DiMarco Kaitlyn G, Beasley Kara M, Shah Karina, Speros Julia P, Elliott Jonathan E, Laurie Steven S, Duke Joseph W, Goodman Randall D, Futral Joel Eben, Hawn Jerold A, Roach Robert C, Lovering Andrew T
Department of Human Physiology, University of Oregon, Eugene, OR, USA.
VA Portland Health Care System, Portland, OR, USA.
Exp Physiol. 2022 Feb;107(2):122-132. doi: 10.1113/EP089948. Epub 2022 Jan 10.
What is the central question to this study? Is there a relationship between a patent foramen ovale and the development of acute mountain sickness and an exaggerated increase in pulmonary pressure in response to 7-10 h of normobaric hypoxia? What is the main finding and its importance? Patent foramen ovale presence did not increase susceptibility to acute mountain sickness or result in an exaggerated increase in pulmonary artery systolic pressure with normobaric hypoxia. This suggests hypobaric hypoxia is integral to the increased susceptibility to acute mountain sickness previously reported in those with patent foramen ovale, and patent foramen ovale presence alone does not contribute to the hypoxic pulmonary pressor response.
Acute mountain sickness (AMS) develops following rapid ascent to altitude, but its exact causes remain unknown. A patent foramen ovale (PFO) is a right-to-left intracardiac shunt present in ∼30% of the population that has been shown to increase AMS susceptibility with high altitude hypoxia. Additionally, high altitude pulmonary oedema (HAPE) is a severe type of altitude illness characterized by an exaggerated pulmonary pressure response, and there is a greater prevalence of PFO in those with a history of HAPE. However, whether hypoxia per se is causing the increased incidence of AMS in those with a PFO and whether a PFO is associated with an exaggerated increase in pulmonary pressure in those without a history of HAPE is unknown. Participants (n = 36) matched for biological sex (18 female) and the presence or absence of a PFO (18 PFO+) were exposed to 7-10 h of normobaric hypoxia equivalent to 4755 m. Presence and severity of AMS was determined using the Lake Louise AMS scoring system. Pulmonary artery systolic pressure, cardiac output and total pulmonary resistance were measured using ultrasound. We found no significant association of PFO with incidence or severity of AMS and no association of PFO with arterial oxygen saturation. Additionally, there was no effect of a PFO on pulmonary pressure, cardiac output or total pulmonary resistance. These data suggest that hypobaric hypoxia is necessary for those with a PFO to have increased incidence of AMS and that presence of PFO is not associated with an exaggerated pulmonary pressor response.
本研究的核心问题是什么？卵圆孔未闭与急性高原病的发生以及在常压低氧7 - 10小时后肺动脉压力过度升高之间是否存在关联？主要发现及其重要性是什么？卵圆孔未闭的存在并未增加急性高原病的易感性，也未导致在常压低氧时肺动脉收缩压过度升高。这表明，低氧性低氧对于先前报道的卵圆孔未闭者急性高原病易感性增加至关重要，仅卵圆孔未闭的存在并不会导致低氧性肺血管加压反应。
急性高原病（AMS）在快速登高后发生，但其确切病因尚不清楚。卵圆孔未闭（PFO）是一种存在于约30%人群中的右向左心内分流，已证明其会增加高海拔低氧时AMS的易感性。此外，高原肺水肿（HAPE）是一种严重的高原病类型，其特征为肺压力反应过度，有HAPE病史者中PFO的患病率更高。然而，低氧本身是否导致PFO者AMS发病率增加以及PFO是否与无HAPE病史者的肺动脉压力过度升高相关尚不清楚。将36名按生物学性别匹配（18名女性）且有无PFO（18名PFO阳性）的参与者暴露于相当于海拔4755米的常压低氧环境7 - 10小时。使用路易斯湖AMS评分系统确定AMS的存在和严重程度。使用超声测量肺动脉收缩压、心输出量和总肺阻力。我们发现PFO与AMS的发病率或严重程度无显著关联，且与动脉血氧饱和度无关联。此外，PFO对肺压力、心输出量或总肺阻力无影响。这些数据表明，低氧性低氧对于PFO者AMS发病率增加是必要的，且PFO的存在与肺血管加压反应过度无关。
