The mechanism of fetal homeostasis in intrauterine growth-retarded fetus

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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.