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Acute pulmonary embolism is a relatively common disease that may become critical and associated with increased mortality. Several pathophysiological and biochemical processes including increased pressure in pulmonary arteries, increased right ventricular afterload and right ventricular pressure, shear stress, inflammation, oxidative stress, certain cytokines, extracellular matrix remodelling, endogenous vascular elastase, plasminogen activator/plasmin system and MMP-s have been identified as potential factors in the development of pathological changes in acute pulmonary embolism. To extend our knowledge about these processes we conducted four studies using experimental animal models and performed clinical studies on acute pulmonary embolism. In our experiments we investigated the oxidative stress, changes in platelet count and platelet aggregation, changes in MMP and TIMP levels as well as alteration of NO consumption. In our book we present the used materials and methods, describe and discuss our results as well as give conclusions to understand the pathophysiological background of pulmonary embolism induced biochemical changes in experimental models and in the clinical setting.

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