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Fibrin D-dimer impairs the accumulation and anticoagulant properties of heparan sulphate and stimulates secretion of plasminogen activator inhibitor-1 by rabbit coronary endothelial cells.

100%

Yevdokimova N. Y., Veselovska L. D., Gogolinska G. K., Buchanevich O. M., Kosyakova G. V., Gritsenko P. G., Lugovskoj E. V., Komisarenko S. V.

2003

vol. 50

issue 1

279-289

Fibrin split product D-dimer (DD) is most probably involved in the development of vascular disorders. At 1.5 μM concentration DD inhibited the incorporation of D-[1-3H]glucosamine hydrochloride and [2-14C]acetate · Na into pericellular heparan sulphate (HS) of rabbit coronary endothelial cells without affecting other groups of glycosaminoglycans (GAGs). At the same time, DD reduced HS ability to bind antithrombin (AT) and suppressed NO production. The effect of DD on pericellular GAGs was similar to that of Nw-methyl-L-arginine, the competitive inhibitor of endothelial NO synthase (eNOS). L-Ascorbic acid, eNOS activator, increased the level of endogenous NO in the DD-treated cells, and restored HS accumulation and antithrombin binding. It is suggested that DD influence on endothelial HS may be mediated by NO production. Another effect of DD, namely, stimulation of plasminogen activator inhibitor-1 (PAI-1) secretion did not depend on the NO level. The decreased HS content, reduced anticoagulant properties of HS, and increased PAI-1 secretion disorganized the endothelial matrix, and promoted fibrin formation and vascular damage. This points to DD as an important factor in the development of vascular disorders.

Elevation of plasma fibrinogen in silent myocardial ischaemia

100%

Grzywacz A., Psuja P., Zozulińska M., Elikowski W., Zawilska K.

Acta Biochimica Polonica

1999

vol. 46

issue 4

985-989

High plasma levels of fibrinogen and plasminogen activator inhibitor (PAI-1) are reported to be correlated with coronary heart disease. Therefore the level of fibrinogen concentration in plasma was examined and verified for the possible correlation with the previously explored PAI-1 antigen and PAI-1 activity in the pathogenesis of premature atherosclerosis (Grzywaczet al., 1998,Blood Coagul Fibrinol. 9, 245-249). Examination included only men, aged 33-46 years, who were in a stable condition for at least six months after the acute event. They were divided into two subgroups: group A (n = 14) with and group B (n = 15) without ischaemic changes in 24 h Holter electrocardiogram. The number of involved vessels visible on the coronarography picture was similar in both groups. In the patients of group A the mean level of fibrinogen (3.92 vs 3.23 g/l, P < 0.05) was higher than in the controls (n = 15). No statistically differences were found between group B and control healthy subjects in any of the parameters measured. There were no correlation between fibrinogen concentration and PAI-1 antigen and activity levels, which were elevated in both groups of patients according to our previous study. Our results indicate that elevated levels of plasma fibrinogen and PAI-1 appeared in the group of patients with more severe disease, as revealed by silent myocardial ischaemia.

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2 Acta Biochimica Polonica

1 2003

1 1999

1 Buchanevich O. M.

1 Elikowski W.

1 Gogolinska G. K.

1 Gritsenko P. G.

1 Grzywacz A.

1 Komisarenko S. V.

1 Kosyakova G. V.

1 Lugovskoj E. V.

1 Psuja P.

1 Veselovska L. D.

1 Yevdokimova N. Y.

1 Zawilska K.

1 Zozulińska M.

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Fibrin D-dimer impairs the accumulation and anticoagulant properties of heparan sulphate and stimulates secretion of plasminogen activator inhibitor-1 by rabbit coronary endothelial cells.

Elevation of plasma fibrinogen in silent myocardial ischaemia