Effects of exercise and conditioning on clotting and fibrinolytic activity in men

1987 ◽  
Vol 62 (4) ◽  
pp. 1416-1421 ◽  
Author(s):  
E. W. Ferguson ◽  
L. L. Bernier ◽  
G. R. Banta ◽  
J. Yu-Yahiro ◽  
E. B. Schoomaker
Keyword(s):  
Fibrinolytic Activity ◽  
Blood Clotting ◽  
Degradation Products ◽  
Clot Lysis ◽  
Plasma Clot ◽  
Fitness Program ◽  
Fibrin Degradation Products ◽  
Before And After ◽  
Plasmin Inhibitor ◽  
Sedentary Subjects

Sixty healthy men in three physical fitness categories (sedentary, on no organized fitness program; joggers, running 5–15 miles/wk; and marathoners, running greater than 50 miles/wk) were evaluated for changes in blood clotting and fibrinolytic activity before and after maximum exercise on a treadmill according to the Bruce protocol. The rate of blood clotting, as measured by prothrombin times, partial thromboplastin times and thrombin times, was accelerated by exercise (all P less than 0.005). The ability of euglobulin clots and plasma clots to lyse incorporated 125I-fibrin, termed 125I-euglobulin clot lysis (IEL) and 125I-plasma clot lysis (IPCL), were used as indexes of fibrinolytic activity. Marathoners had greater increases in fibrinolytic activity with exercise (76% compared with 63% for joggers and 55% for sedentary subjects by IEL; 427% compared with 418% for joggers and 309% for sedentary subjects by IPCL; all P less than 0.05). Fibrin degradation products increased with exercise (P less than 0.005 for the total group of 60 subjects). The absolute concentrations of alpha 2-plasmin inhibitor, alpha 2-macroglobulin, and antithrombin III increased with exercise (all P less than 0.005), but when concentrations were corrected for acute shifts of plasma water during exercise, the quantity of these inhibitors actually decreased (all P less than 0.005). The changes in clotting assays with exercise were not significantly correlated with changes in whole blood lactate, blood pyruvate, or rectal temperatures. Fibrinolytic assays before and after exercise correlated poorly to moderately with blood lactates (IEL: r = 0.441 and r = 0.425, respectively; IPCL: r = 0.294 and r = 0.544, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

A Plasma Clot Lysis Assay Based on the Release of Fibrin Degradation Products: Application to the Diagnosis of Hypofibrinolytic States

1990 ◽  
Vol 63 (01) ◽  
pp. 076-081 ◽  
Author(s):  
Pascale Gaussem ◽  
Sophie Gandrille ◽  
Pascale Molho-Sabatier ◽  
Loïc Capron ◽  
Jean-Noël Fiessinger ◽  
...  
Keyword(s):  
Degradation Products ◽  
Venous Occlusion ◽  
Lower Limbs ◽  
Clot Lysis ◽  
Plasma Clot ◽  
Vein Thrombosis ◽  
Fibrin Degradation Products ◽  
Before And After ◽  
Euglobulin Clot Lysis Time ◽  
Pai 1

SummaryUsing a monoclonal antibody-based assay, we measured the fibrin degradation product release in the supernatant of plasma clots obtained before and after venous occlusion (VO) in 30 patients with definite or suspected vascular thrombosis (19 definite and 2 suspected deep vein thrombosis, 6 recurrent superficial thrombophlebitis, 3 arterial occlusions of lower limbs). tPA and PAI-1 concentrations were determined using ELISA assays; the post-occlusion values were corrected for haemoconcentration. The increase in tPA during VO was correlated with haemoconcentration (r = 0.74), but 3 patients had ineffective VO (<2% increase in proteins). The fibrinolytic response to VO was evaluated using the shortening of the time necessary for the release of 200 μg of fibrin degradation products per mg of fibrinogen (Δ T 200). Two among the 27 patients with effective VO were bad responders with a Δ T 200 <3 h (whereas all the others had Δ T 200 >10 h). These patients had respectively a deficient tPA release (Δ tPA = 1 ng/ml) and an elevated PAI-1 level at rest (33 ng/ml). Several other patients were bad responders in terms of tPA release or of shortening of the euglobulin clot lysis time but they had a normal Δ T 200. This plasma clot test reflects the ability of free tPA to bind to fibrin (the amount of which depends on the level of tPA and PAI-1), and may be useful in the diagnosis of a hypofibrinolytic state.

