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应用伊文思蓝标记白蛋白法，微量滴定法和紫外法观察了急性低压缺氧复合梭曼中毒肺组织伊文思蓝含量，磷脂酶Ａ２（ＰＬＡ２）活力以及支气管肺泡灌洗液（ＢＡＬＦ）中ＰＬＡ２活力，血管紧张素转换酶（ＡＣＥ）活性和蛋白含量的变化。结果表明，低压缺氧（模拟海拔４０００ｍ）６ｈ后，给大鼠梭曼７２μｇ·ｋｇ－１ｓｃ，继续减压可引起肺组织伊文思蓝含量增加，ＢＡＬＦ中ＡＣＥ活性和蛋白含量升高，同时伴有肺组织和ＢＡＬＦ中ＰＬＡ２活性明显升高，提示急性低压缺氧复合梭曼中毒导致的肺损伤可表现为肺微血管通透性（ＰＭＶＰ）增高，微血管内皮细胞损伤和ＰＬＡ２的作用是引起ＰＭＶＰ增高的主要原因。
The Evans blue content, phospholipase A2 (PLA2) activity in lung tissue of bronchoalveolar lavage fluid (BALF) in acute hypobaric anoxia and bronchoalveolar lavage fluid (BALF) were measured by Evans blue labeled albumin method, microtitration and UV method. Vitality, changes in angiotensin-converting enzyme (ACE) activity and protein content. The results showed that after hypobaric hypoxia (simulated altitude of 4000m) for 6h, the rat soman 72μg · kg-1sc continued decompression can cause increased Evans blue content in lung tissue, ACE activity and protein content in BALF increased, accompanied by PLA2 activity in lung tissue and BALF was significantly increased, suggesting that lung injury caused by acute hypobaric hypoxia-combined soman intoxication may be manifested as increased pulmonary microvascular permeability (PMVP), microvascular endothelial cell damage and the role of PLA2 is caused by elevated PMVP The main reason.