Fritz H, Jochum M, Geiger R, Duswald K H, Dittmer H, Kortmann H, Neumann S, Lang H
Folia Histochem Cytobiol. 1986;24(2):99-115.
In severe inflammatory response, various blood and tissue cells, including polymorphonuclear granulocytes, release lysosomal proteinases, extracellularly and into the circulation. Such enzymes, as well as normally intracellular oxidizing agents produced during phagocytosis, enhance the inflammatory response by degrading connective tissue structures, membrane constituents and soluble proteins by proteolysis or oxidation. We first used polymorphonuclear elastase (E) as a marker of such release reactions. The liberated proteinase competes with susceptible substrates, including alpha 1-proteinase inhibitor (alpha 1PI) and alpha 2-macroglobulin, and is eliminated finally as inactive enzyme-inhibitor complexes by the reticulo-endothelial system. Using an enzyme-linked immunosorbent assay, we determined the plasma levels of E-alpha 1PI following major abdominal surgery, multiple trauma and pancreatogenic shock. Whereas the operative trauma was followed by up to 3-fold increase of the E-alpha 1-PI, postoperative septicemia was associated with a 10 to 20 fold increase. The increase of E-alpha 1-PI and a concomitant decrease of plasma factors, such as antithrombin III, clotting factor XIII and alpha 2-macroglobulin, were correlated. Multiple trauma causes a substantial increase of E-alpha 1-PI up to 14 hours after accident. The released elastase seems to correlate with severity of injury, but assessing the relationship to consumption of plasma factors is complicated by concomitant transfusions. In acute pancreatitis, peaks, of E-alpha 1-PI coincide with a massive consumption of antithrombin III and alpha 2-macroglobulin during shock.
在严重的炎症反应中，包括多形核粒细胞在内的各种血液和组织细胞会将溶酶体蛋白酶释放到细胞外并进入循环系统。这些酶以及吞噬作用过程中正常产生的细胞内氧化剂，通过蛋白水解或氧化作用降解结缔组织结构、膜成分和可溶性蛋白质，从而增强炎症反应。我们首先使用多形核弹性蛋白酶（E）作为此类释放反应的标志物。释放的蛋白酶会与包括α1 -蛋白酶抑制剂（α1PI）和α2 -巨球蛋白在内的易感底物竞争，最终作为无活性的酶 - 抑制剂复合物被网状内皮系统清除。我们采用酶联免疫吸附测定法，测定了腹部大手术、多发伤和胰腺源性休克后血浆中E - α1PI的水平。手术创伤后E - α1 - PI水平最多可升高3倍，而术后败血症则与升高10至20倍相关。E - α1 - PI的升高与血浆因子如抗凝血酶III、凝血因子XIII和α2 -巨球蛋白的同时降低相关。多发伤在事故发生后长达14小时会导致E - α1PI大幅升高。释放的弹性蛋白酶似乎与损伤严重程度相关，但由于同时进行输血，评估其与血浆因子消耗的关系变得复杂。在急性胰腺炎中，E - α1 - PI的峰值与休克期间抗凝血酶III和α2 -巨球蛋白的大量消耗同时出现。
