Delii V., Sulaieva O.

CLINICAL AND EXPERIMENTAL MEDICINE

Scentific article

In order to establish signaling mechanisms of platelet dysfunction among patients with acute gastroduodenal ulcer bleeding the assessment of agonist-induced platelet aggregation was performed by means of the spectrophotometric method and inhibitory method at the time of hospitalization of patients and the third day after. It has been shown that on the first day of hospitalization the level of collagen- and ADP- induced platelet aggregation was decreased among patients with acute gastroduodenal ulcer bleeding in comparison with the controlgroup. In cases of medium/high level of platelet aggregation, the reverse aggregation graph was recorded that was associated with the risk of recurrent bleeding. On the third day after hospitalization, the rise of ADP-induced platelet aggregation was found on account of PKA becomes a positive regulator of platelet intracellular signaling system. The assessment of induced platelet aggregation among patients with acute gastroduodenal ulcer bleeding compared with the control group allowed to discover a double decreased platelet aggregation to ADP (p=0.004) and 4.5-times decreased platelet aggregation to collagen (p=0.0001). The characteristics of aggregation graphs to ADP have shown partially inverse and inverse platelet aggregation, that was widely spread among patients with medium/high level of platelet aggregation. The previous issue has been associated with reverse and partially reverse aggregation graphs to collagen. Moreover, the highest rate of recurrent bleeding was found among patients with medium/high level of platelet aggregation to collagen (p=0.02) which was featured by a long latency period. The scrutiny also has revealed the correlation between ADP and collagen-induced platelet aggregation (r=0.28; p=0.01), which indicates that platelet disfunction takes place in the intracellular signaling system. On the first day of hospitalization no effect of PK A inhibitor on ADP-induced platelet aggregation was detected (p=0.71). The examination of effect of PK C inhibitor on ADP-induced platelet aggregation also has revealed no effect (p=0.57). In addition to the level of platelet aggregation inhibitors did not influence the characteristics of aggregation graphs. The comparison of ADP- and collagen-induced platelet aggregation in dynamics (on the first and the third days of hospitalization) has shown 2-times growth of platelet aggregation to ADP (p<0.05) and no changes of collageninduced platelet aggregation (p=0.59). On the third day of hospitalization the increase in the effect of PK A inhibitor on ADP-induced was recorded (p<0.05). The study of the effects of PK C inhibitor on ADP-induced platelet aggregation has revealed no differences (p=0.69).

gastroduodenal ulcer, acute bleeding, hemostasis, platelets, platelet signaling system, protein kinases (A and C).

1. Radenko EE. Otsinka efektivnosti endoskopichnogo gemostazu u hvorih na gostru krovotechu z verhnih viddiliv travnogo kanalu [dysertatsiya]. Donetsk; 2009. 20 s. [in Ukrainian].
2. Barinov EF, Sulaeva OM, Deliy VYu. Zvyazok funktsionalnogo stanu formenih elementiv krovi ta morfogenetichnih protsesiv u krayoviy zoni gastroduodenalnih virazok, uskladnenih krovotecheyu. Aktualni problemi zahvoryuvan shlunkovo-kishkovogo traktu. Donetsk: Donetskiy natsionalniy medichniy universitet im. M. Gorkogo; 2012. s. 11-5. [in Ukrainian].
3. Barinov EF, Sulaeva ON, Deliy VYu. Prognozirovanie reparatsii yazv zheludka putem issledovaniya funktsionalnoy aktivnosti trombotsitov. Zakonomernosti embrio-fetalnyih morfogenezov u cheloveka i pozvonochnyih zhivotnyih: III embriologicheskiy simpozium Yugra-Embrio-2011. Hantyi-Mansiysk; 2011. s. 104. [in Russiаn].
4. Bye AP, Unsworth AJ, Gibbins JM. Platelet signaling: a complex interplay between inhibitory and activatory networks. J Thromb Haemost. 2016 May;14(5):918-30. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26929147 DOI: 10.1111/jth.13302
5. Randriamboavonjy V, Isaak J, Frömel T, Viollet B, Fisslthaler B, Preissner KT, et al. AMPK α2 subunit is involved in platelet signaling, clot retraction, and thrombus stability. Blood. 2010 Sep 23;116(12):2134-40. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20558612 DOI: 10.1182/blood-2010-04-279612
6. Zaid Y, Senhaji N, Naya A, Fadainia C, Kojok K. PKCs in thrombus formation. Pathol Biol (Paris). 2015 Dec;63(6):268-71. Available from: https:// www.ncbi.nlm.nih.gov/pubmed/26476932 DOI: 10.1016/j.patbio.2015.09.001
7. Hardy AR, Conley PB, Luo J, Benovic JL, Poole AW, Mundell SJ. P2Y1 and P2Y12 receptors for ADP desensitize by distinct kinase-dependent mechanisms. Blood. 2005 May 1;105(9):3552-60. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15665114 DOI: 10.1182/ blood-2004-07-2893

«Bulletin of problems biology and medicine» Issue 4 Part 1 (153), 2019 year, 82-85 pages, index UDK 616.33-002.44-089:616.155.291

10.29254/2077-4214-2019-4-1-153-82-85