoneally.Such index,including MTcontent,lactate dehydrogenase(LDH)and creatine ki-nase(CK)leakage,adenosine triphosphate(ATP),myocardial cell Ca 2+ content,Ca 2+ -ATPase activity of mi-tothondia([Ca 2+ -ATPase]m)and its Ca 2+ content m),synthesizing ATP activity of mitochondria(m)were tested.Results When ZnSO 4 was applied over12h,MT begins to express,and24h arrives at the peak,and48h still has high expression.There were markly increase in E 24h and E 48h group in hemodynamics recovery,ATP content,[Ca 2+ -ATPase]m activity,m activity,and markly reduction in LDH and CK leakage,my-ocardial cell Ca 2+ content,m content and the ultrastructure injuries are less than those in C and E 12h group.Conclusions This study demonstrated that MThas markly protective effects on immature myocardial cell by ZnSO 4 ip induced MTexpression.
出处
《中国微循环》
2004年第1期13-15,共3页
Journal of Chinese Microcirculation
关键词
金属硫蛋白
未成熟心肌细胞
心肌保护
Metallothionein
Immature myocardial cell
Cardioprotection