The Measurement of Fibrinolysis in the Rat

1971 ◽  
Vol 26 (02) ◽  
pp. 295-310 ◽  
Author(s):  
M. J Gallimore ◽  
H. M Tyler ◽  
J. T. B Shaw
Keyword(s):  
Whole Blood ◽  
Fibrinolytic Activity ◽  
Factor Xiii ◽  
Degradation Products ◽  
Blood Clot ◽  
Clot Lysis ◽  
Plate Assay ◽  
Fibrin Degradation Products ◽  
Fibrin Plate ◽  
Dilute Blood

SummaryMethods are described for measuring fibrinolytic activity in the rat. These include dilute blood clot lysis, euglobulin clot lysis, a fibrin plate assay with euglobulin solutions, and an accelerated whole blood clot lysis technique in which limited fibrinolysis is induced with urokinase. In addition, methods have been worked out for the estimation of four plasma components closely involved in fibrinolysis: fibrinogen, factor XIII, plasma inhibitors and fibrin degradation products. The sensitivity and validity of the assays were tested by studying their capacity to detect changes resulting from the administration of eledoisin, Neohydrin and turpentine.

Thrombin activatable fibrinolysis inhibitor (TAFI) affects fibrinolysis in a plasminogen activator concentration-dependent manner

2004 ◽  
Vol 91 (03) ◽  
pp. 473-479 ◽  
Author(s):  
Ana Guimarães ◽  
Dingeman Rijken
Keyword(s):  
Plasminogen Activator ◽  
In Vitro Study ◽  
Inhibitory Effect ◽  
Retardation Factor ◽  
Clot Lysis ◽  
Dependent Manner ◽  
Plasma Clot ◽  
Concentration Dependent Manner ◽  
Plasmin Inhibitor

SummaryTAFIa was shown to attenuate fibrinolysis. In our in vitro study, we investigated how the inhibitory effect of TAFIa depended on the type and concentration of the plasminogen activator (PA). We measured PA-mediated lysis times of plasma clots under conditions of maximal TAFI activation by thrombin-thrombomodulin in the absence and presence of potato carboxypeptidase inhibitor. Seven different PAs were compared comprising both tPA-related (tPA, TNK-tPA, DSPA), bacterial PA-related (staphylokinase and APSAC) and urokinase-related (tcu-PA and k2tu-PA) PAs. The lysis times and the retardation factor were plotted against the PA concentration. The retardation factor plots were bell-shaped. At low PA concentrations, the retardation factor was low, probably due to the limited stability of TAFIa. At intermediate PA concentrations the retardation factor was maximal (3-6 depending on the PA), with TNK-tPA, APSAC and DSPA exhibiting the strongest effect. At high PA concentrations, the retardation factor was again low, possibly due to inactivation of TAFIa by plasmin or to a complete conversion of glu-plasminogen into lys-plasminogen. Using individual plasmas with a reduced plasmin inhibitor activity (plasmin inhibitor Enschede) the bell-shaped curve of the retardation factor shifted towards lower tPA and DSPA concentrations, but the height did not decrease. In conclusion, TAFIa delays the lysis of plasma clots mediated by all the plasminogen activators tested. This delay is dependent on the type and concentration of the plasminogen activator, but not on the fibrin specificity of the plasminogen activator. Furthermore, plasmin inhibitor does not play a significant role in the inhibition of plasma clot lysis by TAFI.

scholarly journals Fibrin fragment D-dimer and fibrinogen B beta peptides in plasma as markers of clot lysis during thrombolytic therapy in acute myocardial infarction

Blood ◽  
1990 ◽  
Vol 76 (7) ◽  
pp. 1341-1348 ◽  
Author(s):  
CM Lawler ◽  
EG Bovill ◽  
DC Stump ◽  
DJ Collen ◽  
KG Mann ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Degradation Product ◽  
Degradation Products ◽  
Tissue Type ◽  
Clot Lysis ◽  
Fibrin Degradation Product ◽  
Fibrin Degradation Products ◽  
Group 2 ◽  
D Dimer ◽  
Group 1

