Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is known, that plasmin is capable of specifically activating the complement factors C1 q and C3. In addition plasmin can activate procollagenase to collagenase. Since both mechanisms could possibly play a decisive role in the pathogenesis of rheumatoid arthritis, we have carried out animal experiments to investigate the primary role of plasmin in the development of arthritis. Twenty-two rabbits were subjected to intraarticular injection with an equal dose of plasmin on days 1, 4, and 8. An aspirate was taken on day 9 for a white cell count and a histological investigation of the synovial tissue. Already after a single dose of 0.25 CU plasmin an inflammatory reaction was clearly observed. Increasing amounts of plasmin (2.5 and 12.5 CU) caused an increased inflammatory response. On the basis of these results, it is discussed whether the observed arthritic reaction after plasmin injection is caused by complement activation. Possible analogies with rheumatoid arthritis are discussed.
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PMID:[Experimental plasmin arthritis]. 622 84

Radioactively labeled human fibrin clots were placed into veins of Macaca arctoides monkeys. Thrombolysis was recorded by the disappearance of radioactivity and by angiography. Streptokinase (SK) and urokinase (UK) induced thrombolysis was potentiated by low dose aspirin (ASA) and pentoxifylline (PE). Studies on the mechanisms of action revealed that PE inhibits platelet aggregation, releases tissue plasminogen activator (t-PA) from the endothelium, increases red cell deformability and inhibits white cell adhesion. Thrombolysis by pro-urokinase (pro-UK) was potentiated by low dose SK probably because of streptokinase-plasmin activation of pro-UK to UK. Platelet aggregation inhibitory effects, disaggregation of platelet aggregate inducing effects, and the t-PA releasing activity of PE was demonstrated in patients with obstructive cardiovascular disease. Pharmacodynamic studies suggested that PE metabolites one and five are most effective from this point of view. These metabolites are currently studied in combination with thrombolytic enzymes.
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PMID:Potentiation of thrombolytic therapy by enzyme combinations and with aspirin or pentoxifylline. 799 60

The relation of intravascular fibrin to the leucocytic sticking reaction in ear chambers of rabbits injured by heat was investigated in two ways. First, attempts were made to destroy the thin layer of fibrin believed to coat the surfaces of cells involved in the sticking reaction. Second, white cell sticking was studied after fibrinogen had been removed from the blood stream. The results of these experiments were as follows:- 1. Activation of fibrinolysin in vivo by streptokinase did not impair sticking of white blood cells. 2. Administration of streptokinase parenterally did not lower fibrinogen blood levels appreciably even when the amount used was large. 3. Thromboplastin infusions alone reduced circulating fibrinogen to low levels but leucocytic sticking was not prevented. Furthermore, frequent death of animals due to pulmonary embolism made such experiments prohibitive. 4. Addition of streptokinase to thromboplastin infusions protected against embolic deaths but did not influence sticking even though the fibrinogen levels achieved were quite low. 5. Finally, when thrombin was added to infusions of thromboplastin and streptokinase, no circulating fibrinogen could be detected. Under such circumstances leucocytic sticking following heat injury occurred without reduction. These findings were interpreted as evidence against a primary role of the blood clotting mechanism in causing the sticking of white blood cells to injured endothelium. Alternative explanations were discussed.
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PMID:Studies on the pathogenesis of acute inflammation. II. The relationship of fibrinogen and fibrin to the leucocytic sticking reaction in ear chambers of rabbits injured by heat. 1379 25