Fibrinolytic activity of cerebral tissue after experimental subarachnoid haemorrhage: inhibitory effect of tranexamic acid (AMCA).
The influence of tranexamic acid (AMCA) on the fibrinolytic activity induced by plasminogen activators (PA) of the cerebral leptomeninges, arteries and choroid plexus after artificial subarachnoid haemorrhage (SAH) was studied in 90 rabbits. SAH was induced by injection of 1-2 ml autologous blood into the suboccipital cistern. Half of the rabbits were given AMCA, 200 mg per kg body weight, in daily single i.v. injections. The rabbits were sacrificed after 3-5, 8-10 and 14-15 days respectively. Part of the leptomeninges, basilar artery and choroid plexus were removed for assaying PA by the histochemical fibrin slide and fibrin plate methods, using thiocyanate for extraction of plasminogen activator from the tissues. Quantitative assays for the fibrin plate method showed high PA in the arterial and meningeal tissues from the untreated animals 3-5 days after SAH. The PA had decreased to normal levels 8-10 days after SAH but increased again 14-15 days after SAH. A lower PA in the choroid plexus followed the same pattern. The concentration of the primary plasmin inhibitor in plasma had decreased to half of the normal value 8 days after SAH when compared to the concentration in pooled plasma from normal rabbits. In AMCA treated animals the meningeal PA, assayed by both methods, was decreased 3-5 days after SAH while no or an insignificant decrease in PA was seen 8-10 and 14-15 days after SAH. The PA of the arterial vessel wall and choroid plexus in the AMCA treated animals, assayed by the histochemical method, was moderately decreased 3-5 days after SAH, while no significant differences between untreated and AMCA treated animals were seen after 8-10 or 14-15 days when the tissues were assayed by either method. These findings indicate that AMCA suppresses PA primarily in the leptomeninges during the first few days after SAH and presumably before the meningeal fibrosis has developed.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002536:Cerebral Arteries / Q000378:metabolism; D002831:Choroid Plexus / Q000378:metabolism; D003509:Cyclohexanecarboxylic Acids / Q000627:therapeutic use*; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis; D008297:Male; D008578:Meninges / Q000378:metabolism; D010960:Plasminogen Activators / Q000378:metabolism; D011817:Rabbits; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy* / Q000378:metabolism; D014148:Tranexamic Acid / Q000627:therapeutic use*
D003509:Cyclohexanecarboxylic Acids; D005338:Fibrin Fibrinogen Degradation Products; D014148:Tranexamic Acid; D010960:Plasminogen Activators