The search for a model of high-altitude pulmonary oedema must continue

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.