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

胎儿生长和胎儿窘迫的内分泌代谢机制的综合研究

• 批准号: 60480368
• 负责人: MOCHIZUKI Matsuto
• 金额: $ 3.84万
• 依托单位: Kobe University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1985
• 资助国家: 日本
• 起止时间: 1985 至 1987
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-60480368/
• 关键词: Fetal Growth; Fetal Distress; Pregnancy Induced Yhpertension; Metabolism During Pregnancy; Calcium; 甲状腺ホルモン

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

本研究的目的是确定机制运作的情况下，胎儿宫内发育迟缓（IUGR）和胎儿窘迫。研究了母体内分泌、代谢和生理特征，结果总结如下：（1）母体糖代谢和胎儿生长：（a）使用体内装置，链脲佐菌素诱导的大鼠高血糖导致生长迟缓的后代，并且，大鼠胎儿肝脏中胰高血糖素受体的诱导受损;（B）在使用胎鼠肝培养物的体外研究中，胰岛素样生长因子-I通过促进大鼠胎儿中的糖原合成和细胞增殖而显示出生长促进作用。(2)妊娠高血压综合征（PIH）：（a）在PIH患者中，盐负荷试验导致血压显著升高。血管紧张素II负荷试验不能抑制肾素和缓激肽的分泌。在原位，血管降压系统可被激活，但其对血管紧张素的储备功能， ...更多信息 （B）重度妊高征患者细胞内Na^+浓度显著升高，同时伴有细胞内Ca^+<++>水平升高。这种Ca^<++>水平的增加导致子宫肌层血管收缩。(3)钙代谢：妊高征患者血清Ca^++、P水平明显低于正常妊娠组。但血清PTH升高。这些变化可能是由于活性形式的维生素D3的血清水平较低而导致肠对Ca和P的吸收减少。(4)甲状腺激素：妊高征患者血清中反T3水平较高，游离T3水平较低。这可能是母体代谢低下加剧的结果，其中T4向rT 3的转化比T4向T3的转化更占主导地位。然而，胎盘内部的单脱碘似乎阻止了甲状腺激素从母体到胎儿的主动运动。(5)胎儿生长和胎儿窘迫：这项研究证明，在妊高征的情况下，胎盘功能不全状态引起的胎儿生长迟缓显着有助于慢性胎儿窘迫的发展。产前超声评估胎儿生长可能是有效和适当的预测胎儿窘迫的情况下，高危妊娠。少

项目成果

中山洋: 日本産科婦人科学会雑誌. 38. 1578-1586 (1986)

Hiroshi Nakayama：日本妇产科学会杂志 38. 1578-1586 (1986)。

三村治: 日本内分泌学会雑誌. (1988)

Osamu Mimura：日本内分泌学会杂志（1988）。

丸尾原義: 日本新生児学会雑誌. 23. 492-500 (1987)

Maruohara, Y.：日本新生儿学会杂志 23. 492-500 (1987)

Noriyuki,Ohara: "Calcium Metabolism and Calcium-regulating Hormones during Normal Pregnancy" Folia Endocrinologica Japonica. 62. 1578-1586 (1986)

Noriyuki,Ohara：“正常怀孕期间的钙代谢和钙调节激素”Folia Endocrinologica Japonica。

藤井良造: 日本内分泌学会雑誌. 63. 1241-1254 (1987)

Ryozo Fujii：日本内分泌学会杂志 63. 1241-1254 (1987)。