Experimental models of pulmonary embolism

Abstract

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.

Metabolic Pathway of Cardiospecific Troponins: From Fundamental Aspects to Diagnostic Role (Comprehensive Review)

“…The evidence of the adverse effect of cortisol on CMC is a clinical study that demonstrates that increased levels of the stress hormone (cortisol) are associated with increased levels of cardiospecific TnT ( Lazzarino et al, 2013 ). In addition, a number of researchers associate the increased high activity of the sympathoadrenal system with a larger size of the focus of myocardial necrosis in MI, the incidence of acute CVD and an unfavorable prognosis ( Manfredini et al, 2004 ; Arroyo Úcar et al, 2012 ; Fournier et al, 2014 ; Seneviratna et al, 2015 ; Roos and Holzmann, 2018 ; Chaulin, 2021 ; Chaulin and Duplyakov, 2021g ; Chaulin, 2021h ; Chaulin and Duplyakov, 2022 ; Mullova et al, 2022 ).…”

On the Effect of Heterophilic Antibodies on Serum Levels of Cardiac Troponins: A Brief Descriptive Review

“…In the first case, a 64-year-old woman with PATE had constantly variating elevated levels of cTnI (between 23 μg/L to 0.43 μg/L) in comparison with the reference range (0.13 μg/L). Although the physicians suspected a myocardial injury, which is often typical of PATE [ 47 , 48 ], they were confused by the fact that the ECG data and the CPK-MB values were absolutely normal, therefore, the physicians assumed interference was taking place. After the patient’s sample was treated with the HABA, the cTnI level turned out to be lower than the upper-control limit (<0.13 μg/L).…”