Agostoni A, Gardinali M, Frangi D, Cugno M, Cafaro C, Conciato L, Sponzilli C, Salmoirago E
Istituto di Medicina Interna, Università degli Studi, IRCCS Ospedale Maggiore di Milano.
Ann Ital Med Int. 1994 Jul-Sep;9(3):178-9.
Details of possible complement activation in acute myocardial infarction (AMI) and the in vivo effects of fibrinolytic agents on this activation are not yet known. We measured complement activation in 40 patients with AMI: 20 were treated with streptokinase, and 20 did not receive any fibrinolytic agent. Anaphylatoxin C4a, C3a and membrane attack complexes SC5b-9 increased about 10-fold (p < 0.0001) during streptokinase infusion. There were no increases in complement catabolic products in AMI patients not treated with streptokinase. Significant transient leukopenia (-29.5%, 7.0 SEM, p = 0.001) and a drop in systolic pressure (-29%, 3.4 SEM, p < 0.0001) occurred after 15 min of streptokinase infusion simultaneously with the peak of anaphylatoxins in plasma.
急性心肌梗死(AMI)中补体激活的可能细节以及纤溶药物对此激活的体内效应尚不清楚。我们检测了40例AMI患者的补体激活情况:20例接受链激酶治疗,20例未接受任何纤溶药物。在输注链激酶期间,过敏毒素C4a、C3a和膜攻击复合物SC5b - 9增加了约10倍(p < 0.0001)。未接受链激酶治疗的AMI患者的补体分解产物没有增加。输注链激酶15分钟后,与血浆中过敏毒素峰值同时出现了显著的短暂性白细胞减少(-29.5%,标准误7.0,p = 0.001)和收缩压下降(-29%,标准误3.4,p < 0.0001)。