Experimental models of pulmonary embolism

Pulmonary embolism (PE) ranks third in the structure of acute cardiovascular diseases. Every year there is a rapid increase in morbidity and mortality from PE. Laboratory biomarkers for PE diagnosis do not have the necessary specificity, and therefore are ineffective. PE requires timely active treatment, in particular for the prevention of serious complications. In this regard, further research is needed to study and search for novel promising biomarkers for the early detection of PE, pathophysiological mechanisms and targets for therapeutic effects. To a large extent, novel data on the pathophysiology of cardiovascular diseases, including PE, scientists receive from experimental studies using animal models. In this review, we summarize the main existing experimental models of PE, describe the principles and methods for modeling this disease. There are following models of PE: intravenous thrombin infusion, adenosine diphosphate-induced PE, PE induction by thromboplastin, recombinant human tissue factor or high molecular weight polyphosphates, collagen/adrenaline-induced PE, ex vivo thrombus intravenous administration, surgical model. This publication also presents our own experience in creating an artificial model of PE in animals using an intravenous thrombus. In our model, confirmation of PE was obtained during pathological examination and an increase in the level of following biomarkers: troponin, N-terminal pro-brain natriuretic peptide, and D-dimer. In this pilot study, a PE model was created to study the pathogenesis and novel treatment options for this disease. To confirm the effectiveness of the model, future studies are required.