Toff William D, Jones Chris I, Ford Isobel, Pearse Robert J, Watson Henry G, Watt Stephen J, Ross John A S, Gradwell David P, Batchelor Anthony J, Abrams Keith R, Meijers Joost C M, Goodall Alison H, Greaves Michael
Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester, England.
JAMA. 2006 May 17;295(19):2251-61. doi: 10.1001/jama.295.19.2251.
The link between long-haul air travel and venous thromboembolism is the subject of continuing debate. It remains unclear whether the reduced cabin pressure and oxygen tension in the airplane cabin create an increased risk compared with seated immobility at ground level.
To determine whether hypobaric hypoxia, which may be encountered during air travel, activates hemostasis.
DESIGN, SETTING, AND PARTICIPANTS: A single-blind, crossover study, performed in a hypobaric chamber, to assess the effect of an 8-hour seated exposure to hypobaric hypoxia on hemostasis in 73 healthy volunteers, which was conducted in the United Kingdom from September 2003 to November 2005. Participants were screened for factor V Leiden G1691A and prothrombin G20210A mutation and were excluded if they tested positive. Blood was drawn before and after exposure to assess activation of hemostasis.
Individuals were exposed alternately (> or =1 week apart) to hypobaric hypoxia, similar to the conditions of reduced cabin pressure during commercial air travel (equivalent to atmospheric pressure at an altitude of 2438 m), and normobaric normoxia (control condition; equivalent to atmospheric conditions at ground level, circa 70 m above sea level).
Comparative changes in markers of coagulation activation, fibrinolysis, platelet activation, and endothelial cell activation.
Changes were observed in some hemostatic markers during the normobaric exposure, attributed to prolonged sitting and circadian variation. However, there were no significant differences between the changes in the hypobaric and the normobaric exposures. For example, the median difference in change between the hypobaric and normobaric exposure was 0 ng/mL for thrombin-antithrombin complex (95% CI, -0.30 to 0.30 ng/mL); -0.02 [corrected] nmol/L for prothrombin fragment 1 + 2 (95% CI, -0.03 to 0.01 nmol/L); 1.38 ng/mL for D-dimer (95% CI, -3.63 to 9.72 ng/mL); and -2.00% for endogenous thrombin potential (95% CI, -4.00% to 1.00%).
Our findings do not support the hypothesis that hypobaric hypoxia, of the degree that might be encountered during long-haul air travel, is associated with prothrombotic alterations in the hemostatic system in healthy individuals at low risk of venous thromboembolism.
长途航空旅行与静脉血栓栓塞之间的联系一直是持续争论的话题。与地面久坐不动相比,飞机机舱内气压降低和氧分压降低是否会增加风险仍不清楚。
确定航空旅行期间可能遇到的低压缺氧是否会激活止血过程。
设计、地点和参与者:一项单盲交叉研究,在低压舱内进行,以评估73名健康志愿者在8小时坐位暴露于低压缺氧环境下对止血的影响,该研究于2003年9月至2005年11月在英国进行。对参与者进行凝血因子V Leiden G1691A和凝血酶原G20210A突变筛查,检测呈阳性者被排除。在暴露前后采集血液以评估止血激活情况。
个体交替暴露(间隔≥1周)于低压缺氧环境(类似于商业航空旅行中机舱气压降低的情况,相当于海拔2438米处的大气压)和常压常氧环境(对照条件;相当于地面大气条件,海拔约70米)。
凝血激活、纤维蛋白溶解、血小板激活和内皮细胞激活标志物的比较变化。
在常压暴露期间,一些止血标志物出现了变化,这归因于长时间坐着和昼夜节律变化。然而,低压暴露和常压暴露的变化之间没有显著差异。例如,低压暴露和常压暴露之间变化的中位数差异,凝血酶 - 抗凝血酶复合物为0 ng/mL(95%CI,-0.30至0.30 ng/mL);凝血酶原片段1 + 2为 -0.02[校正]nmol/L(95%CI,-0.03至0.01 nmol/L);D - 二聚体为1.38 ng/mL(95%CI,-3.63至9.72 ng/mL);内源性凝血酶潜力为 -2.00%(95%CI,-4.00%至1.00%)。
我们的研究结果不支持以下假设:长途航空旅行期间可能遇到的低压缺氧程度与静脉血栓栓塞低风险的健康个体止血系统中的促血栓形成改变有关。