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S. Mullan, F. Beckman, G. Vailati, J. Karasick and G. Dobben

treatment could then be carried out with the lower mortality figure indicated a decade ago by Norlén and Olivecrona. 5 Since blood clots (at least partially) disappear under the influence of a lytic enzyme, an antithrombolysin might have some therapeutic merit. Epsilon aminocaproic acid 8 which competes with the activator of plasminogen offers some possibilities worthy of clinical trial. In addition, it might be expected to prolong the life span of any thrombi that might be induced electrically in an experimental animal. Material and Methods Owing to the

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S. Mullan and J. Dawley

by Beller, 2, 3 Pechet, 13 and others. 5, 8, 14, 20 Pharmacologically, it acts by competitive inhibition of the activator, which converts plasminogen into the proteolytic enzyme plasmin. It also appears to inhibit (but to a lesser extent) the direct action of plasmin, namely, the breakdown of the fibrin molecule into plypeptides and animo acids. It is largely excreted unchanged in the urine. Toxic reports have been minimal. It is contraindicated in situations of endovascular thrombosis and in situations of defective renal excretion. Minimal side effects such as

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Temporary Experimental Intracranial Vascular Occlusion

Effect of Massive Doses of Heparin on Brain Survival

Donald R. Smith, Thomas B. Ducker and Ludwig G. Kempe

properties of the blood and effects of anticoagulant drugs in experimental cerebral infarction. New Engl. J. Med. , 1958, 258: 151–159. 24. Meyer , J. S. , Herndon , R. M. , Johnson , J. F. , et al. Treatment of cerebrovascular thrombosis with plasmin and plasminogen activators. Res. Publs Ass. Res. nerv. ment. Dis. , 1966 , 41 : 373 – 398 . Meyer , J. S., Herndon , R. M., Johnson , J. F., et al. Treatment of cerebrovascular thrombosis with plasmin and plasminogen activators. Res. Publs Ass. Res. nerv. ment. Dis. , 1966

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Edwin E. MacGee and William R. Bernell

Normal blood clotting is a dynamic process in which forces leading to coagulation are antagonized by contrary forces, including natural anticoagulants and agents that remove the formed clot. A simplified schematic representation of the clotting process is shown in Fig. 1 . Clot dissolution or fibrinolysis is equally important. Sherry's concept 8 of the human fibrinolytic enzyme system in plasma is shown in Fig. 2 . Central in this process is plasmin, an active fibrinolytic enzyme, and its precursor plasminogen. Clot lysis takes place primarily as the result of

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Tom Ewald, Steve Mahaley Jr., Jack Goodrich, Robert Wilkinson and Don Silver

frequent nor more extensive in the groups treated with EACA, nor was there any associated hydrocephalus. The fibrinolytic activity of the arachnoid and dura resides primarily in the vasa vasorum and small vessels of these structures and is primarily an activator activity ( i.e., converts plasminogen to plasmin). At the time of sampling the meninges (½, 1, 2, and 4 months after the administration of blood and/or EACA), both arachnoid and dura contained similar amounts of fibrinolytic activity as did the meninges from untreated dogs. This indicates that the fibrinolytic

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Robert R. Smith and John J. Upchurch

, acts principally by competitive inhibition of the activator that converts inactive plasminogen into the active fibrinolytic enzyme plasmin. Active plasmin, normally not present in the circulating blood, is probably the most important factor in fibrin clot dissolution. While EACA has been used extensively in the treatment of patients with various fibrinolytic disorders, there is little information on proper dosage, the duration of action, and the complications related to therapy in patients with normal fibrinolytic systems. Several recent studies emphasize that even

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The pathophysiological response to spinal cord injury

The current status of related research

Jewell L. Osterholm

therapy in acute experimental injuries. 25 The rationale for applying Amicar (aminocaproic acid) stems from its known action in bleeding disorders with active fibrinolysis. 135 Amicar lessens bleeding by inhibition of plasminogen activator substance plus a lesser antiplasmin activity. Thus a fibrin clot once formed may be somewhat more stable as the fibrin-destructive system is held in abeyance by treatment. Since hemorrhage is a major factor within acutely injured spinal cord tissues, the logic of clot stabilization and hopeful arrest of further bleeding is obvious

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Volker K. H. Sonntag and Bennett M. Stein

: 153 – 156 , 1953 Ablondi FB, Hagan JJ, Philips M, et al: Inhibition of plasmin, trypsin and the streptokinase-activated fibrinolytic system by ε-aminocaproic acid. Arch Biochem Biophys 82: 153–156, 1953 3. Alkjaersig N , Fletcher AP , Sherry S : ε-aminocaproic acid: an inhibitor of plasminogen activation. J Biol Chem 234 : 832 – 837 , 1959 Alkjaersig N, Fletcher AP, Sherry S: ε-aminocaproic acid: an inhibitor of plasminogen activation. J Biol Chem 234: 832–837, 1959 4

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James B. Campbell, Vincent DeCrescito, John J. Tomasula, Harry B. Demopoulos, Eugene S. Flamm and Bienvenido D. Ortega

known that steroid substances, such as MP, become intercalated into cell membranes and thereby minimize edema consequent to trauma. 13, 14 At the same time, lysosomal membranes are stabilized, preventing the release of proteolytic enzymes and esterases. The latter can cause hydrolytic destruction of phospholipids in myelin. EACA is a highly effective inhibitor of proteolytic enzymes. The activation of plasminogen requires proteolytic action to produce plasmin which then acts on fibrin as a proteolytic enzyme. Thus, EACA, by virtue of its ability to inhibit

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Julian L. Robinson, Christopher S. Hall and Carol B. Sedzimir

also be concerned. These include the high thromboplastin concentration in the uterus, the partial inhibition of the reticulo-endothelial system (which partly clears coagulation products), a possible anaphylactoid reaction because the fetus may be immunologically distinct from the mother, and the presence of large amounts of plasminogen in the myometrium. The initial control of hemorrhage, however, depends on the ability of the feeding vessel to contract so that the flow of blood is sufficiently reduced to allow clotting to occur. The normal feeding artery of an