机构地区:[1]苏州大学附属第一医院胎儿医学研究所,215000 [2]山东省淄博市中心医院妇科,255036
出 处:《中华围产医学杂志》2017年第4期282-286,共5页Chinese Journal of Perinatal Medicine
基 金:国家自然科学基金(81401244);江苏省自然基金(BK20140292);苏州市科技支撑计划(SYS201451)
摘 要:目的探讨孕期缺氧对胎鼠血管功能的影响及其机制。方法将清洁级Sprague—Dawley孕鼠随机分为缺氧组和对照组,各8只。缺氧组大鼠在妊娠第5-21天置入氧含量为10.5%的培养箱中,对照组置入含氧量正常的培养箱中。于妊娠第21天剖宫取出胎鼠,测定胎鼠出生体重、血气及电解质等指标。同时分离胎鼠胸主动脉血管环,并分别进行血管功能实验。观察孕期缺氧对胎鼠胸主动脉在血管紧张素Ⅱ(angiotensin Ⅱ,AngⅡ)介导下的收缩效应及乙酰胆碱介导下的舒张效应的影响,并联合使用内皮型一氧化氮合酶阻断剂左旋硝基精氨酸甲酯(NG—nitro—Larginine methyl ester,L—Name)及L型钙通道阻断剂尼非地平,记录血管舒缩反应的变化。采用t检验、双因素方差检验等进行统计学分析。结果(1)与对照组相比,缺氧组胎鼠的出生体重[(4.40±0.23)与(3.33±0.42)g,t=2.871]、血氧分压[(50.64±2.17)与(42.50±2.32)mmHg(1mmHg=0.133kPa),t=2.6181和血氧饱和度[(58.95±1.97)%与(47.73±2.24)%,t=3.564]均明佩降低(P值均〈0.05)。(2)与对照组相比,缺氧组胎鼠胸主动脉对Ang1I介导的收缩反应增强,但对乙酰胆碱诱导的舒张效应降低(P值均〈0.05)。L—Name能增强AngI/介导的收缩反应,且对照组的升高幅度高于缺氧组(P〈0.05);尼非地平能减弱AngⅡ介导的收缩反应,且缺氧组减弱幅度高于对照组(P〈0.05)。结论孕期母体缺氧不仅能影响胎鼠发育,而且能改变胎鼠的血管功能,可能与L型钙通道改变和内皮型一氧化氮合酶功能受损有关。Objective To explore the effects and mechanisms of prenatal hypoxia on vasomotor functions of fetal rats. Methods Sixteen pregnant Sprague-Dawley rats were randomly divided into two groups: control and hypoxia groups (eight in each group). Rats in the hypoxia group were provided with 10.5% of oxygen from gestation day 5 to 21, while those in the control group were exposed to normoxic condition. Fetuses were removed from the pregnant rats by cesarean section on gestational day 21. Fetal body weight, blood gas and electrolyte levels were measured. Thoracic aorta rings were separated from fetal rats and used in different vascular function tests. Effects of hypoxia during pregnancy on angiotensin Ⅱ(Ang Ⅱ)-mediated vasoconstrictions and acetylcholine (Ach)-mediated vasodilatations in fetal thoracic aortas were measured. Changes in vasomotor functions were observed after both endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-Name) and L-type calcium channel (LTCC) inhibitor nifedipine were administered. T-test and two-way analysis of variance were used for statistical analysis. Results (1) Compared with the control group, fetal body weight [(4.40±0.23) vs (3.33±0.42) g, t=2.871], blood partial pressure of oxygen [(50.64±2.17) vs (42.50±2.32) mmHg (1 mmHg=0.133 kPa), t=-2.618] and blood oxygen saturation [(58.95±1.97)% vs (47.73±2.24)%, t=3.564] in the hypoxia group were significantly reduced (all P〈0.05). (2) Compared with the control group, Ang Ⅱ-mediated vasoconstrictions increased, but Ach- mediated vasodilatations in fetal thoracic aortas decreased in the hypoxia group (both P〈0.05). L-Name induced stronger Ang H -mediated contractions in thoracic aortas in the control group than that in the hypoxia group (P〈0.05). However, nifedipine decreased Ang Ⅱ-induced contractions, especially in the hypoxia group (P〈0.05). Conclusions Maternal hypoxia during pregnancy not only affects the g
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