Project/Area Number |
14571588
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Nippon Medical School |
Principal Investigator |
SAWA Rintaro NIPPON MEDICAL SCHOOL, OBSTETRICS AND GYNECOLOGY, ASSITANT PROFESSOR, 医学部, 講師 (30267174)
|
Co-Investigator(Kenkyū-buntansha) |
YONEYAMA Yoshio NIPPON MEDICAL SCHOOL, OBSTETRICS AND GYNECOLOGY, ASSITANT PROFESSOR, 医学部, 講師 (00201096)
|
Project Period (FY) |
2002 – 2003
|
Project Status |
Completed (Fiscal Year 2003)
|
Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2003: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
Keywords | ADENOSINE / FEATL CARDIOCYTE / HIBERNATION / 5'-NUCLEOTIDASE / ADENOSINE DEAMINASE / ハイバーネーション / 5'-nucleotiduse |
Research Abstract |
During the decrease of coronary blood flow, the compensative mechanism acts to maintain coronary flow by lowering cardiac function in the adults. This mechanism has been known as hibernation. Recently, the relationship between adenosine and hibernation has been well investigated. The bioactivity of adenosine in fetal brain and cardiocyte are much higher than those in adults, which may contribute to the low rate of cardiac diseases in fetus and newborn. We evaluated changes in 5'-nucleotidase and adenosine deaminase levels during fetal ischemic and reperfusion stress in chronically instrumented fetal goats, and demonstrated that fetuses have a compensative mechanism that tends to increase adenosine levels. However, excessive adenosine has cytotoxic effects, so fetuses have also have a self-defense mechanism that dampens excessive adenosine. These compensative mechanisms may induce fetal hibernation to adapt limited oxygen supply in utero, which eventually contribute to adapt the stressful conditions in utero, such as pregnancy-induced hypertension, IUGR, infection and twin pregnancy.
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