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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

inhibits plasminogen activation, should only be used when primary fibrinolysis is clearly the etiological process. 1 There has not been agreement regarding recommended therapy for the secondary fibrinolytic syndromes. Whole, preferably fresh blood, and fibrinogen may be used. There are reports attesting to the efficacy of heparin therapy in disseminated intravascular coagulation and secondary fibrinolysis. 4, 5–7 As a general rule, heparin is indicated in the initial phase, when the intravascular coagulation is taking place, to stop the consumption of the clotting

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Robert R. Smith and John J. Upchurch

all patients with aneurysms and subarachnoid hemorrhage has, however, not been established. Frequent measurement of the fibrinolytic activity in patients receiving these agents may direct modifications in drug administrations so as to obtain optimal antifibrinolysis in the lowest dose range. References 1. Alkjaersig N , Fletcher AP , Sherry S : E-Aminocaproic acid: an inhibitor of plasminogen activation. J Biol Chem 234 : 832 – 837 , 1959 Alkjaersig N, Fletcher AP, Sherry S: E-Aminocaproic acid: an inhibitor of

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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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Chikao Nagashima, Motohide Takahama, Yoshihiro Nakayama and Takao Asano

to the endothelial wall. The platelets may also clump for repair of multiple capillary defects 1, 27 both leading to clot, tissue hypoxia, necrosis, and bleeding. Swelling of endothelial cells, subendothelial hemorrhage, necrosis and hyaline degeneration of the interstitial tissue seen in our case ( Fig. 3 lower left and right ), may reflect these events. Plasminogen activator and other lysis factors released from damaged endothelial cells and interstitial tissue may cause clot lysis, hyperfibrinolysis, consumption of fibrinogen, clotting factors, platelet

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Physiopathogenesis of subdural hematomas

Part 2: Inhibition of growth of experimental hematomas with dexamethasone

David Glover and Enrique L. Labadie

apparently required for the process to continue. 8 Products derived from the breakdown of solid blood elements trigger inflammatory responses in the surrounding meningeal membranes, 4 which promote a fibroblastic reaction that infiltrates the clot surface through the fibrin fibers. Meanwhile, plasminogen activators within the clot and arising from the meninges 13, 17 initiate the fibrinolytic liquefaction that creates the center cavity. In the ongoing inflammatory process, neocapillaries are formed within the fibroblastic membrane. These thin-walled vessels permit the

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Haruhide Ito, Toshio Komai and Shinjiro Yamamoto

-diffusion plate tests for estimating fibrinolytic activity and plasminogen activator in the tissue extract. Wells are filled with extract (upper), and a mixture of extract and serum (lower) . Two wells at the left = extract from the dura mater; middle two wells = extract from outer membrane; two wells at the right = extract from inner membrane. Fig. 3. Tissue fibrinolytic activity in the dura mater, outer membrane, and inner membrane in nine patients with chronic subdural hematoma. Each well is filled with extract. Circles indicate activity as determined by the

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Athanasios Smokovitis and Tage Astrup

A ssays of the fibrinolytic activity in extracts from the brain of man and several animal species show that a plasminogen activator is present in high concentrations in the meninges. 6, 9, 10, 19 The pia mater has a particularly high fibrinolytic activity, and this is true even in species that usually have low concentrations of plasminogen activator in their tissues, such as cattle, 10 or rabbit. 6 In contrast, the dura mater frequently showed a low fibrinolytic activity. Interestingly, in organ cultures of human embryonic pia mater and dura mater, both

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Raymond R. Tubbs, Sanford P. Benjamin and Donald E. Dohn

-activated fibrinolytic system by ϵ-aminocaproic acid. Arch Biochem Biophys 83 : 153 – 160 , 1959 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 83: 153–160, 1959 2. 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