Gagnon R, Rundle H, Johnston L, Han V K
Department of Obstetrics and Gynaecology, St. Joseph's Health Centre, London, Ontario, Canada.
Am J Obstet Gynecol. 1995 May;172(5):1451-8. doi: 10.1016/0002-9378(95)90477-8.
Fetal growth and development are closely related to normal placental growth and function. We performed a study to determine the effect of a 10-day period of fetal hypoxemia induced by umbilical-placental hypoperfusion on tissue deoxyribonucleic acid synthesis rates in the 0.84 to 0.91 of gestation ovine fetus and placenta.
Daily fetal placental embolization was performed in four chronically catheterized sheep fetuses until fetal arterial oxygen content decreased by approximately 30% compared with preembolization values. Five control fetuses received vehicle only. On experimental day 10, the deoxyribonucleic acid synthesis rate was determined by injecting tritiated thymidine (1 mCi/kg) intravenously approximately 8 hours before the end of the study.
Fetal arterial oxygen decreased from 3.2 +/- 0.1 (SEM) mmol/L preembolization to 2.2 +/- 0.2 mmol/L on day 10 (p < 0.001) and remained unchanged in controls. On day 10 deoxyribonucleic acid synthesis rates were significantly reduced in embolized fetuses compared with controls, by 38% in cotyledons (83.0 +/- 15.1 vs 133.7 +/- 9.9 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), 28% in the left ventricular wall (36.8 +/- 3.7 vs 51.0 +/- 4.7 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), and 45% in the quadriceps muscle (15.4 +/- 4.0 vs 28.1 +/- 3.0 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05). Tritiated thymidine autoradiography demonstrated that cotyledonary deoxyribonucleic acid synthesis occurred exclusively in the fetal trophoblasts cells.
We concluded that a reduction in cotyledonary, quadriceps muscle, and left ventricular myocardium deoxyribonucleic acid synthesis rates are the earliest adaptive mechanisms of fetal growth associated with development of umbilical-placental insufficiency. We speculate that alteration in the myocardial deoxyribonucleic acid synthesis rate could be a major contributing factor in the deterioration of fetal myocardial function associated with increased placental vascular resistance.
胎儿生长发育与正常胎盘生长及功能密切相关。我们开展了一项研究，以确定脐-胎盘低灌注诱导的为期10天的胎儿低氧血症对妊娠0.84至0.91期绵羊胎儿及胎盘组织脱氧核糖核酸合成率的影响。
对4只长期插管的绵羊胎儿每日进行胎儿胎盘栓塞，直至胎儿动脉氧含量相较于栓塞前值降低约30%。5只对照胎儿仅接受赋形剂。在实验第10天，在研究结束前约8小时静脉注射氚标记胸腺嘧啶核苷（1 mCi/kg）来测定脱氧核糖核酸合成率。
胎儿动脉氧含量从栓塞前的3.2±0.1（标准误）mmol/L降至第10天的2.2±0.2 mmol/L（p<0.001），而对照组保持不变。在第10天，与对照组相比，栓塞胎儿的脱氧核糖核酸合成率显著降低，子叶中降低38%（83.0±15.1对133.7±9.9次衰变/分钟/微克脱氧核糖核酸，p<0.05），左心室壁降低28%（36.8±3.7对51.0±4.7次衰变/分钟/微克脱氧核糖核酸，p<0.05），股四头肌降低45%（15.4±4.0对28.1±3.0次衰变/分钟/微克脱氧核糖核酸，p<0.05）。氚标记胸腺嘧啶核苷放射自显影显示，子叶脱氧核糖核酸合成仅发生在胎儿滋养层细胞中。
我们得出结论，子叶、股四头肌和左心室心肌脱氧核糖核酸合成率降低是与脐-胎盘功能不全发展相关的胎儿生长的最早适应性机制。我们推测，心肌脱氧核糖核酸合成率的改变可能是与胎盘血管阻力增加相关的胎儿心肌功能恶化的主要促成因素。
