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

The subunit fibrin composition of thrombi of both venous and arterial origin was examined by sodium dodecyl sulphate gel electrophoresis. The thrombi were recovered by surgical intervention and all had the same fibrin subunit composition. The alpha chains were cross-linked as alpha-chain polymers alpha (p), the gamma chains as gamma-chain dimers (gamma-gamma) while the beta chains were not crosslinked; a further subunit of molecular weight 33 000 was shown to be present in all the fibrins examined and was a degradation fragment of the beta or gamma chains. This data suggests that the crosslinked alpha chains are rate limiting to the lysis of thrombi in vivo. The digestion of pulmonary emboli by plasmin yielded soluble degradation products which were identified as D dimer and E, the latter fragments being the major products obtained by the lysis of in-vitro made plasma clots. The similarity of the composition and lysis of thrombus fibrin to that formed in vitro augurs well for the justification of in-vitro research on mechanisms in thrombolysis.
Cardiovasc Res 1976 Jul
PMID:Fibrin subunits in venous and arterial thromboembolism. 13 59

The present concept of physiologic fibrinolysis was reviewed. It was concluded that the nonspecific proteolytic activity of plasmin would essentially be limited to fibrin in vivo in view of (A) the specific adsorption of activator and of plasminogen onto the fibrin surface resulting in local generation of plasmin and (B) the fact that plasmin, adsorbed to fibrin (in contrast to plasmin in the fluid phase) largely escapes from the action of antiplasmin. The hemostatic balance in the resting condition was discussed. It was concluded that under normal conditions, systemic intravascular fibrin deposition or formation must be either nonexistent or extremely limited. On the other hand, there is considerable evidence that a limited systemic fibrinogenolysis is going on in healthy individuals and that this process can be accelerated by simple physiologic procedures, such as strenuous physical exercise.
Prog Cardiovasc Dis
PMID:The role of the fibrinolytic system in thromboembolism. 15 21

Segmentally enclosed thrombolysis (SET) was performed immediately following 34 percutaneous transluminal angioplasties (PTAs) for femoropopliteal occlusions. The dilated segment was sealed off with a double balloon catheter, and recombinant tissue plasminogen activator (rt-PA) 1 mg/ml and heparin 200 IU/ml were injected between the balloons. The catheter was removed after 30 min and heparin treatment was continued for 24 h. Alpha-2-antiplasmin was initially reduced by 13% and normalized 2 h after SET, indicating that only small amounts of free plasmin were liberated during thrombolysis. No clinically relevant changes in plasma fibrinogen occurred. Two puncture site hemorrhages did not coincide with the coagulopathy induced by SET. One-year patency was 80%. Early rethrombosis occurred in 9% versus 41% in our previous series on standard PTA for femoropopliteal occlusions (p less than 0.001). Therefore, SET is considered beneficial in reducing the incidence of early rethrombosis.
Cardiovasc Intervent Radiol
PMID:Segmentally enclosed thrombolysis in percutaneous transluminal angioplasty for femoropopliteal occlusions: a report from a pilot study. 183 37

The protease inhibitor aprotinin interacts with plasmin and kallikrein, which are generated in cardiac surgery during cardiopulmonary bypass (CPB). The influence of high-dose aprotinin application (2 million kallikrein inactivator units given i.v. at the beginning of anaesthesia followed by a 500,000 KIU/h infusion throughout the operation and additional 2 millions KIU added to the priming of the oxygenator) on perioperative blood loss and donor blood requirement was studied in 152 adult cardiac surgical patients. This group was compared to 317 patients having cardiac surgery without the application of aprotinin. Aprotinin reduced the homologous blood requirement by 43% (1783 +/- 100 vs 1015 +/- 131 ml, p less than 0.05), while the reduction of postoperative blood loss was 29% (1070 +/- 43 vs 761 +/- 51 ml, p less than 0.05). Fortytwo percent of the aprotinin treated patients completed their hospital stay without having any donor blood transfusion compared to 18% in the group without aprotinin. The blood saving effect was even more pronounced in operations with prolonged perfusion times. Intra- and postoperative complications were equally distributed in both groups. The blood-saving effect of aprotinin may be due to a platelet-preserving effect and/or kallikrein inhibition during CPB. There were no clinically relevant side effects related to aprotinin observed. It is concluded that high dose aprotinin therapy reduces both postoperative blood loss and homologous blood requirement, and therefore the routine application of aprotinin during cardiac surgical procedures is to be recommended.
Thorac Cardiovasc Surg 1989 Apr
PMID:Reduction of homologous blood requirement in cardiac surgery by intraoperative aprotinin application--clinical experience in 152 cardiac surgical patients. 247 Dec 88

Two different priming solutions for cardiopulmonary bypass (CPB) were studied in regard to possible influence on the plasma protease systems. The study was performed on 20 patients undergoing elective coronary artery bypass grafting. In ten cases the priming solution contained 1,000 ml dextran (MW 70,000) and in ten it consisted only of Ringer's acetate solution. The same level of haemodilution was established during CPB in the two groups. Clinical variables and laboratory data were monitored. Spontaneous kallikrein activity, plasma prekallikrein, functional kallikrein inhibition capacity, spontaneous plasmin activity, plasminogen, functional antiplasmin activity, prothrombin and antithrombin-III were measured, using chromogenic peptide substrate assays before and during CPB as well as in the postoperative period. The antiplasmin activity decreased more in the dextran than in the Ringer group following cardiopulmonary bypass but the difference was without clinical significance. No statistically significant intergroup difference was found in the other measured variables of the kallikrein-kinin, fibrinolytic and coagulation systems.
Scand J Thorac Cardiovasc Surg 1989
PMID:Changes in the plasma protease systems during open-heart surgery with dextran vs. Ringer acetate as priming solution. 248 39

