Schaiff W T, Eisenberg P R
Cardiovascular Division, Washington University School of Medicine, St Louis, Missouri 63110, USA.
Coron Artery Dis. 1997 Jan;8(1):9-18. doi: 10.1097/00019501-199701000-00002.
Complement activation occurs in patients with myocardial infarction treated with fibrinolytic agents and plays a critical role in reperfusion injury. This study was designed to determine whether pharmacologic activation of plasminogen directly induces complement activations.
Whole blood was incubated with plasminogen activators and the plasma was assayed for C3a levels as an indicator of complement activation.
Therapeutic concentrations of tissue-type plasminogen activator, streptokinase, or urokinase increased C3a concentrations from a baseline of approximately 500 ng/ml to an average of 1300-1500 ng/ml with tissue-type plasminogen activator or urokinase, and to an average of approximately 4000 ng/ml with streptokinase (P < 0.01, versus baseline for all plasminogen activators). Plasminogen activation also enhanced complement activation induced by conventional complement activators.
These results indicate that pharmacologic plasminogen activation may exacerbate reperfusion injury either by directly inducing complement activation or by enhancing the activation initiated by other mechanisms, or both.
在接受纤溶药物治疗的心肌梗死患者中会发生补体激活，且其在再灌注损伤中起关键作用。本研究旨在确定纤溶酶原的药物激活是否直接诱导补体激活。
将全血与纤溶酶原激活剂孵育，并检测血浆中C3a水平作为补体激活的指标。
组织型纤溶酶原激活剂、链激酶或尿激酶的治疗浓度可使C3a浓度从基线约500 ng/ml升高，使用组织型纤溶酶原激活剂或尿激酶时平均升高至1300 - 1500 ng/ml，使用链激酶时平均升高至约4000 ng/ml（与所有纤溶酶原激活剂的基线相比，P < 0.01）。纤溶酶原激活还增强了由传统补体激活剂诱导的补体激活。
这些结果表明，药物性纤溶酶原激活可能通过直接诱导补体激活或增强由其他机制引发的激活，或两者兼而有之，从而加重再灌注损伤。
