bivalirudin and Edema

bivalirudin has been researched along with Edema* in 2 studies

Other Studies

2 other study(ies) available for bivalirudin and Edema

ArticleYear
Factor Xa as an interface between coagulation and inflammation. Molecular mimicry of factor Xa association with effector cell protease receptor-1 induces acute inflammation in vivo.
    The Journal of clinical investigation, 1997, May-15, Volume: 99, Issue:10

    Coagulation proteases were tested in a rat model of acute inflammation. Subplantar injection of Factor Xa (10-30 microg) produced a time- and dose-dependent edema in the rat paw, and potentiated carrageenin-induced edema. In contrast, the homologous protease Factor IXa was ineffective. This inflammatory response was recapitulated by the Factor Xa sequence L83FTRKL88(G), which mediates ligand binding to effector cell protease receptor-1 (EPR-1), while a control scrambled peptide did not induce edema in vivo. Conversely, injection of the EPR-1-derived peptide S123PGKPGNQNSKNEPP137 (corresponding to the receptor binding site for Factor Xa) inhibited carrageenin-induced rat paw edema, while the adjacent EPR-1 sequence P136PKKRERERSSHCYP150 was without effect. EPR-1-Factor Xa-induced inflammation was characterized by fast onset and prominent perivascular accumulation of activated and degranulated mast cells, was inhibited by the histamine/serotonin antagonists cyproheptadine and methysergide, but was unaffected by the thrombin-specific inhibitor, Hirulog. These findings suggest that through its interaction with EPR-1, Factor Xa may function as a mediator of acute inflammation in vivo. This pathway may amplify both coagulation and inflammatory cascades, thus contributing to the pathogenesis of tissue injury in vivo.

    Topics: Amino Acid Sequence; Analysis of Variance; Animals; Antithrombins; Blood Coagulation; Carrageenan; Cyproheptadine; Edema; Factor Xa; Hirudins; Histamine H1 Antagonists; Inflammation; Male; Mast Cells; Methysergide; Molecular Sequence Data; Peptide Fragments; Rats; Rats, Wistar; Recombinant Proteins; Serotonin Antagonists; Time Factors

1997
Thrombin functions as an inflammatory mediator through activation of its receptor.
    The Journal of experimental medicine, 1996, Mar-01, Volume: 183, Issue:3

    A rat model of inflammation was used to investigate the biological effects of thrombin. The thrombin-specific inhibitor Hirulog markedly attentuated the carrageenin-induced edema of the paw of the rat. Injection of thrombin into the paw also produced edema. The effect of thrombin was due to activation of its receptor; a thrombin receptor activating peptide (TRAP) reproduced the effects of thrombin in causing edema. TRAP also increased vascular permeability as demonstrated by extravasation of Evans blue and 125I-labeled serum albumin. The release of bioactive amines played an important role in mediating the TRAP-induced edema; the serotonin/histamine antagonist cryproheptadine and the histamine H2 receptor antagonist cimetidine reduced significantly the edema caused by TRAP. Treatment of rats with the mast cell degranulator 48/80 to deplete these cells of their stores of histamine and serotonin abolished completely the ability of TRAP to produce edema. Histochemical examination confirmed that TRAP treatment led to mast cell degranulation. Thus, it has been possible to demonstrate that thrombin acts as an inflammatory mediator in vivo by activating its receptor, which in turn leads to release of vasoactive amines from mast cells.

    Topics: Amino Acid Sequence; Animals; Antithrombins; Carrageenan; Cytoplasmic Granules; Edema; Hirudins; Histamine; Inflammation; Male; Mast Cells; Molecular Sequence Data; Peptide Fragments; Rats; Rats, Wistar; Receptors, Thrombin; Recombinant Proteins; Serotonin; Thrombin

1996