caa a22 4500 465764177 CHVBK 20180323111909.0 cr unu---uuuuu 170327e19900601xx s 000 0 eng 10.1007/BF00915811 doi (NATIONALLICENCE)springer-10.1007/BF00915811 Phospholipase A2-induced lung edema and its mechanism in isolated perfused guinea pig lung [Elektronische Daten] [Si-Feng Chen, Shao-Hua Li, Xia Fei, Zhong-Li Wu] 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 cyclooxy genase and lipoxygenase besides its direct effect. Plenum Publishing Corporation, 1990 Chen Si-Feng Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut Li Shao-Hua Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut Fei Xia Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut Wu Zhong-Li Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut Inflammation Kluwer Academic Publishers-Plenum Publishers 14/3(1990-06-01), 267-273 0360-3997 14:3<267 1990 14 10753 https://doi.org/10.1007/BF00915811 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00915811 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Chen Si-Feng Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut NATIONALLICENCE 700 1- Li Shao-Hua Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut NATIONALLICENCE 700 1- Fei Xia Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut NATIONALLICENCE 700 1- Wu Zhong-Li Department of Pathophysiology, Second Military Medical University, 594 Xiang Ying Road, 200433, Shanghai, China aut NATIONALLICENCE 773 0- Inflammation Kluwer Academic Publishers-Plenum Publishers 14/3(1990-06-01), 267-273 0360-3997 14:3<267 1990 14 10753 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer