THE INDUCTION OF HIBERNATION OF FETAL CARDIOCYTE BY ADENOSINE

在冠状动脉血流量减少的过程中，代偿机制通过降低成人的心功能来维持冠脉流量。这种机制被称为冬眠。近年来，腺苷与冬眠的关系得到了很好的研究。胎儿脑和心肌中腺苷的生物活性远高于成人，这可能是胎儿和新生儿心脏病发病率较低的原因之一。我们评估了5‘-核苷酸酶和腺苷脱氨酶水平在胎儿缺血和再灌流应激过程中的变化，证明了胎儿有一种倾向于增加腺苷水平的代偿机制。然而，过量的腺苷具有细胞毒性作用，因此胎儿也有一种自我防御机制，可以抑制过量的腺苷。这些代偿机制可能诱导胎儿冬眠以适应宫内有限的氧气供应，最终有助于适应宫内应激条件，如妊娠高血压综合征、IUGR、感染和双胎妊娠。

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.