Inflammatory cytokines in BAL fluid and pulmonary hemodynamics in high-altitude pulmonary edema

To evaluate the pathogenesis of high-altitude pulmonary edema (HAPE), we performed bronchoalveolar lavage (BAL) and pulmonary hemodynamic studies in seven patients with HAPE at its early stage. We measured cell counts, biochemical contents, and concentrations of pro-inflammatory cytokines including...

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Published inRespiration physiology Vol. 111; no. 3; pp. 301 - 310
Main Authors Kubo, Keishi, Hanaoka, Masayuki, Hayano, Toshihide, Miyahara, Takashige, Hachiya, Tsutomu, Hayasaka, Muneharu, Koizumi, Tomonobu, Fujimoto, Keisaku, Kobayashi, Toshio, Honda, Takayuki
Format Journal Article
LanguageEnglish
Published Shannon Elsevier B.V 01.03.1998
Amsterdam Elsevier
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Summary:To evaluate the pathogenesis of high-altitude pulmonary edema (HAPE), we performed bronchoalveolar lavage (BAL) and pulmonary hemodynamic studies in seven patients with HAPE at its early stage. We measured cell counts, biochemical contents, and concentrations of pro-inflammatory cytokines including interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor (TNF)- α and of anti-inflammatory cytokines including IL-1 receptor antagonist (ra) and IL-10 in the BAL fluid (BALF). All patients showed increased counts for total cells, alveolar macrophages, neutrophils and lymphocytes, and markedly elevated concentrations of proteins, lactate dehydrogenase, IL-1 β, IL-6, IL-8, TNF- α and IL-1ra. The levels of IL-1 α and IL-10 were not increased. Patients also showed pulmonary hypertension with normal wedge pressure. Both the driving pressure obtained as pulmonary arterial pressure minus wedge pressure and the Pa O 2 under room air were significantly correlated with the concentrations of IL-6 and TNF- α in the BALF. These findings suggest that the inflammatory cytokines play a role at the early stage of HAPE and might be related to pulmonary hypertension.
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ISSN:0034-5687
DOI:10.1016/S0034-5687(98)00006-1