Catecholamines in arterial and venous umbilical blood: placental extraction, correlation with fetal hypoxia, and transcutaneous partial oxygen tension.

In 34 parturient women the levels of free epinephrine (E), norepinephrine (NE), and dopamine (D) were determined by a radioenzymatic method using maternal venous and umbilical arterial and venous blood. The study was conducted to investigate the relationship between fetal catecholamines and hypoxia, fetal heart rate (FHR), and transcutaneous pO2 (tcpO2). The placental catecholamine extraction rates were also calculated. Results The NE concentrations (10,200 pg/ml) and the E concentrations (1,120 pg/ml) in the fetal arterial blood were highly elevated with mean values increased 4-fold over umbilical vein values. Compared with the maternal venous blood, NE values were increased 20-fold, and E values 10-fold. Free D concentrations in fetal arterial blood (130 pg/ml) had risen 2.5-fold over maternal levels. These results suggest that the catecholamines measured in cord blood are of fetal origin and that the placenta has a high capacity for inactivation of free catecholamines. The placental extraction rate is 77 +/- 14% for NE, 76 +/- 16% for E, and 33 +/- 25% for D. The placental extraction rates for E and NE were virtually identical; in agreement with morphological studies they demonstrated absence of sympathetic innervation on the fetal side of the placenta. Highly significant correlations were found between fetal arterial NE concentrations and the 1-minute APGAR score, pH and base deficit in the umbilical artery and alterations of the FHR (deceleration area, baseline FHR). Further analysis of FHR alterations reveals that an increase in deceleration area without tachycardia is not correlated with an increase of fetal arterial NE concentration. A significant rise in NE was only found with additional tachycardia which is often associated with a loss of oscillation amplitude. Fetal arterial E concentrations were found to correlate with the fetal parameters indicating increased adrenal secretion of the hormone during fetal stress. However, correlation coefficients were lower than those obtained for NE. A significant effect of fetal hypoxia on arterial and venous D levels could not be demonstrated. Fetal tcpO2 varies between 0-25 mm Hg during the last two hours before delivery. In most cases tcpO2 was lower than the arterial pO2. Besides epidermal thickness and artifacts, skin perfusion is a major factor influencing the tcpO2 (transcutaneous arterial pO2 difference). Vasoconstriction of the cutaneous vessels induced by increased NE secretion during hypoxia may obviously produce a fall in tcpO2.(ABSTRACT TRUNCATED AT 400 WORDS)