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Oxygen Supplementation to Stabilize Preterm Infants in the Fetal to Neonatal Transition: No Satisfactory Answer.

Torres-Cuevas I, Cernada M, Nuñez A, Escobar J, Kuligowski J, Chafer-Pericas C, Vento M - Front Pediatr (2016)

Bottom Line: Immediately after birth with the initiation of breathing, the lung expands and oxygen availability to tissue rises by twofold, generating a physiologic oxidative stress.However, both lung anatomy and function and the antioxidant defense system do not mature until late in gestation, and therefore, very preterm infants often need respiratory support and oxygen supplementation in the delivery room to achieve postnatal stabilization.Notably, interventions in the first minutes of life can have long-lasting consequences.

View Article: PubMed Central - PubMed

Affiliation: Neonatal Research Group, Health Research Institute La Fe , Valencia , Spain.

ABSTRACT
Fetal life elapses in a relatively low oxygen environment. Immediately after birth with the initiation of breathing, the lung expands and oxygen availability to tissue rises by twofold, generating a physiologic oxidative stress. However, both lung anatomy and function and the antioxidant defense system do not mature until late in gestation, and therefore, very preterm infants often need respiratory support and oxygen supplementation in the delivery room to achieve postnatal stabilization. Notably, interventions in the first minutes of life can have long-lasting consequences. Recent trials have aimed to assess what initial inspiratory fraction of oxygen and what oxygen targets during this transitional period are best for extremely preterm infants based on the available nomogram. However, oxygen saturation nomogram informs only of term and late preterm infants but not on extremely preterm infants. Therefore, the solution to this conundrum may still have to wait before a satisfactory answer is available.

No MeSH data available.


Related in: MedlinePlus

Correlation between amniotic fluid levels of erythropoietin (EPO) and meta-tyrosine, a biomarker of oxidative damage to protein in diabetic type 2 pregnancies treated with insulin (23).
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Figure 4: Correlation between amniotic fluid levels of erythropoietin (EPO) and meta-tyrosine, a biomarker of oxidative damage to protein in diabetic type 2 pregnancies treated with insulin (23).

Mentions: Physiological systems are adapted to sense O2 needs not only to avoid excessive exposures to ROS but also to provide sufficient O2 to allow normal cellular functioning. The most relevant oxygen sensing transcription factors are hypoxia-inducible factor (HIF), cAMP response-binding protein (CREB), nuclear factor kappa B (NFκB), activator protein 1 (AP-1), and p53. These factors regulate gene expression in response to changes in the concentration of oxygen and derived ROS. Low O2 containing environments favor early placental and fetal development. Angiogenesis is stimulated by low oxygen tissue concentrations through transcriptional and post-transcriptional regulation of growth factors, such as vascular endothelial growth factors (VEGFs), erythropoietin (EPO), placental growth factor (PGF), and angiopoietins 1 and 2. The master regulator for the cell’s adaptive responses to hypoxia is HIF-1, a heterodimeric transcription factor comprising HIF-1α and HIF-1β subunits (22). Activated genes, especially VEGF and EPO, enhance O2 delivery to tissue. EPO does not cross the placenta, and it does not accumulate in tissue. Therefore, fetal plasma concentration of EPO is determined by its rate of synthesis and elimination, and amniotic fluid EPO levels correlate well to fetal and neonatal plasma EPO levels obtained simultaneously at elective and emergency cesarean section. Amniotic fluid EPO concentration increases exponentially during fetal hypoxia and correlates to oxidative and nitrosative stress in the fetus (Figure 4). Alteration of EPO concentration in amniotic fluid correlates to immediate postnatal complications and could, therefore, be used as a reliable biomarker to indicate emergency C section (23).


Oxygen Supplementation to Stabilize Preterm Infants in the Fetal to Neonatal Transition: No Satisfactory Answer.

Torres-Cuevas I, Cernada M, Nuñez A, Escobar J, Kuligowski J, Chafer-Pericas C, Vento M - Front Pediatr (2016)

Correlation between amniotic fluid levels of erythropoietin (EPO) and meta-tyrosine, a biomarker of oxidative damage to protein in diabetic type 2 pregnancies treated with insulin (23).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4835680&req=5

Figure 4: Correlation between amniotic fluid levels of erythropoietin (EPO) and meta-tyrosine, a biomarker of oxidative damage to protein in diabetic type 2 pregnancies treated with insulin (23).
Mentions: Physiological systems are adapted to sense O2 needs not only to avoid excessive exposures to ROS but also to provide sufficient O2 to allow normal cellular functioning. The most relevant oxygen sensing transcription factors are hypoxia-inducible factor (HIF), cAMP response-binding protein (CREB), nuclear factor kappa B (NFκB), activator protein 1 (AP-1), and p53. These factors regulate gene expression in response to changes in the concentration of oxygen and derived ROS. Low O2 containing environments favor early placental and fetal development. Angiogenesis is stimulated by low oxygen tissue concentrations through transcriptional and post-transcriptional regulation of growth factors, such as vascular endothelial growth factors (VEGFs), erythropoietin (EPO), placental growth factor (PGF), and angiopoietins 1 and 2. The master regulator for the cell’s adaptive responses to hypoxia is HIF-1, a heterodimeric transcription factor comprising HIF-1α and HIF-1β subunits (22). Activated genes, especially VEGF and EPO, enhance O2 delivery to tissue. EPO does not cross the placenta, and it does not accumulate in tissue. Therefore, fetal plasma concentration of EPO is determined by its rate of synthesis and elimination, and amniotic fluid EPO levels correlate well to fetal and neonatal plasma EPO levels obtained simultaneously at elective and emergency cesarean section. Amniotic fluid EPO concentration increases exponentially during fetal hypoxia and correlates to oxidative and nitrosative stress in the fetus (Figure 4). Alteration of EPO concentration in amniotic fluid correlates to immediate postnatal complications and could, therefore, be used as a reliable biomarker to indicate emergency C section (23).

Bottom Line: Immediately after birth with the initiation of breathing, the lung expands and oxygen availability to tissue rises by twofold, generating a physiologic oxidative stress.However, both lung anatomy and function and the antioxidant defense system do not mature until late in gestation, and therefore, very preterm infants often need respiratory support and oxygen supplementation in the delivery room to achieve postnatal stabilization.Notably, interventions in the first minutes of life can have long-lasting consequences.

View Article: PubMed Central - PubMed

Affiliation: Neonatal Research Group, Health Research Institute La Fe , Valencia , Spain.

ABSTRACT
Fetal life elapses in a relatively low oxygen environment. Immediately after birth with the initiation of breathing, the lung expands and oxygen availability to tissue rises by twofold, generating a physiologic oxidative stress. However, both lung anatomy and function and the antioxidant defense system do not mature until late in gestation, and therefore, very preterm infants often need respiratory support and oxygen supplementation in the delivery room to achieve postnatal stabilization. Notably, interventions in the first minutes of life can have long-lasting consequences. Recent trials have aimed to assess what initial inspiratory fraction of oxygen and what oxygen targets during this transitional period are best for extremely preterm infants based on the available nomogram. However, oxygen saturation nomogram informs only of term and late preterm infants but not on extremely preterm infants. Therefore, the solution to this conundrum may still have to wait before a satisfactory answer is available.

No MeSH data available.


Related in: MedlinePlus