Components of the coagulation and fibrinolytic systems were determined in patients undergoing open heart surgery with cardiopulmonary bypass. The variables studied included prothrombin, antithrombin-III, spontaneous plasmin activity, plasminogen and functional antiplasmin activity. The variables were measured using chromogenic peptide substrate assays. A marked, transitory, increase in spontaneous plasmin activity prior to cardiopulmonary bypass, but after heparin injection was found. A decrease in antiplasmin activity during bypass was observed, while actual plasminogen level, when correcting for hemodilution, was unchanged. Both prothrombin and antithrombin-III paralleled the decrease in hemoglobin concentration during bypass. These findings suggest that the injection of heparin induced a transient activation of the fibrinolytic system, whereas no detectable consumption of the measured coagulation variables was observed.
Thorac Cardiovasc Surg 1989 Jun
PMID:Changes in the coagulation and fibrinolytic systems during and after cardiopulmonary bypass surgery. 252 23

Pharmacologic intervention is critical to the management of myocardial ischemia. Four classes of drugs are now used in therapeutic regimens for ischemia. beta-Adrenergic blockers decrease ischemia by blocking beta 1-mediated inotropic and chronotropic effects, thereby decreasing myocardial oxygen consumption. Calcium channel blockers alter fast- and slow-response action potentials by decreasing transmembrane calcium flux, resulting in decreased conduction velocity and heart rate and prolonged effective refractory period. These effects positively influence ischemia and atrial dysrhythmias. Additionally, these agents decrease excitation-contraction coupling in vascular smooth muscle, resulting in coronary and peripheral vasodilation. Organic nitrates and nitrites decrease vascular smooth muscle contraction and preload, and afterload, precipitating a decrease in myocardial oxygen consumption and ischemia. They also improve blood flow to areas of compromised flow. Thrombolytic agents are administered in acute situations to dissolve the occluding thrombus, but they must be used within a few hours of the injury. These drugs activate the conversion of plasminogen to plasmin, which breaks down the clot into fibrin degradation products. The choice of agents is determined by the etiology of the patient's ischemia, his or her response to the drug, and the presence of concomitant disease processes.
J Cardiovasc Nurs 1989 Aug
PMID:Pharmacologic management of myocardial ischemia. 257 Jan 35

This article describes the interrelated processes and homeostatic controlling mechanisms of hemostasis and fibrinolysis. Hemostasis involves platelets, blood vessels, and coagulation proteins. Primary hemostasis is dependent on platelet adhesion, activation, secretion, and aggregation. Secondary hemostasis consists of intrinsic activation, extrinsic activation, and the common final pathway. Fibrinolysis results in clot dissolution and is initiated endogenously as plasminogen is converted to plasmin.
J Cardiovasc Nurs 1989 Nov
PMID:Physiologic mechanisms of hemostasis and fibrinolysis. 268

Early reperfusion of occluded coronary arteries offers great promise as a method for minimizing myocardial damage after acute myocardial infarction. Such reperfusion is usually attempted via administration of fibrinolytic agents. Urokinase may hold marginal advantages over streptokinase, especially in patients with high preexisting titers of antistreptokinase antibodies. These minor differences, however, pale in comparison to important advantages demonstrated by the newly developed agent, tissue plasminogen activator (t-PA). The advantages of t-PA derive primarily from its property of binding to, and being activated by, fibrin. Consequently the generated plasmin is also fibrin-bound, the bound plasmin is protected from circulating antiplasmin and therefore more efficiently utilized, and circulating fibrinogen is spared. Preliminary clinical experience indicates that the frequency of favorable response after intravenous administration of t-PA is considerably greater than after SK. A major determinant of clinical benefit after reperfusion is the brevity of ischemia. Selective intracoronary infusion of fibrinolytic agent produces faster lysis than does intravenous infusion, and rate of lysis may be further accelerated by transcatheter disruption of clot and intrathrombic injections of highly concentrated urokinase or t-PA. Even maximally accelerated lysis, however, cannot fully compensate for the inherent delay imposed by catheterization. For that reason, prompt intravenous infusion of fibrinolytic agents, presumably t-PA, seems preferable to the intracoronary route. In the effort to initiate fibrinolytic therapy at the earliest feasible time after infarction, administration by paramedics, or even home administration after training, is a program worthy of exploration.
Cardiovasc Intervent Radiol 1986
PMID:Streptokinase, urokinase, and tissue plasminogen activator: pharmacokinetics, relative advantages, and methods for maximizing rates and consistency of lysis. 310 38

The fibrinolytic system is activated by the conversion of plasminogen to plasmin by mediators such as tissue extract, plasma factor XII, or the exogenous activators urokinase (UK) and streptokinase (SK). The foreign protein composition of SK is responsible for the allergic response observed in some patients following administration. Clinical and investigational evidence has also shown a higher incidence of hemorrhagic complications with SK compared with UK. In general, thrombolytic therapy is a safe, effective way to resolve thrombotic obstruction in patients with such problems as acute pulmonary embolism, acute myocardial infarction, or occluded intravascular lines.
Cardiovasc Intervent Radiol 1988
PMID:Fundamentals of fibrinolytic therapy. 313 Oct 5


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