G. M. Shayakhmetova¹*, A. O. Pavlenko², S. I. Zhuk³,
O. V. Gornytska², I. V. Us³, L. B. Bondarenko¹,
N. V. Dobrelia¹, T. M. Platonova²

¹SI “Institute of Pharmacology and Toxicology, National Academy
of Medical Sciences of Ukraine”, Kyiv;
²Palladin Institute of Biochemistry, National Academy
of Sciences of Ukraine, Kyiv;
³Shupyk National Medical Academy of Postgraduate Education, Kyiv, Ukraine.
*e-mail: anna_shayakhmetova@yahoo.com

Received: 03 June 2026; Revised: 17 June 2026;
Accepted: 27 July 2026; Available on-line: August 2026

Background. Preeclampsia (PE) is a multisystem disorder in pregnancy, that results from placental ischemia, oxidative stress-induced placental damage and placental factors dissemination that cause systemic endothelial dysfunction. Patients with preeclampsia often develop a severe prothrombotic state, the mechanisms of which are not fully elucidated. Objectives. The aim of this study was to assess the informativeness of hemostatic system parameters that characterize the degree of coagulation pathway activation and anticoagulant pathway capacity capacity in experimental preeclampsia model in rats for predicting the development of thrombotic complications in PE. Methods. Wistar females rats were used in the study. To induce a preeclampsia-like syndrome, N(ω)-nitro-L-arginine methyl ester (L-NAME), at a concentration of 0.3 g/l in the drinking water was administered ad libitum from the 8^th to the 14^th day of gestation. On gestational day 21 the rats were anesthetized and blood samples were collected. Urinary and serum concentrations of creatinine, urea, and uric acid were determined using a fully automated Chemistry Analyzer and commercially available kits. Fibrinogen, soluble fibrin monomeric complexes and protein C concentrations, prothrombin time and antithrombin III activity in the blood plasma were estimated with a standard spectrophotometric methods. Results. Increased plasma fibrinogen, significant shortening of plasma clotting time, decrease in both protein C and AT III and increase in SFMCs plasma levels were detected in rats with experimentally L-NAME induced preeclampsia, indicating not only activation of the coagulation system but also disruption of the balance between procoagulant and anticoagulant pathways. Conclusions. L-NAME-induced PE in rats resulted in a pronounced imbalance of the hemostatic system and reproduced key pathophysiological features of PE, including excessive procoagulant shift, intravascular thrombin generation and impairment of anticoagulant mechanisms, making this model a valuable tool for studying mechanisms of disease progression. Analysis of hemostasis parameters in this model, indicates that soluble fibrin, protein C and antithrombin III are the most informative markers for assessing the risk of intravascular coagulation during preeclampsia.