1987 Fiscal Year Final Research Report Summary
Integrated Studies on Endocrino-Metabolic Mechanisms of Fetal Growth and Fetal Distress
| Project/Area Number |
60480368
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Kobe University School of Medicine |
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Principal Investigator |
MOCHIZUKI Matsuto Kobe University School of Medicine, Professor, 医学部, 教授 (80030922)
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| Co-Investigator(Kenkyū-buntansha) |
UEDA Yasuo Kobe University School of Medicine, Research Assoc, 医学部, 助手 (20168636)
DEGUCHI Masaki Kobe University School of Medicine Hospital, Research Assoc, 医学部附属病院, 助手 (70163938)
MARUO Takeshi Kobe University School of Medicine, Assist, Professor, 医学部附属病院, 講師 (60135811)
MORIKAWA Hajime Kobe University School of Medicine, Assist. Professor, 医学部, 講師 (30030894)
ASHITAKA Yoshihiko Kobe University School of Medicine, Assoc. Professor, 医学部, 助教授 (10030959)
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| Project Period (FY) |
1985 – 1987
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| Keywords | Fetal Growth / Fetal Distress / Pregnancy Induced Yhpertension / Metabolism During Pregnancy / Calcium / 甲状腺ホルモン |
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| Research Abstract |
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
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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
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