Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor.

@article{Swenson2002PathogenesisOH,
  title={Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor.},
  author={Erik R Swenson and Marco Maggiorini and Stephen M. Mongovin and John Simon Russell Gibbs and I Mauduyt de la Gr{\`e}ve and Heimo Mairb{\"a}url and Peter D B{\"a}rtsch},
  journal={JAMA},
  year={2002},
  volume={287 17},
  pages={2228-35}
}
CONTEXT The pathogenesis of high-altitude pulmonary edema (HAPE) is considered an altered permeability of the alveolar-capillary barrier secondary to intense pulmonary vasoconstriction and high capillary pressure, but previous bronchoalveolar lavage (BAL) findings in well-established HAPE are also consistent with inflammatory etiologic characteristics. OBJECTIVES To determine whether inflammation is a primary event in HAPE and to define the temporal sequence of events in HAPE. DESIGN… CONTINUE READING

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In HAPE cases , there were no elevations in a number of proinflammatory cytokines and eicosanoid and nitric oxide metabolites .
In HAPE cases , there were no elevations in a number of proinflammatory cytokines and eicosanoid and nitric oxide metabolites .
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