Plasma Immunoreactive Endothelin-1 Concentration in Human Fetal Blood: Its Relation to Asphyxia

Abstract

ABSTRACT. To elucidate the effects of birth stress on immunoreactive endothelin-1 (irET-1) concentrations in fetal blood, we determined irET-1 levels in cord plasma in different modes of delivery associated with or without complications such as asphyxia. The irET-1 concentrations in both the umbilical artery and vein were significantly higher than those found in maternal venous blood at delivery, although there was no significant difference between preterm and full-term infants. When plasma irET-1 concentrations of healthy infants born by vaginal delivery and by cesarean section without labor were compared, the former had significantly ( p < 0.05) higher levels than the latter (15.4 f 4.9 pg/mL versus 11.1 f 3.1 pg/mL). Furthermore, umbilical venous plasma obtained from vaginally delivered infants complicated by asphyxia showed significantly ( p < 0.001) higher irET-1 levels (28.2 f 9.4 pg/ mL) than those of nonasphyxiated infants (14.2 f 4.5 pg/ mL). These data suggest that birth stress, especially asphyxia, may contribute to the increase in fetal circulating irET-1 levels. (Pediatr Res 30: 244-247, 1991) Abbreviations CPK, creatine phosphokinase ET-1, endothelin-1 GOT, aspartate aminotransferase irET-1, immunoreactive ET-1 LDH, lactic acid dehydrogenase TFA, trifluoroacetic acid Endothelin-1 is a potent vasoconstrictor peptide with 2 1 amino acid residues, originally isolated and sequenced from the supernatant of cultured porcine aortic endothelial cells, and the first member of the mammalian endothelin family (1-4). Since ET-1 produces very potent vasoconstriction and an extremely longlasting pressor response, ET-1 may play an important role in the control of blood pressure and/or local blood flow (1, 3, 4). Recently, low concentrations of ET-1 have been detected in plasma from healthy subjects (5-7). Raised plasma concentrations of ET-1 have been observed in certain pathophysiologic conditions, such as uremia (8), acute renal failure (9), acute

Endothelin 1-21 Plasma Concentrations on Days 1 and 4 of Life in Healthy and III Preterm Neonates

“…The results of the present study indicate that preterm infants have high plasma ET concentrations on the 1st postpartum day (16.25 ± 8.14 and 21.81 ± 5.87 pmol/1) com pared to the levels reported in the literature for healthy subjects [19][20][21], Other studies [13][14][15][16] have shown that plasma concentra tions of ET-1-like immunoreactivity in cord blood of full-term neonates was much higher than in maternal blood.The cause of elevated plasma ET concentrations in newborns is un known. Active transport of ETs across the pla centa has been excluded in previous studies 319 [14,16] as a cause of this increase due to the absence of umbilical arteriovenous difference of ET concentrations.…”

“…Active transport of ETs across the pla centa has been excluded in previous studies 319 [14,16] as a cause of this increase due to the absence of umbilical arteriovenous difference of ET concentrations. However, the placenta could be a possible source for synthesis and secretion of ET-1, because the peptide was first cloned from a placental cDNA library [22], Nevertheless, birth stress and especially asphyxia most likely trigger ET synthesis and secretion in the fetal circulation at birth [16]. It has been reported that hypoxia directly stimulates ET-1 release from rat mesenteric arteries in vitro [23] and that experimental asphyxia increases plasma ET-1 concentra tions in the pig [24].…”

“…Thus, over production of endothelins or increased pla cental receptor concentrations could result in limitation of fetoplacental blood flow leading to intrauterine growth retardation [9], ETs are believed to be implicated in a variety of pathologic conditions of the newborn, as per sistent pulmonary hypertension, intraventric ular hemorrhage (IVH) or necrotizing entero colitis [9,10], while they may also play a role in the closure of the ductus arteriosus [11]. ET plasma concentrations have been mea sured in children and infants > 3 months [12], in cord blood [13][14][15][16], during the first postpartum days of healthy full-term neo nates [17] and recently in fetuses of 18-24 weeks [18].…”

Stable Precursor Fragments of Vasoactive Peptides in Umbilical Cord Blood of Term and Preterm Infants

“…Previous reports had demonstrated high umbilical cord blood levels of ET-1 which were even more pronounced in newborns with birth asphyxia [19,20] leading to a significant negative correlation between ADM levels and pH in cord blood [21]. These observations could indicate that birth stress may be an acute stimulus for the production of ADM and ET-1 in vascular endothelium.…”

Effect of Meconium Aspiration on Plasma Endothelin-1 Level and Pulmonary Hemodynamics in a Piglet Model

“…ET-1, a 21-amino acid peptide, can be released from the endothelium by various stimuli including shear stress, stretch, pressure, hypoxia, thrombin, epinephrine, phorbol ester, transforming growth factor-ß and other pharmacological agents [3,[21][22][23][24]. Animal studies have shown that hypoxia [25][26][27][28] and vascular injury [29][30] can increase ET-1 level.…”