Cochrane C G
Division of Vascular Biology and Inflammation, Scripps Clinic and Research Foundation, La Jolla, California 92037.
Am J Med. 1988 Jun 24;84(6A):75-9. doi: 10.1016/0002-9343(88)90162-3.
Alpha-1-proteinase inhibitor (A1PI) was examined in various inflammatory conditions in terms of its capacity to inhibit leukocytic proteases and to act as a monitor of the presence of oxidants generated by stimulated leukocytes. Examination of bronchoalveolar lavage fluid from patients with pulmonary inflammatory disease indicated that oxidants are generated in situ in the inflammatory reaction of the lung; the oxidants could potentially injure tissue directly, and, by virtue of the inactivation of A1PI, prevent inhibition of the neutrophil elastase, potentially allowing unencumbered proteolytic attack of the neutrophil elastase on lung structures. Subsequent examination of leukocytic enzymes and oxidants in experimental pulmonary inflammation in animals also demonstrated the generation of oxidants during development of acute pulmonary inflammation and indicated that the neutrophil is the cell mainly responsible for the release of oxidants.
对α1-蛋白酶抑制剂（A1PI）在各种炎症条件下抑制白细胞蛋白酶的能力以及作为受刺激白细胞产生的氧化剂存在的监测指标进行了研究。对患有肺部炎症疾病患者的支气管肺泡灌洗液的检查表明，氧化剂是在肺部炎症反应中原位产生的；这些氧化剂可能直接损伤组织，并且由于A1PI的失活，阻止了对中性粒细胞弹性蛋白酶的抑制，这可能使中性粒细胞弹性蛋白酶对肺结构进行不受阻碍的蛋白水解攻击。随后对动物实验性肺部炎症中的白细胞酶和氧化剂的检查也证明，在急性肺部炎症发展过程中会产生氧化剂，并且表明中性粒细胞是主要负责氧化剂释放的细胞。
