Erythropoietin does not have effects on the ventilatory and pulmonary vascular response to acute hypoxia in men and women

Sustained and chronic hypoxia lead to a rise 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 intravenous dose of recombinant human erythropoietin (rHuEPO,50 IU kg⁻¹) on the isocapnic HVR and HPV in 7 male and 7 female subjects by exposing them to hypoxia for 20 min (end-tidal PO₂ ∼ 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 (ΔPmax) with echocardiography. In placebo, after 5 and 20 min, men responded with a rise in ventilation by 0.0056 and 0.0023 l/min/kg/%SpO₂, respectively, indicating the presence of hypoxic ventilatory depression. In women, the rise in ventilation was 0.0067 and 0.0047 l/min/kg/%SpO₂, respectively. In both sexes, EPO did not alter these responses significantl . In placebo, mean ΔPmax rose 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 PCO₂. EPO did not alter these responses: in men a rise in ΔPmax by 7.5 ± 1.1 mmHg (NS vs. placebo) and in women by 9.7 ± 2.2 mmHg (NS vs. placebo). We conclude that women tended to have a greater HPV in placebo and that a clinical dose of EPO has no effect on the HVR and HPV in either sex

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