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Thesis summary:

In blood vessels there is a balance between clot formation and its dissolution. Normally, fibrinolysis allows the breakdown of blood clots during the repairing process of injured blood vessels. This process is mediated by the activation of a blood enzyme (plasmin) which breaks down a meshed protein (fibrin) that hold blood clots at the site of vessel injury.  In some diseases the activation of plasmin become excessive leading to bleeding tendencies (hyperfibrinolysis), which can especially occur when the fibrinogen (the fibrin precursor) decreases.
In normal condition abdominal and thoracic cavities are filled with a small amount of fluid deriving from the blood. It is not clear whether the balance between coagulation and fibrinolysis occurring in the blood vessel also occurs in the body cavities when there is an excess of pathological fluid accumulation. The results of this thesis showed that in dogs all types of intracavitary fluids have an increased fibrinolytic activity. This increased fibrinolytic activity was also present in their blood, reaching in some instance a hyperfibrinolic state. These results were evident when the fibrinolysis was studied by detection of FDPs and/or D-dimers (break down products of fibrinogen and blood clots), but also when studied by viscoelastometry (ROTEM). Nevertheless, the agreement between the two detection systems was poor. 
Finally, the result of this thesis also showed that cardiopathic dogs with ascites have hyperfibrinolysis with bleeding tendencies rather than thrombotic events as commonly documented some cardiac diseases in humans and cats.