Chen S F, Li S H, Fei X, Wu Z L
Department of Pathophysiology, Second Military Medical University, Shanghai, China.
Inflammation. 1990 Jun;14(3):267-73. doi: 10.1007/BF00915811.
Lung injury induced by phospholipase A2 (PLA2, 0.046 IU/ml perfusate) was studied in a continuous weighing system of isolated perfused guinea pig lungs. The results revealed that lung weight increased progressively during the 30-min perfusion of PLA2. No change of pulmonary arterial pressure was observed in the same period. Albumin permeability-surface area product, lung index, lung water content, exudate from pleura, and angiotensin-converting-enzyme activity increased significantly at the end of 30 min PLA2 perfusion. p-Bromophenacyl bromide, a PLA2 inhibitor, may block the above changes nearly completely. The effects of inhibitors of cyclooxygenase (indomethacin, IM), lipoxygenase (diethylcarbamaxine, DE), and platelet-activating factor (SRI 63-441) on PLA2-induced lung injury were also studied. We found: (1) PLA2 may induce high permeability lung edema. The role of endothelial injury in the permeability change remains to be further investigated. (2) DE ameliorated lung injury significantly within 10 min of PLA2 treatment but showed no effect after 15 min. IM ameliorated lung injury during the whole experimental period. SRI 63-441 had no effect. It is suggested that PLA2 may damage lung by inducing products of cyclooxygenase and lipoxygenase besides its direct effect.
在离体灌注豚鼠肺脏的连续称重系统中，研究了磷脂酶A2（PLA2，灌注液中浓度为0.046 IU/ml）诱导的肺损伤。结果显示，在PLA2灌注的30分钟内，肺重量逐渐增加。同期肺动脉压未见变化。在PLA2灌注30分钟结束时，白蛋白通透表面积乘积、肺指数、肺含水量、胸膜渗出液以及血管紧张素转换酶活性均显著增加。PLA2抑制剂对溴苯甲酰溴几乎可完全阻断上述变化。还研究了环氧化酶抑制剂（吲哚美辛，IM）、脂氧化酶抑制剂（二乙卡巴嗪，DE）和血小板活化因子抑制剂（SRI 63 - 441）对PLA2诱导的肺损伤的影响。我们发现：（1）PLA2可诱导高通透性肺水肿。内皮损伤在通透性变化中的作用仍有待进一步研究。（2）DE在PLA2处理后10分钟内可显著减轻肺损伤，但15分钟后则无作用。IM在整个实验期间均可减轻肺损伤。SRI 63 - 441无作用。提示PLA2除直接作用外，可能通过诱导环氧化酶和脂氧化酶产物损伤肺脏。
