Catecholamine Levels and Their Correlation to Blood Gases in Umbilical Venous Blood Obtained by Cordocentesis

Abstract

The plasma catecholamine concentration was evaluated in umbilical venous blood obtained by cordocentesis performed in 77 fetuses for indications including: nonimmune hydrops; Rh incompatibility; intrauterine growth retardation; polyhydramnios; anomalies; immunological disorders, and possible viral infection. The pH as well as pO₂ of the umbilical venous blood showed a notably significant negative correlation with the norepinephrine concentration (r = ––0.5607, r = ––0.4467); while pCO₂ was also significantly correlated with the norepinephrine concentration (r = 0.4955). When the pCO₂/pO₂ ratio was tentatively put up for comparison, the ratio was undoubtedly better correlated (r = 0.60442) with the fetal norepinephrine concentration than any other biochemical variable. Moreover, the ratio over 2.0 suggests that fetal catecholamine values have reached abnormal levels.

Catecholamines Mediate Multiple Fetal Adaptations during Placental Insufficiency That Contribute to Intrauterine Growth Restriction: Lessons from Hyperthermic Sheep

“…Poor nutrient supply necessitates metabolic adaptations by the fetus that result in asymmetrical intrauterine growth restriction (IUGR) [2–4]. Although specific etiology of PI is rarely determined and is likely case-specific, common results of placental dysfunction include fetal hypoxemia and hypoglycemia that worsen in concert with increasing fetal demands over the last half of gestation, causing hypercatecholaminemia and hypoinsulinemia [4–7]. Parallels for characteristics observed in human PI-IUGR fetuses have been demonstrated in an ovine model of hyperthermia-induced PI [8].…”

Islet adaptations in fetal sheep persist following chronic exposure to high norepinephrine

“…Fetal stress associated with placental dysfunction chronically elevates catecholamines (Okamura et al 1990; Greenough et al 1990). In this study, we demonstrate that sustained exposure to elevated NE directly produces lasting adaptations in fetal β-cells.…”

“…Fetal stress imposed by complications such as ischemic placental disease leads to prolonged increases in fetal circulating catecholamines (Okamura et al 1990; Greenough et al 1990; Ananth & Vintzileos 2006; Ananth & Friedman 2014). Elevated epinephrine and norepinephrine (NE) concentrations in the fetus are primary determinants for adaptive changes in metabolism and reduced growth rates (Apatu & Barnes 1991; Milley 1997; Bassett & Hanson 1998; Davis et al 2015).…”

Relation between Fetal Blood Gas Levels and the Outcome of Babies in Severe Preeclampsia.

“…In other words, the fetal blood pH may not be a reliable clue in predicting the subsequent outcome of the fetus. In the fetus with severe hypoxemia and without acidemia, although renal compensation to maintain the homeostasis may still work, functional impairment in critical organs may become irreversible probably because of long-lasted hypoxia and blood redistribution induced by catecholamine release (Okamura et al 1990b). We think that the extent of the deviation of fetal blood p02 value, not pH value, from the norm may serve as a marker for the risk of fetal demise.…”