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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

(A) Under normal circumstances, nitric oxide produced by the action of NO synthase activates guanylate cyclase, which catalyzes the formation of cGMP and subsequently lung vessel vasodilatation. In addition, superoxide anion, derived from air-borne oxygen by the action of superoxide dismutases, is catalyzed to hydrogen peroxide, which acts also as lung vessel vasodilator. (B) In the presence of oxygen in excess (resuscitation and ventilation), anion superoxide will sequester nitric oxide and produce highly reactive peroxynitrite. The amount of available cGMP is reduced and also the production of hydrogen peroxide. Under these circumstances, there is a potent tendency toward vasoconstriction (17, 25, 27).
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Figure 5: (A) Under normal circumstances, nitric oxide produced by the action of NO synthase activates guanylate cyclase, which catalyzes the formation of cGMP and subsequently lung vessel vasodilatation. In addition, superoxide anion, derived from air-borne oxygen by the action of superoxide dismutases, is catalyzed to hydrogen peroxide, which acts also as lung vessel vasodilator. (B) In the presence of oxygen in excess (resuscitation and ventilation), anion superoxide will sequester nitric oxide and produce highly reactive peroxynitrite. The amount of available cGMP is reduced and also the production of hydrogen peroxide. Under these circumstances, there is a potent tendency toward vasoconstriction (17, 25, 27).

Mentions: Oxygen content of the inspiratory gas admixture decisively influences lung vascular tone and is considered one of the main factors causing vasodilatation in the fetal to neonatal transition (36). Traditionally, high oxygen inspiratory fractions have been recommended to enhance newly born infants postnatal adaptation, especially in asphyxiated term babies but also in preterm. However, experimental and clinical studies have shown that fetal to neonatal transition and oxygen supplementation cause an increased production of oxygen free radicals, especially anion superoxide (37). Under normal circumstances, exposure to a brief period of hyperoxia triggers the expression of SODs, which dismutate anion superoxide to hydrogen peroxide (Figure 5). H2O2 has a vasodilatation effect upon the lung vasculature, thus reducing vascular resistance and increasing pulmonary blood flow. However, in the presence of an excess of oxygen, non-dismutated anion superoxide may cause vasoconstriction by reducing the bioavailability of nitric oxide through the blocking the activity of eNOS and favoring the formation of the highly toxic peroxynitrite; moreover, in smooth muscle cells, free radicals inactivate soluble guanyl cyclase and activate phosphodiesterase P5, resulting in decreased levels of cyclic guanidine monophosphate. Altogether, these mechanisms lead to pulmonary vasoconstriction (Figure 5) (38, 39).


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)

(A) Under normal circumstances, nitric oxide produced by the action of NO synthase activates guanylate cyclase, which catalyzes the formation of cGMP and subsequently lung vessel vasodilatation. In addition, superoxide anion, derived from air-borne oxygen by the action of superoxide dismutases, is catalyzed to hydrogen peroxide, which acts also as lung vessel vasodilator. (B) In the presence of oxygen in excess (resuscitation and ventilation), anion superoxide will sequester nitric oxide and produce highly reactive peroxynitrite. The amount of available cGMP is reduced and also the production of hydrogen peroxide. Under these circumstances, there is a potent tendency toward vasoconstriction (17, 25, 27).
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Related In: Results  -  Collection

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

Figure 5: (A) Under normal circumstances, nitric oxide produced by the action of NO synthase activates guanylate cyclase, which catalyzes the formation of cGMP and subsequently lung vessel vasodilatation. In addition, superoxide anion, derived from air-borne oxygen by the action of superoxide dismutases, is catalyzed to hydrogen peroxide, which acts also as lung vessel vasodilator. (B) In the presence of oxygen in excess (resuscitation and ventilation), anion superoxide will sequester nitric oxide and produce highly reactive peroxynitrite. The amount of available cGMP is reduced and also the production of hydrogen peroxide. Under these circumstances, there is a potent tendency toward vasoconstriction (17, 25, 27).
Mentions: Oxygen content of the inspiratory gas admixture decisively influences lung vascular tone and is considered one of the main factors causing vasodilatation in the fetal to neonatal transition (36). Traditionally, high oxygen inspiratory fractions have been recommended to enhance newly born infants postnatal adaptation, especially in asphyxiated term babies but also in preterm. However, experimental and clinical studies have shown that fetal to neonatal transition and oxygen supplementation cause an increased production of oxygen free radicals, especially anion superoxide (37). Under normal circumstances, exposure to a brief period of hyperoxia triggers the expression of SODs, which dismutate anion superoxide to hydrogen peroxide (Figure 5). H2O2 has a vasodilatation effect upon the lung vasculature, thus reducing vascular resistance and increasing pulmonary blood flow. However, in the presence of an excess of oxygen, non-dismutated anion superoxide may cause vasoconstriction by reducing the bioavailability of nitric oxide through the blocking the activity of eNOS and favoring the formation of the highly toxic peroxynitrite; moreover, in smooth muscle cells, free radicals inactivate soluble guanyl cyclase and activate phosphodiesterase P5, resulting in decreased levels of cyclic guanidine monophosphate. Altogether, these mechanisms lead to pulmonary vasoconstriction (Figure 5) (38, 39).

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