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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 effect of prenatal hypoxia on cardiac diastolic function in 7-month-old offspring and its related molecular mechanisms. Methods Pregnant SD pregnant rats of the same period were randomly divided into control group (21% O2, n = 5) and hypoxia group (10% O2, n = 5). Corresponding interventions were recorded on day 7 of gestation. The end of 21 days, natural childbirth. Two male neonatal rats were randomly housed in each litter, with 10 male neonatal rats (n = 10) in each group and housed until 7 months of age. The cardiac diastolic function of 7-month-old offspring was measured. The expression of eNOS, heat shock protein 90 (Hsp90) expression, the use of isotope determination of endothelial nitric oxide synthase activity. Results Compared with the control group, left ventricular end diastolic pressure (LVEDP) [(7.02 ± 0.68) vs (6.05 ± 0.97) mm Hg], left ventricular end systolic pressure (LVESP) (60.72 ± 7.76) vs (69.37 ± 6.38) mm Hg], the maximal rate of increase of left ventricular pressure (+ dp / dtmax [5462 ± 77 vs 5545 ± 62 mm Hg / s] The maximum rate of descending pressure (-dp / dtmax [(4202 ± 83) vs (4285 ± 41) mm Hg / s] 0.60 ± 0.22 vs 1.00 ± 0.27) (all P <0.05). The protein expressions of eNOS (0.030 ± 0.002 vs 0.050 ± 0.003) and Hsp90 (0.015 ± 0.001 vs 0.030 ± 0.002) in myocardium decreased (all P <0.05) ; Myocardial tissue eNOS activity [(3059 ± 309) vs (4431 ± 357) counts / (min · μg)] decreased (P <0.05). Conclusion Prenatal hypoxia can reduce diastolic function by reducing the expression and activity of eNOS and Hsp90 in myocardium of 7-month-old mice.