产前缺氧降低7月龄子鼠心脏舒张功能及其相关分子机制  

Effects of perinatal hypoxia on cardiac diastolic function and expression of related genes of myocardium from 7 months rats

作　　者：陈幼芳 杜心清[2] 吴淳淳[2] 林惠通[2] 林文东 

机构地区：[1]福建省泉州医学高等专科学校临床医学院内科学教研室,福建泉州362011 [2]福建医科大学附属第二临床学院

出　　处：《中华高血压杂志》2016年第12期1142-1146,共5页Chinese Journal of Hypertension

基　　金：泉州市科委重点项目(2012Z72);福建省卫计委中青年骨干人才培养项目(2013-ZQN-JC-28)

摘　　要：目的研究产前缺氧对7月龄子鼠心脏舒张功能影响及其相关分子机制。方法同期怀孕的SD孕鼠随机分为对照组(21%O2,n=5)、缺氧组(10%O2,n=5),于妊娠第7天开始相应的干预、记录,至妊娠第21天结束,自然分娩。每窝随机留2只雄性新生鼠饲养,每组共10只雄性新生鼠(n=10),饲养至7月龄。测定7月龄子鼠心脏舒张功能,利用实时逆转录聚合酶链反应(RT-PCR)、免疫组织化学技术检测7月龄子鼠心肌组织内皮型一氧化氮合酶(eNOS)、热休克蛋白90(Hsp90)表达,利用同位素方法测定内皮型一氧化氮合酶活性。结果与对照组比较,产前缺氧组7月龄子鼠左心室舒张末压(LVEDP)[(7.02±0.68)比(6.05±0.97)mm Hg]升高,左心室收缩末压(LVESP)[(60.72±7.76)比(69.37±6.38)mm Hg]、左心室内压最大上升速率(+dp/dtmax)[(5462±77)比(5545±62)mm Hg/s]和左心室内压最大下降速率(-dp/dtmax)[(4202±83)比(4285±41)mm Hg/s]降低(均P<0.05);心肌组织eNOS(0.41±0.21比1.00±0.25)、Hsp90(0.60±0.22比1.00±0.27)mRNA表达降低(均P<0.05);心肌组织eNOS(0.030±0.002比0.050±0.003)、Hsp90(0.015±0.001比0.030±0.002)蛋白表达降低(均P<0.05);心肌组织eNOS活性[(3059±309)比(4431±357)计数/(min·μg)]降低(P<0.05)。结论产前缺氧通过降低7月龄子鼠心肌组织eNOS和Hsp90表达及活性,降低心脏舒张功能。Objective To investigate the effects and mechanisms of perinatal hypoxia on cardiac diastolic function and expression of endothelial nitric oxide synthase（eNOS）and heat shock protein 90（Hsp90）in myocardium of 7 months rats. Methods Ten pregnant rats from the 7th to the 21 st day of their pregnancy were randomly divided into 2 groups：perinatal hypoxia group（10% O_2,n=5）and normoxic control group（21% O_2,n=5）. Pregnant rats had spontaneous deliveries. Two male offsprings from each litter were selected randomly and fed for 7 months.Cardiac diastolic function was examined and myocardium were obtained from 7 months old rats. The expression of eNOS and Hsp90 in myocardium from both group were examined. Results Compared to control group,hypoxia induced a significant increase in left ventricular end diastolic pressure（LVEDP）[（7.02±0.68）vs（6.05±0.97）mm Hg],and decreases in left ventricular end systolic pressure（LVESP）[（60.72±7.76）vs（69.37±6.38）mm Hg],＋dp/dtmax [（5462±77）vs（5545±62）mm Hg/s]and-dp/dtmax [（4202±83）vs（4285±41）mm Hg/s].Hypoxia also induced decrease in mRNA（eNOS 0.41±0.21 vs 1.00±0.25,Hsp90 0.60±0.22 vs 1.00±0.27）and protein level（eNOS 0.030±0.002 vs 0.050±0.003,Hsp90 0.015±0.001 vs 0.030±0.002）of eNOS and Hsp90.A decrease in eNOS activities was observed in 7-months rats＇ myocardium of hypoxia group compared to normoxic control[（3059±309）vs（4431±357）counts/（min·μg）,all P〈0.05]. Conclusion Perinatal hypoxia can induce impairment in cardiac diastolic function in 7 months old rats.The molecular mechanism may be related to decrease of eNOS and Hsp90 expression and eNOS activities in myocardium induced by perinatal hypoxia.

关 键 词：产前缺氧 心脏舒张功能 内皮型一氧化氮合酶 热休克蛋白90 

分 类 号：R722[医药卫生—儿科]