INFLUENCE OF GLUCOSAMINE HYDROCHLORIDE ON THE EFFECT OF STREPTOKINASE IN REGIONAL THROMBOLYSIS ON VENOUS THROMBOSIS MODEL

Oklei D. V., Shtrygol’ S. Yu., Larianovska Yu. В.

CLINICAL AND EXPERIMENTAL MEDICINE

Scentific article

The aim of this study was to determine the effect of glucosamine hydrochloride on hemostasiological disorders and the state of the vascular wall during regional thrombolysis with streptokinase in the acute phase of experimental venous thrombosis. Stenosis up to 1 sq. mm posterior vena cava below the confluence of the renal veins in rats causes expressive thrombosis of this vessel and its tributaries. Under the conditions of regional thrombolysis, streptokinase (150,000 IU/kg into the tail vein) has a pronounced fibrinolytic effect, which is histologically confirmed. It quickly destroys a blood clot, small fragments of which are located freely along the vascular wall, blood flow in the vessels is restored. After the administration of streptokinase, the thrombus area decreased by 3 times compared with that in the control group, and the vessel lumen area by 1.5 times. However, against the background of streptokinase use, edema of endothelial cells and disordered orientation of the nuclei of smooth muscle cells of the venous wall were observed, which is a predictor of endothelial dysfunction. Glucosamine hydrochloride (50 mg/kg intragastrically) does not enhance the thrombolytic effect of streptokinase, but prevents endothelial edema and disorientation of the venous wall myocyte nuclei, which may be associated with the protective effect of glucosamine on the vascular wall. The content of D-dimer in the blood plasma of untreated animals in the acute stage of thrombosis (after 30 minutes) does not undergo changes, streptokinase statistically significantly reduces it by 38.3%. Therefore, in the studied acute period of experimental thrombosis, an increase in the content of D-dimer in the blood of untreated rats is not a decisive diagnostic criterion. This situation may be due to the fact that the destruction of a blood clot in these animals after 30 minutes after modeling, thrombosis does not have time to occur. A decrease in the content of D-dimer in both groups of rats that received fibrinolytic therapy indicates a lesser degree of thrombosis, which is confirmed histologically. The results experimentally substantiate the feasibility of a combination of streptokinase with glucosamine hydrochloride to improve the quality of thrombolytic action in venous thrombosis.

glucosamine hydrochloride, streptokinase, regional thrombolysis, acute venous thrombosis, experiment.

1. Wendelboe AM, McCumber M, Hylek EM, Buller H, Weitz JI, Raskob G. ISTH Steering Committee for World Thrombosis Day. Global public awareness of venous thromboembolism. Journal of thrombosis and haemostasis. 2015;13:365-71.
2. Boiko VV, Prasol VO, Taraban IA, Anreieshchev SA, Oklei DV, Boldizhar PO, ta in. Efektyvnist suchasnykh metodiv khirurhichnoho likuvannia hostroho trombozu v systemi nyzhnoi porozhnystoi veny. Klinichna khirurhiia. 2016;11:67-70. [in Ukrainian].
3. Comerota AJ. Catheter-directed thrombolysis for iliofemoral deep vein thrombosis: helpful or hurtful? Expert Rev Hematol. 2015;8(2):131-3.
4. Lin M, Hsieh JC, Hanif M, McDaniel A, Chew DK. Evaluation of thrombolysis using tissue plasminogen activator in lower extremity deep venous thrombosis with concomitant femoral-popliteal venous segment involvement. J. Vasc. Surg. Ven. Lymph. Disord. 2017;5(5):613-20.
5. Gromova OA, Torshin IYu, Lila AM, Naumov AV, Rudakov KV. Hemoreaktomnyy analiz antitromboticheskih effektov glyukozamina sul’fata i nesteroidnyh protivovospalitel’nyh preparatov. Sovremennaya revmatologiya. 2019;13(1):129-34. [in Russian].
6. Denisov SD, Morozkina TS. Trebovaniya k nauchnomu eksperimentu s ispol’zovaniem zhivotnyh. Zdravoohranenie. 2001;4:40-2. [in Russian].
7. Vladimirskaya TE, Adzeriho IE, Shved IA, Zhavnerko GK, Sherstyuk GV, Veyalkina NN, i dr. Tromboliticheskaya terapiya venoznogo tromboza c primeneniem nanokonteynerov: eksperimental’noe issledovanie. Flebologiya. 2014;(3):25-30. [in Russian].
8. Bondarev EV, Shtrygol’ SYu. Sostoyanie svertyvayuschey sistemy krovi pod deystviem preparatov glyukozamina i acetilsalicilovoy kisloty v usloviyah lokal’noy holodovoy travmy. OŃTÚSTIK QAZAQSTAN MEMLEKETTIK FARMATsEVTIKA AKADEMIIaSYNYŃ HABARShYSY. 2017;2(79):30- 7. [in Russian].
9. Bondariev YeV, Shtryhol SIu, Zupanets IA, Otrishko IA. Ahrehatsiia trombotsytiv pid vplyvom preparativ hliukozaminu hidrokhlorydu ta atsetylsalitsylovoi kysloty pry hostrii kholodovii travmi. Klinichna farmatsiia. 2017;1:50-6. [in Ukrainian].
10. Merkulov GA. Kurs patologogistologicheskoy tehniki. L.: Medicina; 1969. 424 s. [in Russian].
11. Volkova OV, Eleckiy YuK, Dubovaya TK. Gistologiya, citologiya i embriologiya: Atlas. Medicina; 1996. 544 s. [in Russian].
12. Rebrova OYu. Statisticheskiy analiz medicinskih dannyh. Primenenie paketa prikladnyh programm STATISTICA. M.: MediaSfera; 2006. 312 s. [in Russian].
13. Yamshchikov NV, Kruglyakov PP, Koshev VI, Petrov ES, Rudenko EYu, Yamshchikova EN. Gistogenez i strukturnaya organizatsiya stenki polykh i legochnykh ven krysy. Morfologiya. 2004;5:30-3. [in Russian].
14. Kalinin RE, Suchkov IA, Pshennikov AS, Novikov AN. Varianty eksperimentalnogo modelirovaniya venoznoy endotelialnoy disfunktsii: sovremennoye sostoyaniye problemy. Rossiyskiy mediko-biologicheskiy vestnik imeni akademika I.P. Pavlova. 2014;3:143-7. [in Russian].
15. Gabinskiy YaL, Kalinina SG. Vliyaniye razlichnykh rezhimov tromboliticheskoy terapii streptokinazoy pri ostrom infarkte miokarda na pokazateli koagulyatsionnogo gemostaza i fibrinoliza. Kardiovaskulyarnaya terapiya i profilaktika. 2006;5(6):61-9. [in Russian].

«Bulletin of problems biology and medicine» Issue 3 (152), 2019 year, 165-171 pages, index UDK 615.273.55:547.459.5:616.151.511: 615.015.21: 612.084

10.29254/2077-4214-2019-3-152-165-171