Fibrinolytic and fibrin stabilizing activity of synovial membranes.

Most tissues exhibit fibrinolytic activity because of their content of plasminogen activator (Albrechtsen, 1958; Astrup and Stage, 1952; Pandolfi, Nilsson, Robertson, and Isacson, 1967; Sayers, Tyler, and Lack, 1965). This activity might be demonstrated by applying the tissue itself or a tissue extract on a fibrin plate (Astrup and Permin, 1947; Caughey and Highton, 1967) or by the histiochemical fibrin slide technique (Todd, 1959). The activity appears, as is shown by the "fibrinolysis autograph" technique, to be connected to the endothelium of veins and venules and of pulmonal arteries (Todd, 1964; Warren, 1964), although blood vessels may not be the only source of tissue activator activity (Astrup and Sj6lin, 1958; Sayers and others, 1965). The "fibrinolysis autograph" technique has recently been used to demonstrate the tissue fibrin stabilizing factor. (Sayers and others, 1965). Increased deposition.,of fibrin in tissue, in joint cavities, and on syrovial membrane has been noticed in cases of rheumatoid arthritis (RA). The findings of Bamhart, Riddle, Bluhm, and Quintana (1967), Bluhm, Riddle, and Barnhart (1966) Riddle, Bluhm, and Barnhart (1965), Dumonde and Glynn (1962), Glynn (1963), and Lack (1964, 1968) have led to the hypothesis that fibrin plays an important role in perpetuating the chronic inflammation of RA. The purpose of this study has been to examine by means of the fibrinolysis autograph technique the plasminogen activator activity in synovial membranes, and to test its ability to degrade isolated human fibrin, fibrin from the plasma of patients with active RA, and fibrin from normal plasma, and also to test the fibrin stabilizing activity of the membranes by their ability to stabilize human fibrin deprived of the fibrin stabilizing factor (FSF).