Institute of Mountain Emergency Medicine, Eurac Research, Bolzano, Italy.
Department of Anesthesia and Intensive Care Medicine, "F. Tappeiner" Hospital, Merano, Italy.
Am J Physiol Regul Integr Comp Physiol. 2021 Apr 1;320(4):R526-R531. doi: 10.1152/ajpregu.00313.2020. Epub 2021 Feb 3.
We investigated whether low arterial oxygen tension ([Formula: see text]) or hypoxia-induced plasma volume (PV) contraction, which reduces central blood volume (BV) and atrial distension, explain reduction in circulating atrial natriuretic peptide (ANP) after prolonged hypoxic exposure. Ten healthy males were exposed for 4 days to hypobaric hypoxia corresponding to an altitude of 3,500 m. PV changes were determined by carbon monoxide rebreathing. Venous plasma concentrations of midregional proANP (MR-proANP) were measured before and at the end of the exposure. At the latter time point, the measurement was repeated after ) restoration of [Formula: see text] by breathing a hyperoxic gas mixture for 30 min and ) restoration of BV by fluid infusion. Correspondingly, left ventricular end-diastolic volume (LVEDV), left atrial area (LAA), and right atrial area (RAA) were determined by ultrasound before exposure and both before and after fluid infusion at the end of the exposure. Hypoxic exposure reduced MR-proANP from 37.9 ± 18.5 to 24.5 ± 10.3 pmol/L ( = 0.034), LVEDV from 107.4 ± 33.5 to 91.6 ± 26.3 mL ( = 0.005), LAA from 15.8 ± 4.9 to 13.3 ± 4.2 cm ( = 0.007), and RAA from 16.2 ± 3.1 to 14.3 ± 3.5 cm ( = 0.001). Hyperoxic breathing did not affect MR-proANP (24.8 ± 12.3 pmol/L, = 0.890). Conversely, fluid infusion restored LVEDV, LAA, and RAA to near-baseline values (108.0 ± 29.3 mL, 17.2 ± 5.7 cm, and 17.2 ± 3.1 cm, respectively, > 0.05 vs. baseline) and increased MR-proANP to 29.5 ± 13.3 pmol/L ( = 0.010 vs. preinfusion and = 0.182 vs. baseline). These findings support that ANP reduction in hypoxia is at least partially attributed to plasma volume contraction, whereas reduced [Formula: see text] does not seem to contribute.
我们研究了低动脉氧分压 ([Formula: see text]) 或低氧诱导的血浆容量(PV)收缩,这会降低中心血容量(BV)和心房扩张,是否可以解释延长低氧暴露后循环心房利钠肽(ANP)的减少。10 名健康男性在低压缺氧环境下暴露 4 天,相当于海拔 3500 米的高度。通过一氧化碳再呼吸来确定 PV 的变化。在暴露前和暴露结束时测量静脉血浆中 midregional proANP(MR-proANP)的浓度。在后者时间点,通过呼吸 30 分钟富氧混合气来恢复 [Formula: see text] 后和通过输液来恢复 BV 后,再次进行测量。相应地,在暴露前、暴露结束时输液前后,通过超声确定左心室舒张末期容积(LVEDV)、左心房面积(LAA)和右心房面积(RAA)。低氧暴露使 MR-proANP 从 37.9±18.5 降至 24.5±10.3 pmol/L( = 0.034),LVEDV 从 107.4±33.5 降至 91.6±26.3 mL( = 0.005),LAA 从 15.8±4.9 降至 13.3±4.2 cm( = 0.007),RAA 从 16.2±3.1 降至 14.3±3.5 cm( = 0.001)。高氧呼吸不会影响 MR-proANP(24.8±12.3 pmol/L, = 0.890)。相反,输液将 LVEDV、LAA 和 RAA 恢复到接近基线值(108.0±29.3 mL、17.2±5.7 cm 和 17.2±3.1 cm,分别为 >0.05 与基线值),并使 MR-proANP 增加至 29.5±13.3 pmol/L( = 0.010 与输液前相比, = 0.182 与基线相比)。这些发现支持在低氧血症中 ANP 的减少至少部分归因于血浆体积收缩,而降低的 [Formula: see text] 似乎没有贡献。