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1 DAN Europe Research Division, Roseto, Italy; I.S.E.P.K., Universite Libre de Bruxelles, Brussels, Belgium; Department of Environmental & Occupational Physiology, Haute Ecole Paul Henri Spaak, Brussels, Belgium
2 DAN Europe Research Division, Roseto, Italy; Center for Hyperbaric Oxygen Therapy, Military Hospital Queen Astrid, Brussels, Belgium
3 DAN Europe Research Division, Roseto, Italy; I.S.E.P.K., Universite Libre de Bruxelles, Brussels, Belgium
4 DAN Europe Research Division, Roseto, Italy
* To whom correspondence should be addressed. E-mail: peter.germonpre{at}mil.be.
Renal (peritubular) tissue hypoxia is a well known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 hours and a period of breathing 100% oxygen at 2.5 ATA (atmospheres absolute) for 90 minutes (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay (RIA) at various time points during 24-36 hours. A 60% increase (P<0.001) in serum EPO was observed 36h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (for example after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger - the "normobaric oxygen paradox" - does not appear to be present after hyperbaric oxygen breathing.
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