Johnson D D, Singh M B, Cheung C Y
Department of Reproductive Medicine, University of California, San Diego, La Jolla 92093-0802, USA.
Am J Obstet Gynecol. 1997 Jan;176(1 Pt 1):42-8. doi: 10.1016/s0002-9378(97)80009-9.
The current study investigated the effects of 3 hours of hypoxia on atrial natriuretic factor gene expression and peptide content in each of the four cardiac chambers of the near-term ovine fetus.
Twenty-three chronically catheterized ovine fetuses at 125 to 129 days' gestation (term 145 days) were used for this study. Fetal hypoxia was induced for 3 hours in 12 fetuses by infusion of nitrogen into the maternal trachea. The remaining fetuses were used as controls. Fetal arterial PO2 and plasma atrial natriuretic factor concentrations were measured during hypoxia. At the end of the hypoxic period atrial natriuretic factor peptide contents and messenger ribonucleic acid levels in each cardiac chamber were determined by radioimmunoassay and Northern blot analysis, respectively.
With infusion of nitrogen into the maternal trachea, fetal arterial PO2 was reduced within 30 minutes by an average of 8.0 +/- 0.3 (SEM) mm Hg (p < 0.0001) and remained reduced at this level throughout the entire hypoxic period. Plasma atrial natriuretic factor concentrations increased by 1152 +/- 212 pg/ml (p < 0.003) and the increase was sustained for the duration of hypoxia. Atrial natriuretic factor peptide and messenger ribonucleic acid levels were much higher in the atria than in the ventricles. Hypoxia did not result in alterations of atrial natriuretic factor peptide content or messenger ribonucleic acid abundance in each cardiac chamber.
In the near-term ovine fetus, 3 hours of hypoxia resulted in greatly elevated plasma atrial natriuretic factor concentrations; this response was sustained for the duration of hypoxia. However, the increase was not associated with a detectable change in atrial natriuretic factor peptide content or an induction of atrial natriuretic factor gene expression in the atria and ventricles.
本研究调查了3小时缺氧对近足月绵羊胎儿四个心腔中心房利钠因子基因表达及肽含量的影响。
本研究使用了23只妊娠125至129天(足月为145天)且已长期插管的绵羊胎儿。通过向母体气管内注入氮气,使12只胎儿诱发缺氧3小时。其余胎儿作为对照。在缺氧期间测量胎儿动脉血氧分压(PO2)和血浆心房利钠因子浓度。在缺氧期结束时,分别通过放射免疫测定法和Northern印迹分析确定每个心腔中心房利钠因子肽含量和信使核糖核酸水平。
向母体气管内注入氮气后,胎儿动脉PO2在30分钟内平均降低8.0±0.3(标准误)毫米汞柱(p<0.0001),并在整个缺氧期维持在该水平。血浆心房利钠因子浓度增加1152±212皮克/毫升(p<0.003),且在缺氧期间持续升高。心房利钠因子肽和信使核糖核酸水平在心房中比在心室中高得多。缺氧并未导致每个心腔中心房利钠因子肽含量或信使核糖核酸丰度的改变。
在近足月绵羊胎儿中,3小时的缺氧导致血浆心房利钠因子浓度大幅升高;这种反应在缺氧期间持续存在。然而,这种增加与心房和心室中心房利钠因子肽含量的可检测变化或心房利钠因子基因表达的诱导无关。