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Normobaric oxygen paradox and erythropoietin production in critically ill patients: a prospective observational study

Introduction

The normobaric oxygen paradox (NOP) postulates that a period of normobaric hyperoxia followed by a rapid return to normoxia will create a condition of relative hypoxia, which acts in turn as a stimulus for erythropoietin (EPO) production [1]. Variations in GSH and oxygen free radical (ROS) levels may be involved in this process. We tested the NOP in critically ill patients.

Methods

A prospective observational study on 38 mechanically ventilated (FiO2 <50%) patients with no active bleeding, no blood transfusion needed, and no kidney failure. Eighteen patients underwent a 2-hour period of normobaric hyperoxia (FiO2 = 100%), 20 patients were evaluated as controls (no FiO2 variations). EPO was assayed at baseline (t0), 24 hours (D1) and 48 hours (D2). Serum GSH and ROS were assayed at t0 (baseline), t1 (2-hour FiO2 100%) and t2 (2hour return to normoxia) in 12 patients in the hyperoxia group.

Results

EPO tended to increase in the hyperoxia group over time (P = 0.05), while it remained stable in the control group (P = 0.53) (Figure 1). ROS levels increased at t1 and decreased at t2, GSH tended to decrease at t1 and increased at t2 in the hyperoxia group.

figure1

Figure 1

Conclusion

Relative hypoxia after a transient period of normobaric hyperoxia induces an increase in GSH levels, thus enhancing ROS scavenging. This may act as a stimulus for EPO production.

References

  1. 1.

    Balestra , et al: J Appl Physiol. 2006, 100: 512-8. 10.1152/japplphysiol.00964.2005.

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Zuccari, S., Donati, A., Damiani, E. et al. Normobaric oxygen paradox and erythropoietin production in critically ill patients: a prospective observational study. Crit Care 19, P320 (2015). https://doi.org/10.1186/cc14400

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Keywords

  • Erythropoietin
  • Oxygen Free Radical
  • Prospective Observational Study
  • Kidney Failure
  • Active Bleeding