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.

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.

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 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.

Histopathological Proof of the Pathogenetic Role of a Rare GFAP Mutation in Alexander´s Disease with Isolated Flaccid Paraparesis

2017 ◽  
Vol 48 (S 01) ◽  
pp. S1-S45
Author(s):  
F. Brackmann ◽  
R. Coras ◽  
K. Rössler ◽  
O. Rompel ◽  
R. Trollmann
Keyword(s):  
Pathogenetic Role

A Monoclonal Antibody-Based Enzyme Immunoassay for Fibrin Degradation Products in Plasma

1988 ◽  
Vol 59 (02) ◽  
pp. 310-315 ◽  
Author(s):  
P W Koppert ◽  
E Hoegee-de Nobel ◽  
W Nieuwenhuizen
Keyword(s):  
Enzyme Immunoassay ◽  
Degradation Products ◽  
Blood Clot ◽  
Tissue Type ◽  
Fibrin Degradation Products ◽  
Type Plasminogen Activator ◽  
Strong Positive Reaction ◽  
Sandwich Type ◽  
Capture Antibody

SummaryWe have developed a sandwich-type enzyme immunoassay (EIA) for the quantitation of fibrin degradation products (FbDP) in plasma with a time-to-result of only 45 minutes.* The assay is based on the combination of the specificities of two monoclonal antibodies (FDP-14 and DD-13), developed in our institute. FDP-14, the capture antibody, binds both fibrinogen degradation products (FbgDP) and FbDP, but does not react with the parent fibrin(ogen) molecules. It has its epitope in the E-domain of the fibrinogen molecule on the Bβ-chain between amino acids 54-118. Antibody DD-13 was raised using D-dimer as antigen and is used as a tagging antibody, conjugated with horse-radish peroxidase. A strong positive reaction is obtained with a whole blood clot lysate (lysis induced by tissue-type plasminogen activator) which is used as a standard. The EIA does virtually not detect FbgDP i. e. purified fragments X, Y, or FbgDP generated in vitro in plasma by streptokinase treatment. This indicates that the assay is specific for fibrin degradation products.We have successfully applied this assay to the plasma of patients with a variety of diseased states. In combination with the assay previously developed by us for FbgDP and for the total amount of FbgDP + FbDP (TDP) in plasma, we are now able to study the composition of TDP in patients plasma in terms of FbgDP and FbDP.

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