窒息新生鼠心肌线粒体膜通透性转换孔开放度的变化  

Opening of the myocardial mitochondrial permeability transition pores in neonatal rats after asphyxia

作　　者：房晓祎[1] 林霓阳[1] 李玉光[2] 陈俭琴[2] 

机构地区：[1]汕头大学医学院第一附属医院新生儿科,515041 [2]汕头大学医学院第一附属医院心血管内科,515041

出　　处：《中国小儿急救医学》2013年第2期162-164,共3页Chinese Pediatric Emergency Medicine

基　　金：广东省科技计划项目（20098030801377）;汕头市重点科技计划项目（汕市财教[2012]165号）

摘　　要：目的 观察新生鼠窒息后心肌组织缺血损伤情况以及心肌细胞线粒体膜通透性转换孔（mitochondrial permeability transition pore,MPTP）开放度的变化,以期揭示MPTP开放在窒息后心肌缺氧缺血及再灌注损伤的作用机制.方法 成年SD母鼠妊娠第21天行剖宫产,随机分为正常分娩组及动脉夹闭组,正常分娩组不夹闭子宫动脉,所分娩新生鼠为对照组；以夹闭动脉夹闭组孕鼠子宫动脉方法制作宫内窒息新生大鼠模型,为窒息组,每组各30只,于出生24 h处死新生鼠.以ELISA法检测血清心肌肌钙蛋白Ⅰ（cardiac troponin Ⅰ,cTn Ⅰ）,以荧光分光光度法检测MPTP开放度；以TTC染色法检测心肌缺血面积；以HE染色法观察心肌细胞形态变化.结果 HE染色观察发现,窒息组心肌细胞排列紊乱、细胞肿胀、部分细胞溶解.对照组、窒息组新生鼠血清cTn Ⅰ分别为（0.08 ±0.04） μg/L、（0.40±0.29） μg/L,窒息组明显升高,差异有统计学意义（P＜0.01）.对照组、窒息组新生鼠TTC染色心肌缺血面积分别为（8.01±3.48）％、（42.50±15.90）％（P ＜0.01）.窒息组出现心肌点状坏死,缺血面积增大.对照组、窒息组新生鼠MPTP相对荧光单位分别为118.10±19.10、79.40±10.57 （P＜0.01）,窒息组心肌MPTP开放度增大.各组新生大鼠血清cTn Ⅰ值与MPTP开放度呈正相关（r=-0.384,P＜0.01）.结论 窒息新生大鼠出现心肌损伤,表现为血清cTn Ⅰ升高、心肌缺血及坏死.窒息后心肌MPTP开放度增大是导致心肌损伤的重要原因.Objective To detect the opening of the myocardial mitochondrial permeability transition pores （MPTP） after intrauterine asphyxia in neonatal rats,and to explore the mechanism of the myocardial hypoxic-ischemic and reperfusion injury caused by the opening of MPTP after asphyxia.Methods Cesarean sections were undertaken in female SD rats at the 21st day after pregnancy.The uterine arteries were clamped for 30 minutes followed by releasing for 1 hour and the pups were allocated into the asphyxia group.The uterine arteries were isolated but not clamped and the pups were allocated into the control group.There were 30 neonatal rats in either group and all of them were sacrificed 24 h after birth.Serum cardiac troponin Ⅰ （cTn Ⅰ） levels were detected by enzyme linked immunosorbent assay.The opening degree of MPTP was detected by fluorospectro-photometry.Myocardial ischemic areas were detected by TTC staining.Tissues from the cardiac apex were taken and the pathologic changes of the myocardium were explored by hematoxylin-eosin staining.SPSS for Windows 13.0 was used for statistic analyses.Results In HE staining slices,the myocardial cells in asphyxia group were disarranged and edematous.In control and asphyxia group,the serum cTn Ⅰ levels were （0.08 ±0.04） μg/L and （0.40 ±0.29） μg/L （P 〈0.01）,the myocardial ischemic areas were （8.01 ±3.48） % and （42.50 ± 15.90）% （P 〈0.01）,and the opening degrees of MPTP were （118.10 ± 19.10） RFU and （79.40 ± 10.57） RFU （P 〈 0.01） respectively.The serum levels of cTn Ⅰ,the myocardial ischemic areas,and the opening degrees of MPTP were significantly increased in asphyxia group compared with control group.The serum level of cTn Ⅰ was positive correlated with the opening degree of MPTP in either group（r =-0.384,P 〈 0.01）.Conclusion There are myocardial injuries in neonatal rats after asphyxia,which represent as high level of serum cTn Ⅰ,myocardial ischemia and necrosis.Opening of the myocardial MPTP is one of the cau

关 键 词：线粒体膜通透性转换孔 窒息 心肌损伤 新生鼠 

分 类 号：R722[医药卫生—儿科]