High Altitude Pulmonary Edema
The aim of this section is to present the latest results on HAPE research and to discuss their implications for understanding the pathophysiology of HAPE. Although high pulmonary artery pressure appears to be a condition ‘sine qua non’ it is not clear what causes the exaggerated pressure response and how it accounts for the leak. Animal models and findings in bronchoalveolar lavage fluid indicate a role for increased permeability due to inflammation. Furthermore, data obtained in cell cultures suggest that hypoxia may reduce fluid clearance from the alveoli. Simon Gibbs will review the data on pulmonary circulation in HAPE-susceptible subjects and discuss hemodynamic concepts. Urs Scherrer will evaluate a possible role of transepithelial sodium transport on edema formation and present data obtained in vivo supporting the hypothesis of decreased alveolar fluid clearance in HAPE.