THE LUNG AT HIGH-ALTITUDE - BRONCHOALVEOLAR LAVAGE IN ACUTE MOUNTAIN-SICKNESS AND PULMONARY-EDEMA
THE LUNG AT HIGH-ALTITUDE - BRONCHOALVEOLAR LAVAGE IN ACUTE MOUNTAIN-SICKNESS AND PULMONARY-EDEMA
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DOI：
10.1152/jappl.1988.64.6.2605
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发表时间：
1988-06-01
影响因子：
3.3
通讯作者：
MARTIN, TR
中科院分区：
文献类型：
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作者：
SCHOENE, RB;SWENSON, ER;MARTIN, TR
高原肺水肿（HAPE）是一种严重的高原疾病，可发生在年轻健康个体中，是一种非心源性水肿，与支气管肺泡灌洗液（BAL）中高浓度的蛋白质和细胞有关（Schoene et al.， J. Am.）。中华医学杂志，26(6):663 - 669,1986)。我们假设急性高山病（AMS）中气体交换受损程度较轻是HAPE的前兆。因此，我们在麦金利山上4400米（气压= 440托），通过纤维支气管镜对8名受试者进行了0.89% NaCl的BAL，以评估高海拔时肺部的细胞和生化反应。健康对照1例（动脉氧饱和度= 83%），HAPE攀登者3例（平均动脉氧饱和度= 55.0 +-）。动脉氧饱和度= 70.0 .+-。2.4%)。立即在BAL液上进行细胞计数和分化，其余的冷冻后进行蛋白质和生化分析。这一结果和上面提到的早期研究表明，白细胞总数（.）倍。105/ml)， BAL液为3.5 +-。HAPE 2.0, 0.9 +-。AMS为0.4,+- 0.7。对照组为0.6，HAPE中主要是肺泡巨噬细胞。总蛋白浓度（mg/dl）为616.0 +-。HAPE为3.3,10.4 +-。AMS为8.3,12.0 +-。对照组为3.4，HAPE中存在大（免疫球蛋白M）和小（白蛋白）分子量蛋白。HAPE患者有补体激活（C5a）和血栓素B2和白三烯B4释放的证据，而对照组和AMS患者没有。尽管AMS中存在气体交换障碍，但BAL液没有显示异常蛋白质或细胞浓度的证据。
High-altitude pulmonary edema (HAPE), a severe form of altitude illness that can occur in young healthy individuals, is a noncardiogenic form of edema that is associated with high concentrations of proteins and cells in bronchoalveolar lavage (BAL) fluid (Schoene et al., J. Am. Med. Assoc. 256: 63-69, 1986). We hypothesized that acute mountain sickness (AMS) in which gas exchange is impaired to a milder degree is a precursor to HAPE. We therefore performed BAL with 0.89% NaCl by fiberoptic bronchoscopy in eight subjects at 4,400 m (barometric pressure = 440 Torr) on Mt. McKinley to evaluate the cellular and biochemical responses of the lung at high altitude. The subjects included one healthy control (arterial O2 saturation = 83%), three climbers with HAPE (mean arterial O2 saturation = 55.0 .+-. 5.0%), and four with AMS (arterial O2 saturation = 70.0 .+-. 2.4%). Cell counts and differentials were done immediately on the BAL fluid and the remainder was frozen for protein and biochemical analysis to be performed later. The results of this and of the earlier study mentioned above showed that the total leukocyte count (.times. 105/ml) in BAL fluid was 3.5 .+-. 2.0 for HAPE, 0.9 .+-. 0.4 for AMS, and 0.7 .+-. 0.6 for controls, with predominantly alveolar macrophages in HAPE. The total protein concentration (mg/dl) was 616.0 .+-. 3.3 for HAPE, 10.4 .+-. 8.3 for AMS, and 12.0 .+-. 3.4 for controls, with both large- (immunoglobulin M) and small- (albumin) molecular-weight proteins present in HAPE. There was evidence of complement activation (C5a) and release of thromboxane B2 and leukotriene B4 in HAPE but not in controls or AMS. Despite gas exchange impairment in AMS, the BAL fluid showed no evidence of abnormal protein or cell concentrations.