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

机译:高海拔肺水肿中BAL液中的炎性细胞因子和肺血流动力学。

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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)-alpha 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-1beta, IL-6, IL-8, TNF-alpha and IL-1ra. The levels of IL-1alpha 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 PaO2 under room air were significantly correlated with the concentrations of IL-6 and TNF-alpha 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.
机译:为了评估高海拔肺水肿(HAPE)的发病机理,我们对7例HAPE早期患者进行了支气管肺泡灌洗(BAL)和肺血流动力学研究。我们测量了细胞计数,生化含量以及促炎细胞因子(包括白介素(IL)-1,IL-6,IL-8和肿瘤坏死因子(TNF)-α)以及包括IL-1受体在内的消炎细胞因子的浓度拮抗剂(ra)和BAL液(BALF)中的IL-10。所有患者的总细胞,肺泡巨噬细胞,嗜中性粒细胞和淋巴细胞计数均增加,蛋白质,乳酸脱氢酶,IL-1β,IL-6,IL-8,TNF-α和IL-1ra的浓度显着升高。 IL-1alpha和IL-10的水平没有增加。患者还显示肺动脉高压,楔形压正常。以肺动脉压力减去楔形压力获得的驱动压力和室内空气下的PaO2均与BALF中IL-6和TNF-α的浓度显着相关。这些发现表明,炎性细胞因子在HAPE的早期起作用,并且可能与肺动脉高压有关。

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