Fibrinolytic shutdown after cardiopulmonary bypass surgery is caused by circulating cytokines during operation, accompanied by endothelial injury.

It has been hypothesized that increased cytokines during cardiopulmonary bypass surgery cause postoperative fibrinolytic shutdown. To investigate the role of cytokines and to elucidate its mechanism, tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), plasminogen activator inhibitor-1 antigen (PAI-1 Ag), PAI-1 activity, and thrombomodulin in 16 patients undergoing elective cardiopulmonary bypass surgery were analyzed after induction of anesthesia, before and after cardiopulmonary bypass, and at the end of the operation. during surgery, TNF-α and LI-1β were detected in 44% and 63% of the cases, respectively. PAI-1 Ag (P<0.01), PAI-1 activity (P<0.001) and thrombomodulin (P<0.01) were significantly increased at the end of the operation. The patients were divided into two groups and examined: Group 1 with either cytokine detected (n=12); and group 2 without detection of cytokines (n=4). At the end of the operation, both PAI-1 Ag (P<0.05) and PAI-1 activity (P<0.01) were significantly increased in group 1 compared with group 2. In group 1, there was a significant positive correlation between thrombomodulin and PAI-1 Ag (r (2)=0.117,P<0.05) and PAI-1 activity (r (2)=0.124,P<0.05). In conclusion, TFN-α and IL-1β were released into the systemic circulation during cardiopulmonary bypass surgery, and this release may have been caused by vascular endothelial injury. These cytokines increased PAI-1 activity.