Key result
A clinical intravenous dose of erythropoietin (50 IU/kg) did not significantly alter the ventilatory and pulmonary vascular responses to acute hypoxia in healthy men or women compared to placebo.
Why the study?
Does a clinically relevant intravenous dose of erythropoietin affect the hypoxic ventilatory response and/or hypoxic pulmonary vasoconstriction in healthy humans?
RCT (n=14)
Does a clinically relevant intravenous dose of erythropoietin affect the hypoxic ventilatory response and/or hypoxic pulmonary vasoconstriction in healthy humans?
p-value: p=n.s.
A clinical dose of intravenous erythropoietin does not affect the ventilatory or pulmonary vascular responses to acute hypoxia in healthy men or women.
No effect of clinical-dose erythropoietin on acute hypoxic responses in healthy adults; leaves open relevance in disease or chronic hypoxia.
New Findings What is the central question of this study? Does a clinically relevant intravenous dose of erythropoeitin affect the hypoxic ventilatory response and/or hypoxic pulmonary vasoconstriction in healthy humans? What is the main finding and its importance? Erythropoeitin does not influence the ventilatory and pulmonary vascular responses to acute hypoxia in men or women. Sustained and chronic hypoxia lead to an increase in pulmonary ventilation (hypoxic ventilatory response, HVR) and to an increase in pulmonary vascular resistance (hypoxic pulmonary vasoconstriction, HPV). In this study, we examined the effect of a clinical i.v . dose of recombinant human erythropoietin (50 IU kg −1 ) on the isocapnic HVR and HPV in seven male and seven female subjects by exposing them to hypoxia for 20 min (end‐tidal ∼50 mmHg) while measuring their ventilation and estimating pulmonary arterial pressure from the maximal velocity of the regurgitant jet over the tricuspid valve during systole (Δ P max ) with echocardiography. In the placebo session, after 5 and 20 min men responded with an increase in ventilation by 0.0056 and 0.0023 l min −1 kg −1 , respectively, indicating the presence of hypoxic ventilatory depression. In women, the increase in ventilation was 0.0067 and 0.0047 l min −1 kg −1 , respectively. In both sexes, erythropoietin did not alter these responses significantly. In the placebo session, mean Δ P max increased by 6.1 ± 0.7 mmHg in men ( P = 0.035) and by 8.4 ± 1.4 mmHg in women ( P = 0.020) during the hypoxic exposure, whereby women had a ∼5 mmHg lower end‐tidal . Erythropoietin did not alter these responses; in men, Δ P max increased by 7.5 ± 1.1 mmHg (n.s. versus placebo) and in women by 9.7 ± 2.2 mmHg (n.s. versus placebo). We conclude that women tended to have a greater HPV in placebo conditions and that a clinical dose of erythropoietin has no effect on the HVR and HPV in either sex.
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Berendsen et al. (2016) conducted an RCT in Healthy (n=14). Recombinant human erythropoietin vs. Placebo was evaluated on Isocapnic hypoxic ventilatory response and hypoxic pulmonary vasoconstriction (estimated by ΔPmax) (p=n.s.). A clinical intravenous dose of erythropoietin (50 IU/kg) did not significantly alter the ventilatory and pulmonary vascular responses to acute hypoxia in healthy men or women compared to placebo.
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