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Background:Over the past few decades,there has been a steady increase in work-related travel to mountain and high plain regions; this pattern of transient migration has been accompanied by a concomitant increase in high-altitude pulmonary edema (HAPE).Studies of HAPE have suggested a genetic component to susceptibility and implicated the angiotensin converting enzyme (ACE) gene of the renin-angiotensin-aldosterone-system pathway and the nitric oxide synthase 3 (NOS3) gene of the NO pathway in HAPE development.This study was designed to assess whether genetic variants in the ACE and NOS3 genes are associated with HAPE risk.