The mechanism of fetal homeostasis in intrauterine growth-retarded fetus

宫内生长迟缓被认为是一种慢性胎儿窘迫的情况。众所周知，胎儿在应激时会分泌儿茶酚胺。因此，研究宫内发育迟缓胎儿体内儿茶酚胺的变化具有重要意义。方法：临床研究对象为足月胎儿宫内发育迟缓（IUGR）分娩前剖宫产。取羊水和脐动脉血浆进行儿茶酚胺分析。本文测定了实验性IUGR大鼠羊水、胎儿肾上腺和胎儿血浆中的儿茶酚胺含量。同时测定了胎儿肾上腺中苯乙醇胺-N-甲基转移酶（PNMT）的活性。结果如下：临床IUGR组羊水及脐动脉血中的儿茶酚胺水平，尤其是肾上腺素水平，均显著高于AFD组。即使在反应性非应激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中，羊水中儿茶酚胺浓度升高，胎儿肾上腺素含量下降。然而，PNMT的活性，将去甲肾上腺素转化为肾上腺素的酶，显示IUGR和正常发育的胎儿之间没有差异。与正常胎儿相比，IUGR胎儿急性失血性休克后肾上腺素的释放明显减少。结论：生长迟缓的胎儿分泌儿茶酚胺类物质，尤其是肾上腺素，作为对抗慢性应激的一种保护机制，IUGR时羊水中儿茶酚胺水平升高是胎儿受损的一个早期迹象。IUGR时肾上腺素含量降低可能是IUGR防御机制储备能力降低的原因。

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.