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Many factors, such as endothelial dysfunction, inflammation and hemostatic disturbances, affect formation and progression of atherosclerotic plaque. In our study, we have focused on hemostatic disturbances with particular emphasis on the extrinsic pathways of coagulation. Thrombin is a main enzyme of coagulation and it is engaged in many different subprocesses. It leads to activation of factors of the coagulation cascade, transition of fibrinogen to fibrin monomer, endothelial damage, inflammation, activation of platelets and proliferation. In our study, selected aspects of disorders in prothrombotic states influenced by cigarette smoke have been modeled and analyzed. Tobacco-induced increased tissue factor, which is associated with less plasminogen activator and increased plasminogen activator-1 inhibitor, has been included in the presented model. These disorders together with accompanying inflammatory state are closely related to thrombus formation and cardiovascular disease promotion. The proposed model has been built using Petri nets and the analysis has been based mainly on t-invariants. Using the Petri net theory to model and analyze the investigated phenomena allows to better understand them by revealing some interesting dependencies in the studied biological system. It explains how tobacco smoke affects the analyzed processes and how harmful these effects are.

Selected Aspects of Tobacco-Induced Prothrombotic State, Inflammation and Oxidative Stress: Modeled and Analyzed Using Petri Nets