Fibrin Degradation Products and Vascular Permeability

Increased vascular permeability plays an important role in the pathogenesis of the delayed microembolism syndrome. Fibrin degradation products (FDP) may play a role for this permeability disturbance. Fractions of lymph from the cannulated right lymphatic duct in dogs with induced microembolism syndrome and lysate from fibrin clots obtained by gel chromatography were used. The effect on vascular permeability was determined in the hamster cheek pouch and in the dorsal skin of the rat. Increased permeability was determined by leakage of fluorescein labelled dextran in the first model and by use of isotope labelled albumin in the second model. Lymph from the lymphatic duct and fractions of lysate from fibrin clots caused an increased vascular permeability of the same character in both models, the effect being partly due to high molecular weight products and partly due to low molecular weight products. The effect of high molecular weight products may possibly be due to their continous cleavage releasing low molecular weight vasoactive FDP. The effect of FDP on vascular permeability was enhanced by pretreatment with the β-adrenergic inhibitor propranolol and inhibited by the β2-adrenergie stimulator terbutaline. Bredykinin and PGE1 both increased macromolecular leakage in the hamster cheek pouch. This increase was also counteracted by terbutaline. The FDP effect on permeability might be due to contraction of the endothelial cells.

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Activated Thrombin-activatable Fibrinolysis Inhibitor Reduces the Ability of High Molecular Weight Fibrin Degradation Products to Protect Plasmin from Antiplasmin

Journal of Biological Chemistry ◽

10.1074/jbc.m313211200 ◽

2004 ◽

Vol 279 (14) ◽

pp. 13340-13345 ◽

Cited By ~ 23

Author(s):

Mark Schneider ◽

Nicole Brufatto ◽

Erin Neill ◽

Michael Nesheim

Keyword(s):

Molecular Weight ◽

High Molecular Weight ◽

Degradation Products ◽

Thrombin Activatable Fibrinolysis Inhibitor ◽

Fibrin Degradation Products ◽

Fibrinolysis Inhibitor

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Plasma Fibrin Degradation Products Evolution in Patients with Deep-Vein Thrombosis Treated with a Low Molecular Weight Heparin Fraction (CY222) and Standard Heparin

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1989.tb22530.x ◽

1989 ◽

Vol 556 (1 Heparin and R) ◽

pp. 441-443

Author(s):

RENE FAIVRE ◽

ERIC NEUHART ◽

CLAUDINE SORIA ◽

JEANNETTE SORIA ◽

YVONNE KIEFFER ◽

...

Keyword(s):

Molecular Weight ◽

Deep Vein Thrombosis ◽

Low Molecular Weight Heparin ◽

Degradation Products ◽

Low Molecular Weight ◽

Vein Thrombosis ◽

Fibrin Degradation Products ◽

Deep Vein

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The Fibrin Assay Comparison Trial (FACT)

Thrombosis and Haemostasis ◽

10.1055/s-0037-1615652 ◽

2001 ◽

Vol 85 (04) ◽

pp. 671-678 ◽

Cited By ~ 82

Author(s):

Sybille Zips ◽

Hanimsah Ergül ◽

Dieter Heene ◽

Carl-Erik Dempfle ◽

Keyword(s):

Molecular Weight ◽

High Molecular Weight ◽

Degradation Products ◽

Plasma Samples ◽

Fibrin Degradation Products ◽

Comparison Trial ◽

Clinical Conditions ◽

D Dimer

SummaryAlthough D-dimer has gained widespread clinical use as a parameter for detection of in vivo fibrin formation, the issue of standardization of D-dimer assays remains to be resolved. The FACT study was performed to generate basic data for development of calibrators and standard preparations.A set of 86 samples, including plasma samples from patients with DIC, DVT, and other clinical conditions, serial dilutions of pooled plasma samples, and plasma samples containing fibrinogen- and fibrin derivatives, were distributed to 12 manufacturers of D-dimer assays.D-dimer assays differ concerning specificity for crosslinked fibrin, and preference for either high molecular weight fibrin complexes, or low molecular weight fibrin degradation products. Terminal plasmin digests of fibrin clots for calibration produce aberrant results in some assays, especially those with preference for high molecular weight crosslinked fibrin derivatives. The best conformity is achieved by the use of pooled plasma samples from patients with high levels of D-dimer antigen in plasma. In vitro preparations containing a comparable composition of fibrin derivatives to clinical plasma samples may also serve as reference material.

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Effect of low molecular weight fibrin degradation products on endothelial cells in culture

Thrombosis Research ◽

10.1016/0049-3848(81)90306-6 ◽

1981 ◽

Vol 22 (1-2) ◽

pp. 33-39 ◽

Cited By ~ 26

Author(s):

Christer Busch ◽

Bengt Gerdin

Keyword(s):

Molecular Weight ◽

Endothelial Cells ◽

Degradation Products ◽

Low Molecular Weight ◽

Cells In Culture ◽

Fibrin Degradation Products

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Measurement of Autoantibodies Against Fibrinogen and Fibrin Degradation Products by Enzyme-Linked Immunoassay

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661241 ◽

1985 ◽

Vol 53 (01) ◽

pp. 080-085 ◽

Cited By ~ 5

Author(s):

A N Whitaker ◽

J R McFarlane ◽

E A Rowe ◽

K Lee ◽

P P Masci

Keyword(s):

Molecular Weight ◽

Enzyme Immunoassay ◽

High Molecular Weight ◽

Degradation Products ◽

Normal Subjects ◽

Fibrin Degradation Products ◽

Derivatives Of ◽

D Dimer

SummaryWe have devised a simple enzyme immunoassay to detect and quantitate autoantibodies against derivatives of fibrinogen. This assay has been applied with a range of antigens including a fibrinogen lysate (containing X, Y, D and E), D dimer, D dimerE and a preparation of high molecular weight complexes derived from crosslinked fibrin. We have found that autoantibodies interacting with these antigens can be detected in varying concentrations in most sera from both normal subjects and patients with a variety of diseases and are evidently of mixed Ig class. These autoantibodies are directed against at least several cryptic antigens which appear during fibrinogen/fibrin degradation and some appear to be directed specifically against cross- linked fibrin derivatives. No clear disease correlates have yet emerged but a relationship between elevated levels and prior infective, thrombotic, inflammatory or traumatic disorders is likely. It is suggested that these autoantibodies may contribute to the catabolism of fibrinogen derivatives, provide a marker of thrombosis, and sometimes produce pathologic effects.

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