Haemoconcentration can influence hypoxic pulmonary vasoconstriction (HPV) via increased frictional force and vasoactive signalling from erythrocytes, but whether the balance of these mechanism is modified by the duration of hypoxia remains to be determined. We performed three sequential studies: (i) at sea level, in normoxia and isocapnic hypoxia with and without isovolumic haemodilution (n=10, aged 29±7 years); (ii) at altitude (6±2 days acclimatization at 5050 m), before and during hypervolumic haemodilution (n=11, aged 27±5 years) with room air and additional hypoxia (FiO₂ = 0.15), and; (iii) at altitude (4340 m) in Andean high-altitude natives with excessive erythrocytosis (EE; n=6, aged 39±17 years), before and during isovolumic haemodilution with room air and hyperoxia (end-tidal PO₂ = 100 mmHg). Results: At sea level, haemodilution mildly increased pulmonary artery systolic pressure (PASP; +1.6±1.5 mmHg, P=0.01) and pulmonary vascular resistance (PVR; +0.7±0.8 wu, P=0.04). In contrast, after acclimation to 5050 m, haemodilution did not significantly alter PASP (22.7±5.2 vs. 24.5±5.2 mmHg, P=0.14) or PVR (2.2±0.9 vs. 2.3±1.2 wu, p=0.77), although both remained sensitive to additional acute hypoxia. In Andeans with EE at 4340 m, haemodilution lowered PVR in room air (2.9±0.9 vs. 2.3±0.8 wu, P=0.03), but PASP remained unchanged (31.3±6.7 vs. 30.9±6.9 mmHg, P=0.80) due to an increase in cardiac output. Collectively, our series of studies reveal that HPV is modified by the duration of exposure and the prevailing haematocrit level. In application, these findings emphasize the importance of accounting for haematocrit and duration of exposure when interpreting the pulmonary vascular responses to hypoxemia.

中文翻译：

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血液浓缩对急性、长期和终生低氧血症中缺氧性肺血管收缩的影响。

血液浓缩可以通过增加的摩擦力和来自红细胞的血管活性信号来影响缺氧性肺血管收缩 (HPV)，但这些机制的平衡是否因缺氧持续时间而改变仍有待确定。我们进行了三项连续研究：(i) 在海平面、常氧和等二氧化碳缺氧条件下，有或没有等容血液稀释（n=10，年龄 29±7 岁）；(ii) 在高海拔地区（在 5050 m 处适应 6±2 天），在使用室内空气和额外缺氧 (FiO ₂ = 0.15)进行高容量血液稀释之前和期间（n = 11，年龄 27±5 岁），以及；(iii) 在高海拔（4340 米）安第斯高海拔土著人红细胞过多（EE；n=6，年龄 39±17 岁），在用室内空气和高氧进行等容血液稀释之前和期间（呼气末 PO ₂= 100 毫米汞柱）。结果：在海平面，血液稀释轻度增加肺动脉收缩压（PASP；+1.6±1.5 mmHg，P=0.01）和肺血管阻力（PVR；+0.7±0.8 wu，P=0.04）。相反，在适应 5050 m 后，血液稀释并未显着改变 PASP（22.7±5.2 对 24.5±5.2 mmHg，P=0.14）或 PVR（2.2±0.9 对 2.3±1.2 wu，p=0.77），尽管两者都对额外的急性缺氧保持敏感。在 EE 位于 4340 m 的安第斯山脉中，血液稀释降低了室内空气中的 PVR（2.9±0.9 对 2.3±0.8 wu，P=0.03），但 PASP 保持不变（31.3±6.7 对 30.9±6.9 mmHg，P=0.80）以增加心输出量。总的来说，我们的系列研究表明 HPV 会受到暴露时间和主要血细胞比容水平的影响。在应用中，