Regulation of anterior chamber fibrinolysis

Levels of plasminogen activator (PA), plasminogen (Plg), and antiplasmin activity (APli) were compared in feline aqueous humor obtained from normal eyes, eyes inflamed by chronic mycobacterial-induced uveitis (CMIU), opposite eyes, and in plasma. Fibrin-agar plate microassays were utilized to visually confirm the extent of differences in in vitro fibrinolysis, per se. Chromogenic peptide (S2251) microassays were utilized to quantify differences. Normal AH showed much more available PA than did plasma. However, when APli activity was first neutralized their levels of total PA were comparable. Available PA activity in both normal and CMIU AH was considerably amplified in the presence of trace amounts of free plasmin. Plasma failed to show this response. AH levels of circulating Plg and APli in normal eyes were far below plasma levels. During CMIU, total PA levels remained approximately normal while levels of Plg and APli were greatly increased. The net effect of these concurrent rises was that antiplasmin activity (APli) prevailed over free plasmin formation; i.e., in vitro fibrinolysis was suppressed. Plasma levels of PA, Plg and APli did not change during CMIU. Changes in the normal PA+Plg/APli balance induced by CMIU suggested a hypothetical model of AH fibrinolysis wherein exclusion of APli from the normal anterior chamber and the high levels attained during CMUI are posited as key determinants of AH fibrinolytic capability.