Abstract
Experimental and clinical observations indicate that the systemic deposition of fibrin in disseminated intravascular coagulation (DIC) is insufficiently counteracted by endogenous fibrinolysis. In fact, a marked suppression of fibrinolytic activity, due to elevated levels of PAI-1, can be observed in experimental DIC as well as in patients with DIC from various causes. Relatively impaired plasmin generation is in dysbalance with enhanced thrombin generation and may contribute to the occurrence of systemic microvascular thrombosis and subsequent organ dysfunction.
Original language | English |
---|---|
Pages (from-to) | 119-124 |
Number of pages | 6 |
Journal | Sepsis |
Volume | 3 |
Issue number | 2 |
DOIs | |
Publication status | Published - 1999 |