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首页> 外文期刊>JAMA: the Journal of the American Medical Association >Effect of hypobaric hypoxia, simulating conditions during long-haul air travel, on coagulation, fibrinolysis, platelet function, and endothelial activation.
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Effect of hypobaric hypoxia, simulating conditions during long-haul air travel, on coagulation, fibrinolysis, platelet function, and endothelial activation.

机译:模拟长途航空旅行时的低压缺氧对凝血,纤维蛋白溶解,血小板功能和内皮激活的影响。

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CONTEXT: 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. OBJECTIVE: 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. INTERVENTIONS: 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). MAIN OUTCOME MEASURES: Comparative changes in markers of coagulation activation, fibrinolysis, platelet activation, and endothelial cell activation. RESULTS: 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); -0.20 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%). CONCLUSION: 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.
机译:背景:长途航空旅行与静脉血栓栓塞之间的联系是不断争论的主题。与地面静止不动相比,机舱压力和氧气压力的降低是否会增加风险还不清楚。目的:确定在航空旅行中可能遇到的低压缺氧是否激活止血功能。设计,地点和参与者:在低压舱中进行的单盲,交叉研究,评估了在73名健康志愿者中进行8小时静置低压氧暴露对止血的影响,该研究在英国进行, 2003年9月至2005年11月。筛选参与者V因子Leiden G1691A和凝血酶原G20210A突变,如果测试呈阳性,将其排除。在暴露前后抽血以评估止血的激活。干预措施:使个体交替(相隔>或= 1周)接受低压缺氧,这与商业航空旅行期间机舱压力降低(相当于2438 m的大气压)和常压常氧(对照条件;相当于海拔70米左右的地面大气条件)。主要观察指标: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。结果:在常压暴露期间观察到一些止血标志物的变化,这归因于长时间的坐着和昼夜节律的变化。但是,在低压和正常气压下的变化之间没有显着差异。例如,凝血酶-抗凝血酶复合物(95%CI,-0.30至0.30 ng / mL)在低压和常压暴露之间的变化中位数差异为0 ng / mL;凝血酶原片段1 + 2为-0.20 nmol / L(95%CI,-0.03至0.01 nmol / L); D-二聚体1.38 ng / mL(95%CI,-3.63至9.72 ng / mL);内源性凝血酶电位为-2.00%(95%CI,-4.00%至1.00%)。结论:我们的发现不支持这样的假设,即在长途航空旅行中可能遇到的程度的低压缺氧与低静脉血栓栓塞风险的健康个体的止血系统血栓形成改变有关。

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