We read and studied with great anticipation the article by Gojkovic et al. (1) and the accompanying editorial by Nikinmaa (2) in the present issue reporting on a new mouse model of high altitude pulmonary edema (HAPE). For investigators in the field, particularly those of us researching and treating HAPE in humans, an animal model for HAPE has been a quest for the holy grail for 60 years (3). A good small animal model would permit more extensive and high throughput experiments to better understand the pathophysiology and screen for preventative and therapeutic medications or non-pharmacologic strategies. For an animal model to serve in this role, however, it must closely reproduce the human pathophysiology. HAPE in humans only develops with the hypoxia of high altitude exposure. In most individuals, the rise in pulmonary artery pressure from hypoxic pulmonary vasoconstriction (HPV) is exaggerated and leads to high enough pressures in the microvasculature to cause pulmonary edema.

中文翻译：

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寻找高原肺水肿模型的工作必须继续进行。

我们非常期待阅读和研究Gojkovic等人的文章。（1）和Nikinmaa（2）随附的社论在本期中报道了一种新的高原肺水肿（HAPE）小鼠模型。对于该领域的研究者，特别是我们在人类中研究和治疗HAPE的研究者而言，HAPE的动物模型一直是圣杯的追寻目标（3）。一个好的小型动物模型将允许进行更广泛和更高通量的实验，以更好地了解病理生理，并筛选预防和治疗药物或非药物策略。但是，要使动物模型发挥这种作用，它必须紧密复制人类的病理生理学。人类的HAPE仅随着高海拔暴露的低氧而发展。在大多数人中