中国小儿急救医学
中國小兒急救醫學
중국소인급구의학
CHINESE PEDIATRIC EMERGENCY MEDICINE
2013年
2期
162-164
,共3页
房晓祎%林霓阳%李玉光%陈俭琴
房曉祎%林霓暘%李玉光%陳儉琴
방효의%림예양%리옥광%진검금
线粒体膜通透性转换孔%窒息%心肌损伤%新生鼠
線粒體膜通透性轉換孔%窒息%心肌損傷%新生鼠
선립체막통투성전환공%질식%심기손상%신생서
Mitochondrial permeability transition pore%Asphyxia%Myocardial injury%Neonatal rats
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.
目的 觀察新生鼠窒息後心肌組織缺血損傷情況以及心肌細胞線粒體膜通透性轉換孔(mitochondrial permeability transition pore,MPTP)開放度的變化,以期揭示MPTP開放在窒息後心肌缺氧缺血及再灌註損傷的作用機製.方法 成年SD母鼠妊娠第21天行剖宮產,隨機分為正常分娩組及動脈夾閉組,正常分娩組不夾閉子宮動脈,所分娩新生鼠為對照組；以夾閉動脈夾閉組孕鼠子宮動脈方法製作宮內窒息新生大鼠模型,為窒息組,每組各30隻,于齣生24 h處死新生鼠.以ELISA法檢測血清心肌肌鈣蛋白Ⅰ(cardiac troponin Ⅰ,cTn Ⅰ),以熒光分光光度法檢測MPTP開放度；以TTC染色法檢測心肌缺血麵積；以HE染色法觀察心肌細胞形態變化.結果 HE染色觀察髮現,窒息組心肌細胞排列紊亂、細胞腫脹、部分細胞溶解.對照組、窒息組新生鼠血清cTn Ⅰ分彆為(0.08 ±0.04) μg/L、(0.40±0.29) μg/L,窒息組明顯升高,差異有統計學意義(P＜0.01).對照組、窒息組新生鼠TTC染色心肌缺血麵積分彆為(8.01±3.48)％、(42.50±15.90)％(P ＜0.01).窒息組齣現心肌點狀壞死,缺血麵積增大.對照組、窒息組新生鼠MPTP相對熒光單位分彆為118.10±19.10、79.40±10.57 (P＜0.01),窒息組心肌MPTP開放度增大.各組新生大鼠血清cTn Ⅰ值與MPTP開放度呈正相關(r=-0.384,P＜0.01).結論 窒息新生大鼠齣現心肌損傷,錶現為血清cTn Ⅰ升高、心肌缺血及壞死.窒息後心肌MPTP開放度增大是導緻心肌損傷的重要原因.
목적 관찰신생서질식후심기조직결혈손상정황이급심기세포선립체막통투성전환공(mitochondrial permeability transition pore,MPTP)개방도적변화,이기게시MPTP개방재질식후심기결양결혈급재관주손상적작용궤제.방법 성년SD모서임신제21천행부궁산,수궤분위정상분면조급동맥협폐조,정상분면조불협폐자궁동맥,소분면신생서위대조조；이협폐동맥협폐조잉서자궁동맥방법제작궁내질식신생대서모형,위질식조,매조각30지,우출생24 h처사신생서.이ELISA법검측혈청심기기개단백Ⅰ(cardiac troponin Ⅰ,cTn Ⅰ),이형광분광광도법검측MPTP개방도；이TTC염색법검측심기결혈면적；이HE염색법관찰심기세포형태변화.결과 HE염색관찰발현,질식조심기세포배렬문란、세포종창、부분세포용해.대조조、질식조신생서혈청cTn Ⅰ분별위(0.08 ±0.04) μg/L、(0.40±0.29) μg/L,질식조명현승고,차이유통계학의의(P＜0.01).대조조、질식조신생서TTC염색심기결혈면적분별위(8.01±3.48)％、(42.50±15.90)％(P ＜0.01).질식조출현심기점상배사,결혈면적증대.대조조、질식조신생서MPTP상대형광단위분별위118.10±19.10、79.40±10.57 (P＜0.01),질식조심기MPTP개방도증대.각조신생대서혈청cTn Ⅰ치여MPTP개방도정정상관(r=-0.384,P＜0.01).결론 질식신생대서출현심기손상,표현위혈청cTn Ⅰ승고、심기결혈급배사.질식후심기MPTP개방도증대시도치심기손상적중요원인.
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 causes of myocardial injury.
