The role of ligand-ligand interactions in competition by fibrinogen and fibrin degradation products for fibrinogen binding to human platelets

1983 ◽  
Vol 757 (3) ◽  
pp. 282-287 ◽  
Author(s):  
J PASQUA ◽  
S PIZZO
Keyword(s):  
Degradation Products ◽  
Human Platelets ◽  
Fibrin Degradation Products ◽  
Fibrinogen Binding ◽  
Ligand Interactions

Exercise-Induced Fibrinolysis – Fact or Fiction?

1982 ◽  
Vol 48 (02) ◽  
pp. 201-203 ◽  
Author(s):  
N A Marsh ◽  
P J Gaffney
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Coagulation Factors ◽  
Vascular Wall ◽  
Strenuous Exercise ◽  
Fibrin Degradation Products ◽  
Real Increase ◽  
Exercise Induced ◽  
Male Subjects

SummaryThe effect of strenuous exercise on the fibrinolytic and coagulation mechanisms was examined in six healthy male subjects. Five min bicycle exercise at a work-rate of 800 to 1200 kpm. min−1 produced an abrupt increase in plasma plasminogen activator levels which disappeared after 90 min. However, there was no change in early or late fibrin degradation products nor was there a change in fibrinopeptide A levels or βthromboglobulin levels after exercise although activated partial thromboplastin times were significantly shortened. It is concluded that strenuous exercise does not produce any real increase in fibrinogen-fibrin conversion nor any real increase in the breakdown of these proteins. The role of exercise-induced release of plasminogen activator remains unclear, but probably helps to maintain plasma levels in a discontinuous manner concurrently with the continuous low-level secretion from the vascular wall. The shortening of partial thromboplastin time may be due to the raised levels of plasminogen activator changing the activation state of other coagulation factors.

The Regulatory Role Of Camp In Induction Of Human Platelet Receptor For Fibrinogen

1981 ◽  
Author(s):  
S E Graber ◽  
J Hawiger
Keyword(s):  
Human Platelets ◽  
Membrane Receptor ◽  
Fibrinogen Receptor ◽  
Fibrinogen Binding ◽  
Platelet Receptor ◽  
The Relationship ◽  
Camp Levels ◽  
Dose Dependent ◽  
Stimulation Of

Membrane receptor for fibrinogen plays an essential role in adhesion and aggregation of human platelets by allowing fibrinogen to bridge two or more platelets together. Whereas in normal, unstimulated platelets fibrinogen receptor is not available, it becomes mobilized upon stimulation of platelets with thrombin, ADP, and other stimuli. The mechanism(s) regulating availability of membrane receptor for fibrinogen remains unknown. Following our recent demonstration that prostacyclin (PGI2) prevents mobilization of fibrinogen receptor by thrombin and ADP (Nature 1980, 283,195), we investigated the relationship between cAMP levels and fibrinogen receptor availability. Platelets separated from plasma proteins were briefly exposed to a low thrombin concentration (0.05 U/ml) followed by hirudin to inactivate free thrombin. Binding of 125I-fi- brinogen and cAMP levels were determined in parallel samples. A dose-dependent rise in platelet cAMP levels from 3.3 pM to 10.3 pM/108 platelets in response to PGI2 (3×10-9M - 3×108M) was accompanied by a corresponding inhibition of 125I-fibrinogen binding. The degree of the cAMP increment correlated with binding inhibition (r=0.96). The inhibition of 125I-fibrinogen binding by PGI2 was sustained up to 120 min and was paralleled by a persistent rise in cAMP level. Stimulation of platelet cAMP synthesis “from within” by a ribosylation of the nucleotide regulatory component with subunit A1 of cholera toxin also increased cAMP levels and inhibited fibrinogen receptor mobilization.These results provide evidence that “up and down” regulation of fibrinogen receptor in platelets is linked to changes in cAMP levels induced by different types of adenyl cyclase antagonists and agonists.

Elastase Mediated Fibrinolysis in Acute Promyelocytic Leukemia

2000 ◽  
Vol 83 (06) ◽  
pp. 906-908 ◽  
Author(s):  
Erik-Jan Oudijk ◽  
H. Nieuwenhuis ◽  
Rogier Bos ◽  
Rob Fijnheer
Keyword(s):  
Acute Promyelocytic Leukemia ◽  
Degradation Products ◽  
Promyelocytic Leukemia ◽  
Sepsis Group ◽  
Minor Role ◽  
Hemorrhagic Diathesis ◽  
Elastase Activity ◽  
Fibrin Degradation Products ◽  
A Minor

SummaryThe bleeding syndrome of acute promyelocytic leukemia (APL) is complex and consists of disseminated intravascular coagulation (DIC) and hyperfibrinolysis. Elastase, derived from malignant promyelocytes, is believed to mediate the fibrinogeno- and fibrinolysis by aspecific proteolysis. In this study we measured the role of elastase in fifteen patients with APL by using an assay for elastase degraded fibrin(ogen) and the results were compared with those obtained in patients with sepsis induced DIC.High levels of elastase were observed in sepsis and APL. The levels of fibrinogen and fibrin degradation products were significantly higher in APL patients compared to patients with sepsis induced DIC. Nevertheless, the level of elastase degraded fibrin(ogen) was higher in the sepsis group (635.3 ng/ml, compared to 144.3 ng/ml in APL; p <0.0001). So, the enormous increase in fibrin and fibrinogen degradation products in APL cannot be explained by elastase activity. This study suggests a minor role for elastase mediated proteolysis in the hemorrhagic diathesis in APL patients.

