{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T16:43:05Z","timestamp":1787503385460,"version":"build-2736575974"},"edition-number":"1","reference-count":234,"publisher":"Wiley","isbn-type":[{"value":"9780470650714","type":"electronic"}],"license":[{"start":{"date-parts":[[2012,10,1]],"date-time":"2012-10-01T00:00:00Z","timestamp":1349049600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    High\u2010altitude pulmonary edema (HAPE), a not uncommon form of acute altitude illness, can occur within days of ascent above 2500 to 3000 m. Although life\u2010threatening, it is avoidable by slow ascent to permit acclimatization or with drug prophylaxis. The critical pathophysiology is an excessive rise in pulmonary vascular resistance or hypoxic pulmonary vasoconstriction (HPV) leading to increased microvascular pressures. The resultant hydrostatic stress causes dynamic changes in the permeability of the alveolar capillary barrier and mechanical injurious damage leading to leakage of large proteins and erythrocytes into the alveolar space in the absence of inflammation. Bronchoalveolar lavage and hemodynamic pressure measurements in humans confirm that elevated capillary pressure induces a high\u2010permeability noninflammatory lung edema. Reduced nitric oxide availability and increased endothelin in hypoxia are the major determinants of excessive HPV in HAPE\u2010susceptible individuals. Other hypoxia\u2010dependent differences in ventilatory control, sympathetic nervous system activation, endothelial function, and alveolar epithelial active fluid reabsorption likely contribute additionally to HAPE susceptibility. Recent studies strongly suggest nonuniform regional hypoxic arteriolar vasoconstriction as an explanation for how HPV occurring predominantly at the arteriolar level causes leakage. In areas of high blood flow due to lesser HPV, edema develops due to pressures that exceed the dynamic and structural capacity of the alveolar capillary barrier to maintain normal fluid balance. This article will review the pathophysiology of the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung at high altitude, as well as therapeutic and prophylactic strategies to reduce the morbidity and mortality of HAPE. Published 2012.\n                    <jats:italic>Compr Physiol<\/jats:italic>\n                    2:2753\u20102773, 2012.\n                  <\/jats:p>","DOI":"10.1002\/cphy.c100029","type":"other","created":{"date-parts":[[2012,9,19]],"date-time":"2012-09-19T09:15:47Z","timestamp":1348046147000},"page":"2753-2773","source":"Crossref","is-referenced-by-count":121,"title":["High\u2010Altitude Pulmonary Edema"],"prefix":"10.1002","author":[{"given":"Erik 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