Grissom Colin K, Orme James F, Richer Lori D, McIntyre Thomas M, Zimmerman Guy A, Elstad Mark R
Pulmonary and Critical Care Division, Department of Internal Medicine, LDS Hospital, Salt Lake City, UT, USA.
Crit Care Med. 2003 Mar;31(3):770-5. doi: 10.1097/01.CCM.0000053647.82608.29.
Platelet-activating factor (PAF) is a proinflammatory phospholipid that may contribute to inflammation in the acute respiratory distress syndrome (ARDS). PAF acetylhydrolase (PAF-AH) degrades PAF and regulates its biological activity. We characterized PAF-AH in bronchoalveolar lavage fluid from ARDS patients (n = 33, 22 survivors), patients at risk for ARDS (n = 6), and healthy controls (n = 6).
Bronchoalveolar lavage was performed during acute (<96 hrs from onset), plateau (6 to 12 days), and late (> or = 14 days) phases of ARDS.
Intubated patients with ARDS or a risk factor for ARDS.
In ARDS, total bronchoalveolar lavage PAF-AH activity was markedly increased in the acute phase (87 +/- 89 mU/mL, n = 33) and then decreased in the plateau (23 +/- 14 mU/mL, n = 10) and late phases (19 +/- 14 mU/mL, n = 7) (p = .003). Total bronchoalveolar lavage PAF-AH activity during the acute phase of ARDS was also increased as compared with patients at risk for ARDS (16 +/- 13 mU/mL, n = 6) and healthy controls (3 +/- 3 mU/mL, n = 6) (p < .001). In contrast, plasma PAF-AH activities were the same in controls (3215 +/- 858 mU/mL, n = 6), in patients at risk for ARDS (3606 +/- 1607 mU/mL, n = 6), and during the acute phase of ARDS (3098 +/- 2395 mU/mL, n = 33) (p = .18). PAF-AH mRNA was present in alveolar macrophages in the acute phase of ARDS (five of six) and in at-risk patients (two of three) but not in healthy controls.
PAF-AH activity is increased in bronchoalveolar lavage fluid from patients with ARDS. Likely sources include leakage of plasma PAF-AH into alveoli or release of PAF-AH from injured cells; however, the presence of PAF-AH mRNA in alveolar macrophages suggests that PAF-AH may be actively synthesized in the lungs of patients with ARDS. PAF-AH activity in the lungs of ARDS patients may regulate inflammation caused by PAF and related oxidized phospholipids generated in the inflammatory response.
血小板活化因子（PAF）是一种促炎磷脂，可能在急性呼吸窘迫综合征（ARDS）的炎症反应中起作用。PAF 乙酰水解酶（PAF-AH）可降解 PAF 并调节其生物活性。我们对 ARDS 患者（n = 33，22 例存活者）、有 ARDS 风险的患者（n = 6）和健康对照者（n = 6）的支气管肺泡灌洗液中的 PAF-AH 进行了特征分析。
在 ARDS 的急性（发病后<96 小时）、平台期（6 至 12 天）和晚期（≥14 天）阶段进行支气管肺泡灌洗。
患有 ARDS 或有 ARDS 风险因素的插管患者。
在 ARDS 中，支气管肺泡灌洗总 PAF-AH 活性在急性期显著升高（87±89 mU/mL，n = 33），然后在平台期（23±14 mU/mL，n = 10）和晚期（19±14 mU/mL，n = 7）下降（p = 0.003）。与有 ARDS 风险的患者（16±13 mU/mL，n = 6）和健康对照者（3±3 mU/mL，n = 6）相比，ARDS 急性期支气管肺泡灌洗总 PAF-AH 活性也升高（p < 0.001）。相比之下，对照组（3215±858 mU/mL，n = 6）、有 ARDS 风险的患者（3606±1607 mU/mL，n = 6）和 ARDS 急性期患者（3098±2395 mU/mL，n = 33）的血浆 PAF-AH 活性相同（p = 0.18）。PAF-AH mRNA 在 ARDS 急性期的肺泡巨噬细胞中存在（6 例中有 5 例），在有风险的患者中存在（3 例中有 2 例），但在健康对照者中不存在。
ARDS 患者支气管肺泡灌洗液中 PAF-AH 活性升高。可能的来源包括血浆 PAF-AH 漏入肺泡或受损细胞释放 PAF-AH；然而，肺泡巨噬细胞中 PAF-AH mRNA 的存在表明 PAF-AH 可能在 ARDS 患者的肺中被主动合成。ARDS 患者肺中的 PAF-AH 活性可能调节由 PAF 和炎症反应中产生的相关氧化磷脂引起的炎症。
