Cardioprotective Effects of Increased Endogenous Erythropoietin After Normobaric Oxygen Breathing

Overview

Tissue hypoxia is the only accepted trigger for erythropoietin (EPO) production. However, in healthy subjects EPO concentrations have also increased after oxygen breathing. The aim of our study is to confirm these observations. Besides its main function in erythropoiesis, EPO has also shown tissue protective effects. The second goal of our study is to observe the cardioprotective effects of increased endogenous EPO, induced after normobaric oxygen breathing.

Currently, renal tissue hypoxia is the only widely accepted trigger for erythropoietin (EPO) production. However, previous studies in healthy subjects have demonstrated that a sudden and sustained decrease in tissue oxygen level, aside from an absolute low level of tissue oxygen tension, could also act as a trigger for EPO production. To confirm these observations and to clarify an eventual role of free oxygen radicals and antioxidants, hypobaric pure oxygen will be administered to healthy subjects. The major physiologic function of EPO is thought to be the induction of erythropoiesis. However, a growing body of evidence indicates that EPO has tissue-protective effects and prevents tissue damage during ischemia. In an ex vivo proof-of-concept, protective effects of EPO have been shown in human myocardium. The second goal of our study is to observe the cardioprotective effects of increased endogenous EPO, induced after normobaric oxygen breathing.

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