| 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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