scholarly journals Clot retraction facilitates clot lysis

Blood ◽  
1981 ◽  
Vol 57 (1) ◽  
pp. 44-48
Author(s):  
RC Carroll ◽  
JM Gerrard ◽  
JM Gilliam

Platelet facilitation of clot lysis was studied using the dilute clot lysis assay, a standardized assay for fibrinolysis shown to correlate with the development of postoperative deep vein thrombosis. Clots prepared from dilute platelet poor plasma showed prolonged clot lysis when compared with clots prepared in a similar fashion from dilute platelet rich plasma. Since in the presence of platelets clot retraction or contraction occurred, we evaluated a possible direct contribution of retraction to clot lysis. Dilute platelet poor plasma clots were compacted by centrifugation, to a similar extent as that achieved during clot retraction in dilute platelet rich plasma. These clots now lysed at a rate that approached that seen with dilute platelet rich plasma clots. Using an alternate alternate approach, dilute platelet rich plasma clots were treated with cytochalasin B to prevent clot retraction. Such clots now showed prolonged lysis similar to that seen with dilute platelet poor plasma. The prolonged lysis of cytochalasin B treated dilute platelet rich plasma clots was corrected by artificial compaction of the clots. The results suggest that clot retraction markedly facilitates clot lysis, and shows that a major role of platelets to facilitate clot lysis is the effect of these cells to cause clot retraction.

Blood ◽  
1981 ◽  
Vol 57 (1) ◽  
pp. 44-48 ◽  
Author(s):  
RC Carroll ◽  
JM Gerrard ◽  
JM Gilliam

Abstract Platelet facilitation of clot lysis was studied using the dilute clot lysis assay, a standardized assay for fibrinolysis shown to correlate with the development of postoperative deep vein thrombosis. Clots prepared from dilute platelet poor plasma showed prolonged clot lysis when compared with clots prepared in a similar fashion from dilute platelet rich plasma. Since in the presence of platelets clot retraction or contraction occurred, we evaluated a possible direct contribution of retraction to clot lysis. Dilute platelet poor plasma clots were compacted by centrifugation, to a similar extent as that achieved during clot retraction in dilute platelet rich plasma. These clots now lysed at a rate that approached that seen with dilute platelet rich plasma clots. Using an alternate alternate approach, dilute platelet rich plasma clots were treated with cytochalasin B to prevent clot retraction. Such clots now showed prolonged lysis similar to that seen with dilute platelet poor plasma. The prolonged lysis of cytochalasin B treated dilute platelet rich plasma clots was corrected by artificial compaction of the clots. The results suggest that clot retraction markedly facilitates clot lysis, and shows that a major role of platelets to facilitate clot lysis is the effect of these cells to cause clot retraction.


2021 ◽  
Vol 156 (5) ◽  
pp. 251-252
Author(s):  
Francisco Galeano-Valle ◽  
Jorge del-Toro-Cervera ◽  
Pablo Demelo-Rodríguez

2019 ◽  
Vol 8 (8) ◽  
pp. 512-516
Author(s):  
Vijay Bahadur Singh ◽  
Punya Pratap Singh ◽  
Rajesh Malik ◽  
Lovely Kaushal ◽  
Vijay Verma ◽  
...  

2014 ◽  
Vol 9 (4) ◽  
pp. 187-194
Author(s):  
M.G. Vashist ◽  
S. Deswal ◽  
M. Verma ◽  
S. Kharb

1981 ◽  
Author(s):  
V V Kakkar

Thrombolytic therapy has a unique advantage in the treatment of patients suffering from thrombotic disease, since it is capable of inducing the dissolution of intravascular fibrin and thus causing the reduction or elimination of thrombi. The rapidity of thrombus removal distinguishes this form of treatment from anticoagulant therapy, in which normal physiological processes are allowed to restore the obstructed circulation. By quickly removing the obstruction, it should be possible to reduce the mortality arising from acute thromboembolic episodes.The results of therapy for deep-vein thrombosis have been fairly uniform. The published studies can be broadly classified into two main groups; in uncontrolled trials, partial or complete lysis of thrombi was obtained in approximately 65-80% of the patients who received streptokinase, while only 10-25% of the patients receiving heparin showed this change.In patients suffering from acute major or massive pulmonary embolism, a number of trials have demonstrated a more rapid resolution of the embolus than would be expected by treatment with heparin alone.The role of lytic therapy in preventing the late sequelae of deep vein thrombosis at present remains uncertian. Studies involving large numbers of patients and longer periods of follow-up are required to determine the extent to which post phlebitic venous insufficiency is reduced by early thrombolytic therapy.


1981 ◽  
Vol 26 (1_suppl) ◽  
pp. S81-S83 ◽  
Author(s):  
P. E. Jarrett

The postphlebitic syndrome is a result of previous deep vein thrombosis and presents with oedema, pain, induration, pigmentation and ulceration. Extravascular deposition of fibrin is associated with reduced fibrinolytic activity in these patients. In a double-blind crossover study there was evidence of benefit from stanozolol which enhanced fibrinolytic activity. No side effects of any consequence were noted with a dosage of 5 mg twice per day.


1981 ◽  
Author(s):  
G Schöffel ◽  
R Zimmermann ◽  
J Harenberg

In preliminary studies we demonstrated an increased thrombolytic activity with higher dosages of urokinase in the therapy of deep vein thrombosis. From that time this higher urokinase dosage schedule (loading dose 250,000 IU, initial maintenance dosage 2000 IU/kg/h in combination with 1520 U heparin/kg/h) was used and suggested as ideal.In 10 patients with deep vein thrombosis treated according to this dosage schedule following coagulation parameters were determined before the beginning of the therapy, after 1,4,12 h and then at least once per day up to 7-14 days:aPTT, thrombin clotting time, fibrinogen (according to Clauss, Ratnoff and Menzie and radial immunodiffusion), TEG, euglobulin clot lysis time, inhibitors of fibrinolysis, plasminogen, antithrombin III, fpA, clotting factors V and VIII. The coagulation analysis showed a progressive decrease of fibrinogen to 50100 mg% and of plasminogen to about 40 % within 12-36 h. At this time a reduction of the urokinase dose by 30-40 % and further only slight corrections became necessary. Additional investigations demonstrated a more pronounced fibrinogenolytic effect when dissolving and applying urokinase in plastic material and avoiding contact with glass surfaces. These findings suggested a 30% saving of urokinase.The highly effective urokinase dosage schedule here described has been proved practicable and rendered too frequent coagulation controls superfluous. The saving of urokinase by using plastic material introduced a modification of our urokinase regimen:Loading dose 250,000 IU, followed by 2000 IU/kg/h for only 8 h, then 1000 IU/kg/h with further slight individual dose corrections.


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