Tagan M C, Markert M, Schaller M D, Feihl F, Chiolero R, Perret C H
Institut de Physiopathologie Clinique, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Am J Med. 1991 Sep 30;91(3C):72S-78S. doi: 10.1016/0002-9343(91)90287-8.
Among the different mechanisms involved, polymorphonuclear leukocytes (PMNs) may play a central role in the pathogenesis of adult respiratory distress syndrome (ARDS). PMNs were evaluated in 15 patients with ARDS, in 21 at risk of developing ARDS (AR), and in 36 controls (C). Spontaneous and opsonized zymosan (OZ), phorbol myristate acetate (PMA), and F-Met-Leu-Phe (F-M-L-P)-stimulated oxygen radical production was measured by luminol- and lucigenin-enhanced chemiluminescence (CL). Spontaneous CL activity of PMNs from ARDS patients was significantly greater than that from the PMN control (luminol CL, 2.8 +/- 0.6 vs. 0.8 +/- 0.1 mV, p less than 0.001; lucigenin CL, 2.0 +/- 0.6 vs. 0.30 +/- 0.04 mV, p less than 0.001), and the CL value from AR patients (luminol CL, 1.3 +/- 0.2 mV, p less than 0.001 vs. C; lucigenin CL, 0.8 +/- 0.1 mV, p less than 0.001 vs. C) was found to be between the ARDS and C patients. The peak of PMA-stimulated CL occurred earlier and it was significantly higher in ARDS patients than in AR patients (p less than 0.05) and controls (p less than 0.001). When the CL response was elicited with F-M-L-P, no difference among the three groups was found. When stimulated with OZ, the peak CL generated by PMNs from ARDS patients was significantly depressed compared with controls (luminol CL, 26.7 +/- 1.8 vs. 40.9 +/- 2.3 mV, p less than 0.01; lucigenin CL, 5.0 +/- 0.4 vs. 7.4 +/- 0.5 mV, p less than 0.005) with a similar result being obtained from AR patients (luminol CL, 32.1 +/- 2.5 mV, p less than 0.01 vs. C). Plasma from ARDS and AR patients showed a defective opsonizing capacity, suggesting in vivo complement consumption in both patient groups. No correlation between the severity of hypoxemia, the cause of ARDS, the outcome, and the different PMN functions could be established. Our results are in agreement with a determinant role of PMNs in the development of ARDS. The opposite metabolic responses may explain both the pulmonary injury and the increased susceptibility to infections observed in patients at risk of or with ARDS.
在涉及的不同机制中，多形核白细胞（PMN）可能在成人呼吸窘迫综合征（ARDS）的发病机制中起核心作用。对15例ARDS患者、21例有发生ARDS风险（AR）的患者和36例对照者（C）的PMN进行了评估。通过鲁米诺和光泽精增强化学发光（CL）测定自发和调理酵母聚糖（OZ）、佛波酯肉豆蔻酸酯乙酸酯（PMA）以及F-甲硫氨酰-亮氨酰-苯丙氨酸（F-M-L-P）刺激产生的氧自由基。ARDS患者PMN的自发CL活性显著高于PMN对照者（鲁米诺CL，2.8±0.6对0.8±0.1 mV，p＜0.001；光泽精CL，2.0±0.6对0.30±0.04 mV，p＜0.001），AR患者的CL值（鲁米诺CL，1.3±0.2 mV，与C组相比p＜0.001；光泽精CL，0.8±0.1 mV，与C组相比p＜0.001）介于ARDS患者和C组患者之间。PMA刺激的CL峰值出现得更早，且ARDS患者显著高于AR患者（p＜0.05）和对照者（p＜0.001）。当用F-M-L-P引发CL反应时，三组之间未发现差异。用OZ刺激时，ARDS患者PMN产生的CL峰值与对照者相比显著降低（鲁米诺CL，26.7±1.8对40.9±2.3 mV，p＜0.01；光泽精CL，5.0±0.4对7.4±0.5 mV，p＜0.005），AR患者也得到类似结果（鲁米诺CL，32.1±2.5 mV，与C组相比p＜0.01）。ARDS和AR患者的血浆显示调理能力缺陷，提示两组患者体内补体均有消耗。低氧血症的严重程度、ARDS的病因、转归与不同的PMN功能之间未发现相关性。我们的结果与PMN在ARDS发生中的决定性作用相符。相反的代谢反应可能解释了有ARDS风险或患有ARDS的患者所观察到的肺损伤和感染易感性增加。
