Integrated Studies on Endocrino-Metabolic Mechanisms of Fetal Growth and Fetal Distress

本研究的目的是确定在宫内生长迟缓（IUGR）和胎儿窘迫的情况下运作的机制。研究了母鼠的内分泌、代谢和生理特征，并总结了以下结果：(1)母鼠的葡萄糖代谢和胎儿生长：(a)在体内实验中，链霉素-佐佐毒诱导的高血糖导致了生长迟缓的后代；也;大鼠胎儿肝脏胰高血糖素受体的诱导功能受损；(b)在胚胎大鼠肝脏培养物的体外研究中，胰岛素样生长因子- 1通过促进大鼠胎儿糖原合成和细胞增殖而显示出促进生长的作用。(2)妊高征（PIH）：(a)妊高征患者盐负荷试验导致血压显著升高。血管紧张素ⅱ负荷试验未能抑制肾素和缓激素的分泌。在原位妊娠中，血管抑制系统可能受到刺激，但其抗血管增生的储备功能仍可能低于正常妊娠；(b)严重PIH细胞内Na^+浓度显著升高，细胞内Ca^<++>水平升高。Ca^<++>水平升高导致血管肌层收缩。(3)钙代谢：妊高征患者血清Ca^<++>、P水平明显低于正常妊娠。然而，血清甲状旁腺激素升高。这些变化可能归因于钙和磷从肠道吸收的减少，因为与之相关的血清活性形式维生素d3水平较低。利用大鼠肠道，hPL激活Vit。D3增强Ca^<++>吸收。(4)甲状腺激素：PIH患者血清中逆转录T3较高，游离T3较低。这可能是母体低代谢加剧的结果，其中T4到rT3的转化比T4到T3的转化更占优势。然而，胎盘内部的单去碘作用似乎阻止了甲状腺激素从母体到胎儿的活跃运动。(5)胎儿生长与胎儿窘迫：本研究证实，在妊高征病例中，胎盘功能不全导致的胎儿生长发育迟缓对慢性胎儿窘迫的发展起着重要作用。超声产前胎儿生长评估可能是预测高危妊娠胎儿窘迫的有效方法。少

The purpose of this study is to determine the mechanisms operating in cases of intrauterine growth retardation (IUGR) and fetal distress. Maternal endocrine, metabolic, and physiologic profiles were investrigated and the results are summarized as follows: (1) Maternal glucose metabolism and fetal growth: (a)Using an in-vivo setup, strepto- zotocine-induced hyperglycemia in rats resulted to growth-retarded offsprings; also; the induction of glucagon receptors in rat fetuses' liver was impaired; (b)In an invitro study using fetal rat liver cultures, insulin-like growth factor-l showed a growth-promoting effect by fecilitating glycogen synthesis and cell proliferation in the rat fetuses. (2) Pregnancy-induced hypertension (PIH): (a) In patients with PIH, salt loading test led to a remarkable rise in blood pressure. Angiotensin II loading test failed to suppress secretion of renin and bradykinin. In situ, the vasodepressor system could be stimulated but its reserve function against angiote … More nsin II may stili be less than in mormal pregnancy; (b) Intracellular Na^+ concentration in severe PIH was significantly increased with an associated rise in intracellular Ca^<++> level. Such increase in Ca^<++> level results to myometrial contraction of blood vessels. (3) Calcium metabolism: Serum levels of Ca^<++> and P in PIH were significantly lower than in mormal pregnancy. However, serum PTH was elevated. These changes could be attributed to a reduction in Ca and P absorption from the intestines because of an associated low serum levels of the active form of Vit.D3.Using rat intestine, hPL activated Vit.D3 enhanced Ca^<++> absorption. (4) Thyroid hormone: Higher reverse T3 and lower free T3 levels were observed in PIH patients' sera. These could be the result of intensified maternal hypometabolism where T4 to rT3 conversion is more dominant than T4 to T3 conversion. However, placental inner monodeiodination seems to prevent active movement of thyroid hormone from mother to the fetus. (5) Fetal growth and fetal distress: This study proves that in cases of PIH, fetal growth retardation induced by a state of placental insufficiency significantly contributes to the development of chronic fetal distress. Ultrasonographic antepartum assessment of fetal growth might be effective and appropriate in predicting fetal distress in cases of high risk pregnancy. Less