Valen G, Eriksson E, Risberg B, Vaage J
Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden.
Eur J Cardiothorac Surg. 1994;8(6):324-30. doi: 10.1016/s1010-7940(05)80093-4.
Endothelial release of tissue plasminogen activator (t-PA) may initiate fibrinolysis. Fibrinolysis and coagulation were investigated in 12 patients undergoing elective coronary artery bypass surgery. Cardiopulmonary bypass (CPB) was 108 +/- 7 min (mean +/- SEM), the time of cold, crystalloid, retrograde cardioplegia 53 +/- 5 min. Arterial and coronary sinus blood were sampled concomitantly before cardioplegia and after release of the aortic cross-clamp, for measurement of t-PA antigen (Ag) and activity, plasminogen activator inhibitor (PAI-1) Ag and activity, t-PA/PAI-1 complex, single chain urokinase (sc-uPA) and urokinase (uPA) plasminogen activators, the fibrin split product D-dimer, thrombin-antithrombin complex (TAT), and the prothrombin split product F 1 + 2. Cardiopulmonary bypass significantly increased t-PA Ag and activity, t-PA/PAI complex, D-dimer, TAT, and F 1 + 2, and decreased PAI-1 Ag and activity in arterial blood; uPA and sc-uPA were unchanged. The tissue plasminogen activator antigen was higher in coronary sinus than arterial blood after 1 (39 +/- 5 vs 24 +/- 4 ng/ml, P < 0.003), 4 (P < 0.003), and 10 min (P < 0.004) reperfusion. Tissue plasminogen activator activity and t-PA/PAI complex increased, PAI-1 activity decreased, while all other parameters were unchanged across the coronary circulation. In conclusion, CPB induces fibrinolysis and coagulation. Cold cardioplegia induces t-PA release in the coronary circulation, denoting a postischemic antithrombotic function of the coronary endothelium. Tissue plasminogen activator may be used to evaluate endothelial stimulation or injury induced by CPB, or by different regimens of myocardial protection.
内皮细胞释放组织型纤溶酶原激活剂（t-PA）可能启动纤维蛋白溶解过程。对12例行择期冠状动脉搭桥手术的患者的纤维蛋白溶解和凝血情况进行了研究。体外循环（CPB）时间为108±7分钟（均值±标准误），冷晶体逆行心脏停搏时间为53±5分钟。在心脏停搏前和主动脉阻断钳松开后，同时采集动脉血和冠状窦血，用于测定t-PA抗原（Ag）和活性、纤溶酶原激活剂抑制剂（PAI-1）Ag和活性、t-PA/PAI-1复合物、单链尿激酶（sc-uPA）和尿激酶（uPA）纤溶酶原激活剂、纤维蛋白降解产物D-二聚体、凝血酶-抗凝血酶复合物（TAT）以及凝血酶原裂解产物F1+2。体外循环显著增加了动脉血中的t-PA Ag和活性、t-PA/PAI复合物、D-二聚体、TAT以及F1+2，并降低了PAI-1 Ag和活性；uPA和sc-uPA未发生变化。再灌注1分钟（39±5 vs 24±4 ng/ml，P<0.003）、4分钟（P<0.003）和10分钟（P<0.004）后，冠状窦中的组织型纤溶酶原激活剂抗原高于动脉血。组织型纤溶酶原激活剂活性和t-PA/PAI复合物增加，PAI-1活性降低，而冠状动脉循环中所有其他参数均未改变。总之，体外循环诱导纤维蛋白溶解和凝血。冷心脏停搏诱导冠状动脉循环中t-PA释放，表明冠状动脉内皮具有缺血后抗血栓形成功能。组织型纤溶酶原激活剂可用于评估体外循环或不同心肌保护方案诱导的内皮刺激或损伤。
