The mechanism of fetal homeostasis in intrauterine growth-retarded fetus

胎儿宫内发育迟缓(IUGR)被认为是慢性胎儿窘迫的一种状态。众所周知，胎儿在应对压力时会分泌儿茶酚胺。因此，对胎儿宫内发育迟缓中儿茶酚胺的研究是很有意义的。本研究的目的是利用人和实验动物研究生长迟缓胎儿中的儿茶酚胺。方法：临床研究对象为临产前剖宫产足月胎儿宫内发育迟缓。取羊水和脐动脉血浆进行儿茶酚胺分析。对实验性IUGR大鼠羊水、胎儿肾上腺和胎儿血浆中的儿茶酚胺进行了测定。测定胎儿肾上腺苯乙醇胺-N-甲基转移酶(PNMT)活性。结果：临床IUGR组羊水和脐动脉血儿茶酚胺水平，尤其是肾上腺素水平均显著高于AFD组。即使在反应性无负荷试验的病例中，也观察到羊水中儿茶酚胺的增加。在实验性IUGR大鼠中，羊水中儿茶酚胺浓度升高伴随着胎儿肾上腺素含量的下降。然而，将去甲肾上腺素转化为肾上腺素的酶PNMT的活性在IUGR和正常发育的胎儿之间没有差异。IUGR组胎儿急性失血性休克后肾上腺肾上腺素释放较正常胎儿显著减少。结论：生长迟缓胎儿分泌儿茶酚胺，尤其是肾上腺肾上腺素，作为对慢性应激的保护机制，IUGR羊水中儿茶酚胺水平升高是胎儿受损的早期迹象。IUGR大鼠肾上腺肾上腺素含量降低可能是其防御机制储备能力下降的原因之一。

Intrauterine growth retardation (IUGR) is thought to be a condition of chronic fetal distress. It is well known that fetus secretes catecholamine in response to stress. So, it is of interest to investigate the catecholamine in IUGR.The aim of this work was to study the catecholamine in growth-retarded fetus using both humans and experimental animals. Methods : The clinical subjects were term IUGR delivered by cesarean section prior to the onset of labor. Amniotic fluid and umbilical arterial plasma were obtained for the analysis of catecholamines. In experimental rat IUGR,catecholamines in the amniotic fluid, the fetal adrenal glands and the fetal plasma were measured. Phenylethanolamine-N-methyltransferase (PNMT) activities in the fetal adrenal glands were also assayd. Results : In clinical IUGR,amniotic fluid and umbilical arterial catecholamine levels, especially epinephrine, were significantly higher than those of the AFD cases before labor. This increase in amniotic fluid catecholamines was observed even in the cases which showed reactive nonstress test. In experimental rat IUGR,higher concentrations of amniotic fluid catecholamines were accompanied by the decrease of fetal adrenal epinephrine contents. However, activities of PNMT,the enzyme which converts norepinephrine into epinephrine, showed no difference between the IUGR and the normally developed fetuses. Adrenal epinephrine release following acute fetal hemorrhagic shock in the IUGR was significantly decreased compared to the normal fetuses. Conclusions : Growth-retarded fetus secrets catecholamines, especially adrenal epinephrine, as a protective mechanism against the chronic stress, and elevation in amniotic fluid catecholamine levels in IUGR is a carly sign of fetal compromise. The decrease in adrenal epinephrine contents in IUGR might be responsible for the reduced reserve power in the defense mechanism.