Fibrin Degradation Products and Vascular Permeability

Abstract

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.