Abstract

BackgroundThe effectiveness of sodium bicarbonate (SB) has recently been questioned although it is often used to correct metabolic acidosis of neonates. The aim of the present study was to examine its effect on hemodynamic changes and hydrogen peroxide (H2O2) generation in the resuscitation of hypoxic newborn animals with severe acidosis.MethodsNewborn piglets were block-randomized into a sham-operated control group without hypoxia (n = 6) and two hypoxia-reoxygenation groups (2 h normocapnic alveolar hypoxia followed by 4 h room-air reoxygenation, n = 8/group). At 10 min after reoxygenation, piglets were given either i.v. SB (2 mEq/kg), or saline (hypoxia-reoxygenation controls) in a blinded, randomized fashion. Hemodynamic data and blood gas were collected at specific time points and cerebral cortical H2O2 production was continuously monitored throughout experimental period. Plasma superoxide dismutase and catalase and brain tissue glutathione, superoxide dismutase, catalase, nitrotyrosine and lactate levels were assayed.ResultsTwo hours of normocapnic alveolar hypoxia caused cardiogenic shock with metabolic acidosis (pH: 6.99±0.07, HCO3 −: 8.5±1.6 mmol/L). Upon resuscitation, systemic hemodynamics immediately recovered and then gradually deteriorated with normalization of acid-base imbalance over 4 h of reoxygenation. SB administration significantly enhanced the recovery of both pH and HCO3− recovery within the first hour of reoxygenation but did not cause any significant effect in the acid-base at 4 h of reoxygenation and the temporal hemodynamic changes. SB administration significantly suppressed the increase in H2O2 accumulation in the brain with inhibition of superoxide dismutase, but not catalase, activity during hypoxia-reoxygenation as compared to those of saline-treated controls.ConclusionsDespite enhancing the normalization of acid-base imbalance, SB administration during resuscitation did not provide any beneficial effects on hemodynamic recovery in asphyxiated newborn piglets. SB treatment also reduced the H2O2 accumulation in the cerebral cortex without significant effects on oxidative stress markers presumably by suppressing superoxide dismutase but not catalase activity.

Highlights

  • Sodium bicarbonate (SB) has been used by many clinical practitioners to treat metabolic acidosis of asphyxiated neonates during and after resuscitation

  • Using an acute swine model of neonatal asphyxia, we investigated the effects of sodium bicarbonate (SB) on hemodynamic recovery and H2O2 generation after hypoxiareoxygenation

  • We examined secondary outcomes including pulmonary and carotid hemodynamics, enzymes and metabolites related to H2O2 production including superoxide dismutase (SOD) and catalase, nitrotyrosine and glutathione redox (oxidized glutathione (GSSG)/total glutathione (GSH)) ratio, a marker of oxidative stress [15,16,17]

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Summary

Introduction

Sodium bicarbonate (SB) has been used by many clinical practitioners to treat metabolic acidosis of asphyxiated neonates during and after resuscitation. It may be dangerous to use SB during hypoxia-ischemia of neonates because of paradoxical acidosis [2,6,7]. In a recent questionnaire survey, over 40% of consultant neonatologists in Europe would prescribe SB to asphyxiated neonates with severe metabolic acidosis [8]. The effectiveness of sodium bicarbonate (SB) has recently been questioned it is often used to correct metabolic acidosis of neonates. The aim of the present study was to examine its effect on hemodynamic changes and hydrogen peroxide (H2O2) generation in the resuscitation of hypoxic newborn animals with severe acidosis

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