Mäntysaari Matti, Joutsi-Korhonen Lotta, Siimes Martti A, Siitonen Simo, Parkkola Kai, Lemponen Marja, Lassila Riitta
Aeromedical Centre and Diving Medical Centre, Centre for Military Medicine, Finnish Defence Forces, Helsinki, Finland.
Aviat Space Environ Med. 2011 Jul;82(7):699-703. doi: 10.3357/asem.3012.2011.
Acute hypoxia has been suspected to cause blood coagulation and platelet activation. Our aim was to study blood coagulation and platelet function during a short hypoxic exposure.
Healthy nonsmoking men (N = 10) inhaled a normobaric hypoxic gas mixture containing 8% of oxygen (92% nitrogen) for 7 min via a face mask. Venous blood was collected 5 min before and during the 5 to 7 min of hypoxia exposure (i.e., pretest and hypoxia samples, respectively) while monitoring arterial oxygen saturation (SaO2) with pulse oximetry. Blood sampling was completed in 2 min and the face mask was removed. Venous epinephrine and norepinephrine, complete blood counts, and a panel of coagulation markers were analyzed. Platelet aggregation induced by ristocetin, adenosine diphosphate (ADP), arachidonic acid, and thrombin receptor activating peptide was studied with Multiplate and shear force-dependent functions with PFA-100R (collagen/epinephrine and collagen/ADP cartridges), both assays in whole blood.
During hypoxia, SaO2 declined from 98 to 58% (ranges 97-99% vs. 42-85%), while heart rate increased from 69/min to 94/min (SD 11 vs. SD 13). Venous epinephrine and norepinephrine levels also increased. This short hypoxia induced minor but uniform increases in red cells, reticulocytes, and leukocytes and decreases in platelet counts. Plateletfunctions and prothrombin time, APTT, thrombin time, D-dimer, fibrinogen levels or von Willebrand factor (VWF), antithrombin, factor V (FV) or FVIII activities did not change.
Profound acute hypoxia failed to affect blood coagulation or platelet functions in healthy individuals.
急性缺氧被怀疑会导致血液凝固和血小板活化。我们的目的是研究短期缺氧暴露期间的血液凝固和血小板功能。
10名健康不吸烟男性通过面罩吸入含8%氧气（92%氮气）的常压混合气体7分钟。在缺氧暴露的第5至7分钟之前5分钟以及期间（即分别为预测试和缺氧样本）采集静脉血，同时用脉搏血氧饱和度仪监测动脉血氧饱和度（SaO2）。2分钟内完成采血并移除面罩。分析静脉肾上腺素和去甲肾上腺素、全血细胞计数以及一组凝血标志物。用Multiplate研究瑞斯托菌素、二磷酸腺苷（ADP）、花生四烯酸和凝血酶受体激活肽诱导的血小板聚集，并用PFA-100R（胶原/肾上腺素和胶原/ADP检测卡）研究全血中剪切力依赖性功能。
缺氧期间，SaO2从98%降至58%（范围97 - 99%对42 - 85%），而心率从69次/分钟增加到94次/分钟（标准差分别为11和13）。静脉肾上腺素和去甲肾上腺素水平也升高。这种短期缺氧导致红细胞、网织红细胞和白细胞轻微但一致地增加，血小板计数减少。血小板功能、凝血酶原时间、活化部分凝血活酶时间、凝血酶时间、D - 二聚体、纤维蛋白原水平或血管性血友病因子（VWF）、抗凝血酶、因子V（FV）或FVIII活性均未改变。
严重急性缺氧未能影响健康个体的血液凝固或血小板功能。
