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目的：阐明高原缺氧条件下梭曼中毒肺损伤的特点及机理。方法：应用微量滴定，酶联免疫技术，伊文思蓝标记白蛋白技术测定了在模拟高原４０００ｍ梭曼中毒后大鼠肺组织及肺灌洗液的磷脂酶Ａ２（ＰＬＡ２）、血管紧张素转换酶（ＡＣＥ）活性和肺组织肿瘤坏死因子（ＴＮＦα）、伊文思蓝（ＥＢ）含量的变化。结果：中毒４８ｈＰＬＡ２、ＡＣＥ、ＴＮＦα和ＥＢ含量显著高于１２、２４ｈ，在同一时相点，高原中毒组显著高于其它组。结论：提示ＰＬＡ２活性增高和ＴＮＦα含量的增加可使肺微血管通透性升高，在高原梭曼中毒肺水肿发病机理中起重要作用。
Objective: To elucidate the characteristics and mechanism of soman intoxication lung injury under high altitude hypoxia. Methods: The levels of phospholipase A2 (PLA2), angiotensin converting enzyme (ACE) in lung and lung lavage fluid after simulating solarium 4000m soman intoxication were determined by microtitration, enzyme-linked immunosorbent assay (ELISA) and Evans blue labeled albumin (ACE) activity and tumor necrosis factor (TNFα), Evans blue (EB) content in lung tissue. Results: The levels of PLA2, ACE, TNFα and EB were significantly higher at 48 h after poisoning than at 12 h and 24 h, respectively. At the same time point, the plateau poisoning group was significantly higher than the other groups. Conclusions: It is suggested that the increase of PLA2 activity and the increase of TNFα may increase the permeability of pulmonary microvessels, and play an important role in the pathogenesis of somatotrophic pulmonary edema.