Ukr.Biochem.J. 2018; Том 90, № 2, березень-квітень, c. 67-75


Clot formation and lysis in platelet rich plasma of healthy donors and patients with resistant hypertension

I. I. Patalakh1, O. V. Revka1, O. B. Kuchmenko2, O. O. Matova2, T. F. Drobotko2, T. V. Grinenko1

1Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
2National Scientific Center “Strazhesko Institute of Cardiology” NAMS of Ukraine, Kyiv

Hemostatic balance in blood is affected by numerous factors, including coagulation and fibrinolytic proteins, the wide spectrum of their inhibitors, and blood cells. Since platelets can participate in contradictory processes, they significantly complicate the whole picture. Therefore, nowadays the development of global assays of hemostasis, which can reflect the physiological process of hemostasis and can be used for point-of-care diagnosis of thrombosis, is crucial. This paper outlines a new approach we used to analyze the capabilities of clot waveform analysis tools to distinguish the response of platelet-rich plasma from healthy donors and patients with arterial hypertension caused by stimulation of coagulation and lysis (with exogenous thrombin and recombinant tissue-type plasminogen activator, respectively). In donor plasma, when the clot degradation was accompanied by 40 IU/ml of recombinant tissue-type plasminogen activator, platelets potentiated fibrinolysis more than coagulation, which ultimately shifts the overall balance to a profibrinolytic state. At the same time, for patients with hypertension, platelets, embedded in clot obtained from platelet-rich plasma, showed a weaker ability to stimulate fibrinolysis. The obtained data gives the evidence that platelets can act not only as procoagulants but also as profibrinolytics. By simultaneously amplifying coagulation and fibrinolysis, making their rates comparable, platelets would control plasma procoagulant activity, thereby regulating local hemostatic balance, the size and lifetime of the clot. Moreover, clot waveform analysis may be used to distinguish the effects of platelet-rich plasma on clotting or lysis of fibrin clots in healthy donors and patients with essential hypertension.

Ключові слова: , , , ,


  1. von Känel R, Dimsdale JE. Effects of sympathetic activation by adrenergic infusions on hemostasis in vivo. Eur J Haematol. 2000 Dec;65(6):357-69. PubMed, CrossRef
  2. Hrafnkelsdottir T, Gudnason T, Wall U, Jern C, Jern S. Regulation of local availability of active tissue-type plasminogen activator in vivo in man. J Thromb Haemost. 2004 Nov;2(11):1960-8. PubMed, CrossRef
  3. Chapin JC, Hajjar KA. Fibrinolysis and the control of blood coagulation. Blood Rev. 2015 Jan;29(1):17-24. PubMed, PubMedCentral, CrossRef
  4. Michelson A. D. Platelets. Academic Press; 3 edition (January 9, 2013). 1398 p.
  5. Lipets EN, Ataullakhanov FI. Global assays of hemostasis in the diagnostics of hypercoagulation and evaluation of thrombosis risk. Thromb J. 2015 Jan 23;13(1):4. PubMed, PubMedCentral, CrossRef
  6. Lancé MD. A general review of major global coagulation assays: thrombelastography, thrombin generation test and clot waveform analysis. Thromb J. 2015 Jan 12;13:1.  PubMed, PubMedCentral, CrossRef
  7. Kremers RM, Peters TC, Wagenvoord RJ, Hemker HC. The balance of pro- and anticoagulant processes underlying thrombin generation. J Thromb Haemost. 2015 Mar;13(3):437-47.  PubMed, CrossRef
  8. Tripodi A. A(nother) test meant to fill the gap between in vivo and ex vivo hemostasis. Clin Chem. 2014 Sep;60(9):1137-40. PubMed, CrossRef
  9. van Geffen M, Loof A, Lap P, Boezeman J, Laros-van Gorkom BA, Brons P, Verbruggen B, van Kraaij M, van Heerde WL. A novel hemostasis assay for the simultaneous measurement of coagulation and fibrinolysis. Hematology. 2011 Nov;16(6):327-36. PubMed, CrossRef
  10.  Antovic A. The overall hemostasis potential: a laboratory tool for the investigation of global hemostasis. Semin Thromb Hemost. 2010 Oct;36(7):772-9.  PubMed, CrossRef
  11.  Tabak O, Gelisgen R, Uzun H, Kalender B, Balci H, Curgunlu A, Simsek G, Karter Y. Hypertension and hemostatic/fibrinolytic balance disorders. Clin Invest Med. 2009 Dec 1;32(6):E285. CrossRef
  12. Lip GY, Blann AD. Endothelium and fibrinolysis in hypertension: important facets of a prothrombotic state? Hypertension. 2008 Aug;52(2):218-9. PubMed, CrossRef
  13. Jeng JR, Sheu WH, Jeng CY, Huang SH, Shieh SM. Impaired fibrinolysis and insulin resistance in patients with hypertension. Am J Hypertens. 1996 May;9(5):484-90. PubMed, CrossRef
  14. Sevenet PO, Depasse F. Clot waveform analysis: Where do we stand in 2017? Int J Lab Hematol. 2017 Dec;39(6):561-568. PubMed, CrossRef
  15. Semeraro N, Montemurro P, Piccoli C, Muolo V, Colucci M, Giuliani G, Fumarola D, Pece S, Moran AP. Effect of Helicobacter pylori lipopolysaccharide (LPS) and LPS derivatives on the production of tissue factor and plasminogen activator inhibitor type 2 by human blood mononuclear cells. J Infect Dis. 1996 Dec;174(6):1255-60. PubMed, CrossRef
  16. Poli KA, Tofler GH, Larson MG, Evans JC, Sutherland PA, Lipinska I, Mittleman MA, Muller JE, D’Agostino RB, Wilson PW, Levy D. Association of blood pressure with fibrinolytic potential in the Framingham offspring population. Circulation. 2000 Jan 25;101(3):264-9. PubMed, CrossRef
  17. Nordenhem A, Wiman B. Tissue plasminogen activator (tPA) antigen in plasma: correlation with different tPA/inhibitor complexes. Scand J Clin Lab Invest. 1998 Oct;58(6):475-83. PubMed, CrossRef

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License.