1988 Fiscal Year Final Research Report Summary
Research on pathophysiology, the prediction of onset and the prediction of latent fetal distress in toxemic pregnancy.
| Project/Area Number |
61480351
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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 |
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Principal Investigator |
MORIKAWA Hajime Kobe University School of Medicine, Assistant Proffessor, 医学部, 講師 (30030894)
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| Co-Investigator(Kenkyū-buntansha) |
UEDA Yasuo Kobe University School of Medicine, Research Associate, 医学部, 助手 (20168636)
DEGUCHI Masaki Kobe University School of Medicine, Research Associate, 医学部附属病院, 助手 (70163938)
MARUO Takeshi Kobe University School of Medicine, Assistant Proffessor, 医学部附属病院, 講師 (60135811)
ASHITAKA Yoshihiko Kobe University School of Medicine, Associate Proffessor, 医学部, 助教授 (10030959)
MOCHIZUKI Matsuto Kobe University School of Medicine, Proffessor, 医学部, 教授 (80030922)
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| Project Period (FY) |
1986 – 1988
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| Keywords | Pregnancy Induced Hypertension (PIH) / Calcium Metabolism / Vasopressor System / Vasodepressor System / Intracellular Na^+ concentration / Na^+-K^+-ATPase / Latent Fetal Distress / パルスドップラー法 |
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| Research Abstract |
1. Pathophysiology of pregnancy induccd hypertension(PIH) ; in PIH, the vasopressor system (PRA and PAC) was suppressed, and the negative feedback mechanism of renin secretion against angiotensin I (AI) loading was not observed. On the contrary, the vasodepressor system (plasma bradykinin levels and hANP levels) was stimulated in an in-situ condition, and its reserve function against AI of salt loading was decreased. These results suggest that both the vasopressor and the vasodepressor system do not play a causative role on the onset of PIH. From the point of view on vascular resistance, increase of the peripheral vascular resistance was confirmed in PIN, since intracellular Na^+ concentrations were significantly elcvated and a brcakdown of the compensatory increase of the Na^+ -K^+ -ATPase activities was obsorved.
2. Prediction of PIH : High PRA in the lst and 2nd trimester closely correlated to the occurrence of PIH, and in scrial estimation of PRA from 2nd trimester to term, PRA began to dccrease below lower limits of normal pregnancy at several weeks before the onset of PIH.
3. Caleium metabolism ; Calcium metabolism in PIH was characteristic of low scrum levels of total calcium, ionized calcium, 1,25, (OH)_2 vitamin D_3 and high serum levels of parathyroid hormone. Hypocalcemia secmed to be a result of the decrease in intestinal calcium absorption mainly caused by the decrease of the synthesis of 1,25, (OH)_2 vitamin D_3 in feto-placental unit.
4. Prediction of latent fetal distress ; The fetal growth retardation induced by placental insufficiency strongly correlates with latent fetal distross in cases of PIH. Morcover, these findings indicate that ultrasonographical assessments of fetal growth during gestation might also be useful to predict fetal distress at the time of parturition.
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