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Results Ascorbate study Baseline characteristics of participants are shown in Table 1. All infusions were well tolerated. No statistically significant effects of ascorbate infusion were observed for any of the variables measured in this study. Following the ascorbate infusions, plasma ascorbate concentration was substantially higher and exceeded the normal range of 2�C20 ��g/dL (11�C114 ��mol/L) (P Tanespimycin concentration similar on the learn more two study days. Hypoxia induced a large increase in SPAP that was not affected by loading with ascorbate (compared with baseline, mean SPAP during hypoxia was increased by 55 �� 20% with saline control vs. 51 �� 20% with ascorbate, P = 0.61; Fig. ?Fig.2).2). The increase in cardiac output induced by hypoxia was likewise unaffected by ascorbate (mean increase in cardiac output of 27 �� 22% with saline control vs. 22 �� 22% with ascorbate, P = 0.71; Fig. ?Fig.3).3). Baseline ventilation prior to hypoxia was similar on the 2 days (13 �� 7 L/min on the control day vs. 11 �� 5 L/min on the ascorbate day, P = 0.33) and the increase in ventilation caused by hypoxia was not significantly affected by ascorbate (increase of 15 �� 23% with saline control vs. 38 �� 49% with ascorbate, P = 0.21). Figure 1. Plasma ascorbate concentration before and after infusion of saline control or ascorbate. Venous blood samples were taken at the beginning (denoted A.M.) and end (denoted P.M.) of the protocol on each day. *indicates a statistically significant difference ... Figure 2. Arterial oxygen saturation and systolic pulmonary artery pressure during sustained hypoxia. Upper panels show arterial oxygen saturation (SpO2) and lower panels show systolic pulmonary artery pressure (SPAP) in the Ascorbate study and in the Iron study. ... Figure 3. Cardiac output during sustained hypoxia with and without ascorbate loading. The cardiac output response to hypoxia was not affected by increased ascorbate availability. Data are mean �� SD. The initial Adenosine plasma erythropoietin concentration measured prior to the infusions was not significantly different on the two experimental days (6.5 �� 2.1 mIU/mL prior to control infusion and 5.7 �� 2.0 mIU/mL prior to ascorbate infusion, P = 0.28). The elevation in plasma erythropoietin concentration generated by hypoxia was not significantly affected by ascorbate (increase of 49 �� 25% with placebo vs. increase of 60 �� 43% with ascorbate, P = 0.91). Plasma hepcidin concentration was measured at the same time points. Baseline hepcidin levels were not significantly different on the two experimental days (23 �� 12 ng/mL prior to control infusion and 20 �� 19 ng/mL prior to ascorbate infusion; P = 0.63).