ABSTRACT
A combination of reactions at the site of physical or chemical injury leads to local inflammation, especially when pathogenic microorganisms have access to the site. The interference of a secondary messenger seems likely. Both tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) levels rise very early after an acute event. Interestingly, the t-PA peak precedes by some minutes the peak of PAI-1. Theoretically, an abnormal blood level of fibrinolytic enzymes or their inhibitors can be a reflection of extravascular fibrinolysis induced by inflammatory processes. The plasma levels could rise either by simple leakage from extravascular sites, or by stimulation of the production and/or release of these factors from endothelial cells by the locally produced cytokines. The available literature teaches us that all major organs in contact with the environment react with production of fibrinolytic enzymes and inhibitors when confronted with bacterial products or cytokines.
