Carbon monoxide releasing molecule-2 increases the velocity of thrombus growth and strength in human plasma

Vance G. Nielsen, James K. Kirklin, James F. George

Research output: Contribution to journalArticlepeer-review

56 Scopus citations


Carbon monoxide derived from degradation of heme by heme oxygenase or carbon monoxide releasing molecules (CORMs) has been demonstrated to decrease thrombosis in vivo and to weakly inhibit platelet aggregation. We tested the hypothesis that carbon monoxide released from tricarbonyldichlororuthenium (II) dimer (CORM-2) would diminish the velocity of formation and strength of plasma thrombi as determined by thrombelastography. Normal plasma was exposed to 0 or 100 μmol/l CORM-2 or inactivated CORM-2 (iCORM-2), with coagulation initiated with tissue factor or celite (n ≤ 8 per condition). Additional experiments utilized factor XIII (FXIII) deficient plasma activated with celite. Coagulation kinetics was monitored with thrombelastography for 15 min. CORM-2, and to a lesser extent, iCORM-2, significantly (P < 0.05) increased the velocity of formation (122 and 56%, respectively) and strength (66 and 57%, respectively) of plasma clots initiated with either tissue factor or celite compared with thrombi not exposed to CORM-2 or iCORM. In FXIII deficient plasma CORM-2 significantly increased the velocity of clot formation (264%) and strength (240%). Carbon monoxide and iCORM-2 derived from CORM-2 markedly enhance the velocity of clot growth and strength. These findings serve as the rationale for further investigations to determine if CORMs could be utilized as hemostatic agents.

Original languageEnglish
Pages (from-to)377-380
Number of pages4
JournalBlood Coagulation and Fibrinolysis
Issue number5
StatePublished - Jul 2009
Externally publishedYes


  • Carbon monoxide
  • Carbon monoxide releasing molecule
  • Coagulation
  • Thrombelastography


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