Pavlicek V, Marti H H, Grad S, Gibbs J S, Kol C, Wenger R H, Gassmann M, Kohl J, Maly F E, Oelz O, Koller E A, Schirlo C
Institute of Physiology, University of Zürich, Switzerland.
Eur J Appl Physiol. 2000 Apr;81(6):497-503. doi: 10.1007/s004210050074.
In order to investigate whether vascular endothelial growth factor (VEGF) and inflammatory pathways are activated during acute hypobaric hypoxia in subjects who are susceptible to high-altitude pulmonary oedema (HAPE-S), seven HAPE-S and five control subjects were exposed to simulated altitude corresponding to 4000 m in a hypobaric chamber for 1 day. Peripheral venous blood was taken at 450 m (Zürich level) and at 4000 m, and levels of erythropoietin (EPO), VEGF, interleukin-6 (IL-6) and the acute-phase proteins complement C3 (C3), alpha1-antitrypsin (alpha1AT), transferrin (Tf) and C-reactive protein (CRP) were measured. Peripheral arterial oxygen saturation (SaO2) was recorded. Chest radiography was performed before and immediately after the experiment. EPO increased during altitude exposure, correlating with SaO2, in both groups (r = -0.86, P < 0.001). Venous serum VEGF did not show any elevation despite a marked decrease in SaO2 in the HAPE-S subjects [mean (SD) HAPE-S: 69.6 (9.1)%; controls: 78.7 (5.2)%]. C3 and alpha1AT levels increased in HAPE-S during hypobaric hypoxia [from 0.94 (0.11) g/l to 1.07 (0.13) g/l, and from 1.16 (0.08) g/l to 1.49 (0.27) g/l, respectively; P < 0.05], but remained within the clinical reference ranges. No significant elevations of IL-6, Tf or CRP were observed in either group. The post-exposure chest radiography revealed no signs of oedema. We conclude that VEGF is not up-regulated in HAPE-S and thus does not seem to increase critically pulmonary vascular permeability during the 1st day at high altitude. Furthermore, our data provide evidence against a clinically relevant inflammation in the initial phase of exposure to hypoxia in HAPE-S, although C3 and alpha1AT are mildly induced.
为了研究在易患高原肺水肿的受试者（HAPE-S）急性低压缺氧期间血管内皮生长因子（VEGF）和炎症途径是否被激活，将7名HAPE-S受试者和5名对照受试者置于低压舱中，暴露于相当于4000米的模拟海拔高度1天。在450米（苏黎世水平）和4000米处采集外周静脉血，测量促红细胞生成素（EPO）、VEGF、白细胞介素-6（IL-6）以及急性期蛋白补体C3（C3）、α1-抗胰蛋白酶（α1AT）、转铁蛋白（Tf）和C反应蛋白（CRP）的水平。记录外周动脉血氧饱和度（SaO2）。在实验前和实验后立即进行胸部X线摄影。两组在海拔暴露期间EPO均升高，且与SaO2相关（r = -0.86，P < 0.001）。尽管HAPE-S受试者的SaO2显著下降，但静脉血清VEGF未显示任何升高[HAPE-S受试者均值（标准差）：69.6（9.1）%；对照组：78.7（5.2）%]。在低压缺氧期间，HAPE-S受试者的C3和α1AT水平升高[分别从0.94（0.11）g/l升至1.07（0.13）g/l，以及从1.16（0.08）g/l升至1.49（0.27）g/l；P < 0.05]，但仍在临床参考范围内。两组中均未观察到IL-6、Tf或CRP的显著升高。实验后胸部X线摄影未显示水肿迹象。我们得出结论，在HAPE-S中VEGF未上调，因此在高原第一天似乎不会显著增加肺血管通透性。此外，我们的数据表明，尽管C3和α1AT有轻度诱导，但在HAPE-S缺氧暴露初始阶段不存在具有临床相关性的炎症。
