High altitude pulmonary edema: a pressure-induced leak.
High altitude pulmonary edema (HAPE) is a non-cardiogenic pulmonary edema that can occur in healthy individuals who ascend rapidly to altitudes above 3000-4000m. Excessive pulmonary artery pressure (PAP) is crucial for the development of HAPE, since lowering pulmonary artery pressure by nifedipine or tadalafil (phosphodiesterase-5-inhibitor) will in most cases prevent HAPE. Recent studies using microspheres in swine and magnetic resonance imaging in humans strongly support the concept and primacy of nonuniform hypoxic arteriolar vasoconstriction to explain how hypoxic pulmonary vasoconstriction occurring predominantly at the arteriolar level can cause leakage. Evidence is accumulating that the excessive PAP response in HAPE-susceptible individuals is due to a reduced NO bioavailability. HAPE-susceptible individuals show an endothelial dysfunction in the systemic circulation in hypoxia. Lower levels of exhaled NO in hypoxia before and during HAPE suggest that this abnormality also occurs in the lungs and polymorphisms of the eNOS gene are associated with susceptibility to HAPE in the Indian and Japanese population.
Dehnert
Christoph
C
Medical University Clinic, Department of Internal Medicine, Div. of Sports Medicine, Im Neuenheimer Feld 410, D - 69120 Heidelberg, Germany.
Berger
Marc Moritz
MM
Mairbäurl
Heimo
H
Bärtsch
Peter
P
D000064:Acclimatization; D000531:Altitude; D000532:Altitude Sickness / Q000150:complications / Q000503:physiopathology; D000818:Animals; D001274:Atmospheric Pressure; D002199:Capillary Permeability; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology*
D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III