Evidence of circulating fibrin complexes has been alleged to be of diagnostic value in clinical thrombotic states. Measurements of soluble fibrin complexes were performed in an experimental model of thrombosis to determine whether these arise as a consequence of local thrombus formation or are a manifestation of a systemic "hypercoagulable state," or both. Three experimental models were studied in groups of dogs. The induced pathophysiologic changes were: (1) thrombi formation by stasis; (2) the injection of homologous serum as a source of activated clotting factors; (3) combined homologous serum infusion and stasis thrombosis. Soluble fibrin complexes were studied by two methods, i.e., fibrinogen gel chromatography and a serial dilution protamine sulfate test. Serial studies demonstrated that local thrombosis in the absence of circulating activated clotting factors did not generate significant amounts of soluble fibrin complexes. The injection of serum in the absence of stasis thrombosis resulted in only transient increases in circulating fibrin complexes. The infusion of serum combined with the formation of stasis thrombosis consistently gave rise to substantial quantities of soluble fibrin complexes. Thus in these experimental models, soluble fibrin complexes were detectable in association with an underlying "hypercoagulable state" with or without concomitant thrombosis.
|Original language||English (US)|
|Number of pages||11|
|Journal||The Journal of Laboratory and Clinical Medicine|
|Publication status||Published - 1974|
ASJC Scopus subject areas
- Pathology and Forensic Medicine