Carbon monoxide releasing molecule-2 decreases thick diameter fibrin fibre formation in normal and factor XIII deficient plasmas

Carbon monoxide derived from carbon monoxide releasing molecules (CORMs) has been demonstrated to enhance normal plasma thrombus speed of growth and strength as well as diminish vulnerability to fibrinolysis in vitro. We tested the hypothesis that tricarbonyldichlororuthenium (II) dimer (CORM-2) would modify plasma thrombi ultrastructure as determined by electron microscopy. Normal and FXIII-deficient (<1% normal activity) plasmas were exposed to 0 or 100 μmol/l CORM-2, with coagulation initiated with tissue factor followed by a 15 min incubation at 37°C prior to fixation. Transmission electron microscopy of the four conditions was conducted at 5000-60 000-fold magnification. CORM-2 markedly diminished the formation of thick diameter fibrin fibres in normal plasma and FXIII-deficient plasma. The density of thin diameter fibrin fibres did not seem to be changed by CORM-2 in normal plasma, but was increased in FXIII-deficient plasma. CORM-2 significantly modifies thrombin-mediated polymerization of fibrin. This finding may partially explain how CORM-2 exposure results in stronger thrombi resistant to fibrinolysis.