The effect of fibrinolytic inhibition in the resolution of experimental vitreous hemorrhage.
Complete inhibition of vitreous fibrinolytic activity with 4-amino-methylcyclohexane carbonic acid was associated with significantly delayed resolution of vitreous hemorrhages in rabbits. However, polyacrylamide gel electrophoresis indicated but a slight delay in the removal of the fibrin component of vitreous clots, and most of the residual vitreous opacity comprised intact red blood cells. Fibrin degradation products may act as chemotactic agents, promoting the removal of red blood cells by leukocytes; hence, their absence in treated rabbits might explain in part the delayed red blood cell clearance.
D000042:Absorption; D000818:Animals; D002634:Chemotaxis, Leukocyte; D003509:Cyclohexanecarboxylic Acids / Q000494:pharmacology*; D004912:Erythrocytes; D005128:Eye Diseases / Q000378:metabolism; D005337:Fibrin / Q000378:metabolism; D005338:Fibrin Fibrinogen Degradation Products / Q000502:physiology; D005342:Fibrinolysis / Q000187:drug effects*; D006470:Hemorrhage / Q000378:metabolism*; D010587:Phagocytosis; D011817:Rabbits; D014148:Tranexamic Acid / Q000494:pharmacology*; D014822:Vitreous Body / Q000378:metabolism*
D003509:Cyclohexanecarboxylic Acids; D005338:Fibrin Fibrinogen Degradation Products; D014148:Tranexamic Acid; D005337:Fibrin