Lasson A, Ohlsson K
Adv Exp Med Biol. 1984;167:477-87. doi: 10.1007/978-1-4615-9355-3_42.
The protective role of alpha 2-macroglobulin, alpha 1-antitrypsin and Aprotinin against trypsin-induced effects on C3 and kininogen was studied in a human in vitro model. When human cationic trypsin was added to human serum or plasma, there was a gradual saturation of alpha 2-macroglobulin and later of alpha 1-antitrypsin. When alpha 2-macroglobulin was 70% saturated, there was a prompt cleavage of both C3 and kininogen, in spite of 80% free and active alpha 1-antitrypsin. These biochemical changes and antiprotease levels are identical to our findings in patients with acute pancreatitis, especially in their peritoneal exudate. Very high concentrations of Aprotinin, 5-15 times higher than ever used clinically, blocked the cleavage of both C3 and kininogen, while doses commonly used clinically were without significant effect. The clinical implications are: A trypsin-induced activation of both the complement and kinin system with clinical consequence is possible in patients with acute pancreatitis because of very low alpha 2-macroglobulin levels. Aprotinin in adequate doses, 5-15 times higher than ever used clinically, seems to protect against activation of two systems.
在人体体外模型中研究了α2-巨球蛋白、α1-抗胰蛋白酶和抑肽酶对胰蛋白酶诱导的C3和激肽原影响的保护作用。当将人阳离子胰蛋白酶添加到人血清或血浆中时，α2-巨球蛋白会逐渐饱和，随后α1-抗胰蛋白酶也会饱和。当α2-巨球蛋白饱和度达到70%时，尽管α1-抗胰蛋白酶有80%游离且具有活性，但C3和激肽原仍会迅速裂解。这些生化变化和抗蛋白酶水平与我们在急性胰腺炎患者中的发现相同，尤其是在他们的腹腔渗出液中。非常高浓度的抑肽酶，比临床使用过的浓度高5 - 15倍，可阻止C3和激肽原的裂解，而临床常用剂量则无显著效果。临床意义在于：由于α2-巨球蛋白水平极低，急性胰腺炎患者可能因胰蛋白酶诱导补体和激肽系统激活而产生临床后果。适当剂量的抑肽酶，比临床使用过的剂量高5 - 15倍，似乎可防止这两个系统的激活。