The Pathogenetic Role of Disseminated Intravascular Microcoagulation (DIMC) in Progress of Ischemic Heart Disease (IHD)

1979 ◽  
Author(s):  
N.K. Furkalo ◽  
R.M. Bolshakova ◽  
M.A. Dukhina
Keyword(s):  
Degradation Products ◽  
Activity Detection ◽  
Pathogenetic Role ◽  
Perivascular Edema ◽  
Fibrin Degradation Products ◽  
Conjunctival Vessels ◽  
Phase Platelet ◽  
Diagnostic Criterion ◽  
Early Diagnostic

Hemostatic parameters (including the contact activated phase, platelet functional state, anticoagulational activity, detection of soluble fibrin and fibrinogen (fibrin degradation products) as well as blood viscosity and the character of microcirculation disturbances evaluated by biomicroscopy, microphotographing and filming of bulbar conjunctival vessels, were studied in 394 patients with chronic IHD. Microthrombosis parallel with generalized sludge were discovered within the microcirculatory bed. Analysis of hemostatic rheologic and microcirculatory data has revealed features of chronic, moderately pronounced DIMC, which did not result in marked consumption of coagulational factors. At equal severity grades of IHD, myocardial infarction occured more often in those patients, who bore microthrombosis, microhemorrhage and perivascular edema in the microcirculation system. Hence the detection of DIMC features may become an early diagnostic criterion of IHD severity and its possible complications.

The Amidolytic Activity of the SK-Plasminogen Complex Is Enhanced by a Potentiator which Is Generated in the Presence of Vascular Plasminogen Activator - Role of Fibrin Degradation Products

1982 ◽  
Vol 47 (03) ◽  
pp. 193-196 ◽  
Author(s):  
J Soria ◽  
C Soria ◽  
O Bertrand ◽  
F Dunn ◽  
M Samama ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Venous Stasis ◽  
Amidolytic Activity ◽  
Fibrin Degradation Products ◽  
Lysis Time ◽  
Before And After ◽  
Euglobulin Lysis Time ◽  
High Responders

SummaryIn the presence of an excess of streptokinase (SK) the amidolytic activity of the plasminogen-SK complex on chromogenic substrates is 12% lower in serum than in the corresponding plasma. However, in subjects in whom venous stasis lead to a shortening of the euglobulin lysis time to less than 60 min (high responders), the amidolytic activity of the plasminogen-SK complex in serum was 60% higher than in the corresponding plasma. Attempts to find alterations of the plasminogen molecule itself which would account for the enhanced activity in high responder serum were negative. No free plasmin was present and the plasminogens isolated from plasma and serum before and after venous stasis had the same amidolytic activity as glu-plasminogen in the presence of an excess of SK. N-terminal analysis of these four plasminogens revealed in each instance glutamic acid.The enhancement of the amidolytic activity of the SK-plasminogen complex in serum of high responders (potentiator activity) could be reproduced by adding purified tissue plasminogen activator (TA) to native blood before clotting, but not if TA was added to plasma or to prestasis serum. Removal of fibrin degradation products from poststasis serum resulted in the disappearance of potentiator activity. These experiments suggest that fibrin degradation products, generated during clotting in the presence of vascular or tissular plasminogen activator act as a potentiator of the amidolytic activity of the plasminogen SK-complex.

Potentiation by Adrenaline of Ca2+ Influx and Mobilization in Stimulated Human Platelets: Dissociation from Thromboxane Generation and Aggregation

1988 ◽  
Vol 59 (02) ◽  
pp. 212-215 ◽  
Author(s):  
M J Powling ◽  
R M Hardisty
Keyword(s):  
Human Platelets ◽  
The Other ◽  
Fibrinogen Binding ◽  
Thromboxane Production

SummaryIn a medium containing 1 mM extracellular Ca2+ (Ca2+o), the prior addition of 0.5 pM adrenaline to quin 2-loaded human platelets increased both the rate and amplitude of the rise in cytosolic free Ca2+ (Ca2+i) in response to sub-threshold concentrations of thrombin and PAF and these effects were not prevented by blocking either fibrinogen binding and aggregation or cyclo-oxygenase. In the presence of 2 mM EGTA ([Ca2+o] >100 nM), the rate, but not the extent of rise of [Ca2+i] was enhanced by adrenaline, and this was also unaffected by blockade of cyclo-oxygenase. Addition of adrenaline 1 min after the other agonist in the presence of 1 mM Ca2+o resulted in aggregation without further elevation of [Ca2+i]. Adrenaline thus enhances both influx and intracellular mobilization of Ca2+ by a mechanism independent of both fibrinogen binding and thromboxane production, but these effects do not fully explain its potentiation of aggregation by other agonists

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