1994 Fiscal Year Final Research Report Summary
THE STUDY OF ETIOLOGY AND PATHOPHYSIOLOGY OF PREECLAMPSIA,ANALYSIS IN THE ASPECT OF INTRACELLULAR SIGNAL TRANSDUCTION
Project/Area Number |
04454419
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Research Category |
Grant-in-Aid for General Scientific Research (B)
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Allocation Type | Single-year Grants |
Research Field |
Obstetrics and gynecology
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Research Institution | KOBE UNIVERSITY |
Principal Investigator |
MOCHIZUKI Matsuto Kobe University School of Medicine, Professor, 医学部, 教授 (80030922)
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Co-Investigator(Kenkyū-buntansha) |
DEGUCHI Masaki Kobe University School of Medicine, Lecturer, 医学部・付属病院, 助手 (70163938)
YAMASAKI Mineo Kobe University School of Medicine, Lecturer, 医学部・付属病院, 講師 (00220301)
MARUO Takeshi Kobe University School of Medicine, Associate Professor, 医学部・付属病院, 助教授 (60135811)
MORIKAWA Hajime Kobe University School of Medicine, Associate Professor, 医学部, 助教授 (30030894)
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Project Period (FY) |
1992 – 1994
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Keywords | Pregnancy Induced Hypertension / Endothelin-1 / Platelet-Activating Factor / Hyperlipidemia / Fatty Acids / Nitric Oxide / Magnesium / IGF-1 |
Research Abstract |
1. Endothelial cell function : Pregnant women complicated with pregnancy-induced hypertension in severe type (severe PIH) showed increased plasma levels of endothelin-1 than did normal controls. Changes in fat metabolism were also observed in severe PIH as follows ; higher triglyceridemia with lower HDL-cholesterolemia, increased plasma saturated/unsaturated fatty acids ratio, increased plasma concentration of lipid-peroxide and decreased levels of plasma vitamin E.These are considered as factors intiating and/or deteriorating endothelial cell dysfunction. In vitro studies using cultured endothelial cells also demonstrated that altered profiles of sex steroids and that of lipids in the severe PIH are involved in the pathophysiology of the disorder. However, severe PIH patients also showed increased plasma concentration of platelet-activating factor, which has vasodilatory effect, suggesting that endothelium may still function to antagonize high blood pressure. Nitric oxide synthase of
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placental tissue in constitutive type was demonstrated to be equal on Western blot between normal pregnancy and severe PIH.Although the number of cases is small, there was a tendency of decreased urinary excretion of metabolites of nitric oxide in severe PIH. 2. Electrolytes metabolism : Concentrations of ionized Mgin whole blood and these of intracellular Mg were significantly lower in severe PIH than in normal controls, while there was no significant difference in serum Mg levels between the two groups. These suggest altered Mg metabolism exist in severe PIH.The results of MgSO4 loading revealed a relative deficiency in Mg in the disorder. 3. Fetal development : Plasma IGF-1 levels increased along the course of normal pregnancy correlating to fetal development and maternal weight gain. In severe PIH plasma concentrations of IGF-1 was extremely low in spite of maternal weight gain. This suggests change in IGF-1 reflects disorders in maternal circumstances in nutrition which is closely related to fetal growth. Less
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