Abstract The validity of markers in plasma of in vitro thrombolysis was investigated in 12 patients with extensive fibrinogen breakdown (greater than 80%, group 1) and in 12 patients with minimal breakdown (less than 20%, group 2). The patients were treated with 100 mg of recombinant tissue-type plasminogen activator (rt-PA) in the “Thrombolysis in Myocardial Infarction II” (TIMI II) trial. Cross- linked fibrin degradation product levels were measured with two variant enzyme-linked immunosorbent assays (ELISAs), both using a fibrin fragment D-dimer specific capture antibody. In one instance, a tag antibody was used that cross-reacts with fibrinogen (pan-specific tag ELISA); in the other, the tag antibody was specific for fibrin fragment D (fibrin-specific tag ELISA). Apparent concentrations of cross-linked fibrin degradation products at baseline were within normal limits with both assays in most patients. At 8 hours after rt-PA infusion, the measured cross-linked fibrin degradation products were increased about twofold to fourfold in group 2 with both assays. However, in group 1, levels were significantly higher with the pan-specific tag ELISA (5.8 +/- 4.2 micrograms/mL) compared with the fibrin-specific tag ELISA (1.5 +/- 1.3 micrograms/mL). This observation was most likely a result of detection of fibrinogen degradation products in the pan-specific ELISA. Apparent levels of fibrinopeptide B beta 1–42, a marker of fragment X formation, increased during thrombolysis from 4.2 +/- 2.8 pmol/mL to 2,000 +/- 230 pmol/mL in group 1 and from 4.1 +/- 2.1 pmol/mL to 300 +/- 43 pmol/mL in group 2, and were correlated significantly with the extent of fibrinogen breakdown (r = -0.8). Fibrinopeptide beta 15–42 levels increased from 4.3 +/- 3 pmol/mL to 70 +/- 19 pmol/mL in group 1, but did not increase in group 2. The apparent increase in group 1 could be explained by cross-reactivity of fibrinopeptide B beta 1–42 in the fibrinopeptide beta 15–42 assay. We conclude that cross-linked fibrin degradation product levels as measured with a pan-specific tag ELISA and fibrinopeptide beta 15–42 levels as measured with certain monoclonal antibody-based ELISA are influenced by the extent of fibrinogen degradation. Fibrinopeptide B beta 1–42 is a marker specific for fibrinogen breakdown. Cross-linked fibrin degradation product levels, measured with a fibrin-specific tag ELISA, appear to be markers specific for thrombolysis. Consequently, assays similar to the fibrin- specific tag ELISA may provide more accurate information when correlated with clinical endpoints.

scholarly journals Hematologic and Coagulation Measurements in Autotransfused Blood

1977 ◽  
Author(s):  
F.N. McKenzie ◽  
W. Wall ◽  
R.O. Heimbecker ◽  
R. Barr ◽  
A. Robert
Keyword(s):  
Degradation Products ◽  
Autologous Blood ◽  
Significant Risk ◽  
Major Surgery ◽  
Clot Lysis ◽  
Plasma Hemoglobin ◽  
Fibrin Degradation Products ◽  
Excellent Preservation ◽  
The Mean

Reinfusion of blood shed during elective or emergency vascular surgery (autotransfusion) is an under utilized technique. This is due in part to doubts as to the quality of autotransfused blood and concern about the risk of inducing a coagulopathy in the recipient. We have measured coagulation and hematologic parameters in autotransfused blood in the recipient before and at intervals after operation in 62 patients, none of whom received bank blood or blood products at the time of the study. The patients were heparinized (3 mg/Kg) during operation and this was reversed by protamine at the end of the procedure. The salvaged blood was reinfused immediately after appropriate samples had been taken. The mean volume of blood autotransfused was 1.8L in 58 patients and 9.4L in 4 patients. There was excellent preservation of platelets and fibrinogen, normal levels being maintained both in the autotransfused blood and in the recipients. Values for fibrin degradation products and euglobulin clot lysis remained normal. The mean plasma hemoglobin in the autotransfused blood was 416 mg% and this was not correlated to the volume autotransfused. Partial thromboplastin time which was prolonged by heparin during surgery was consistently normal post-operatively. No patient developed complications which could be attributed to autotransfusion and, in particular, re-operation for post-operative bleeding was never required and wound hematoma was not seen. We conclude that autologous blood may be returned to patients in large amounts without significant risk using the technique described. The technique deserves wider application in major surgery.

Fibrinolytic Activity in Patients with Acute Tonsillitis

1979 ◽  
Vol 88 (3) ◽  
pp. 366-367 ◽  
Author(s):  
T. Kosugi ◽  
O. Matsuo ◽  
M. Hamaya ◽  
H. Mihara
Keyword(s):  
Fibrinolytic Activity ◽  
Degradation Products ◽  
Healthy Adults ◽  
Fibrinolytic System ◽  
Acute Tonsillitis ◽  
Fibrin Degradation Products ◽  
Fibrinogen Content

Three parameters in blood fibrinolysis, viz, the levels of fibrinogen, plasminogen, and fibrinogen and/or fibrin degradation products (FDP), were measured in patients with acute tonsillitis and the results were compared with those for healthy adults. The fibrinogen content in acute tonsillitis increased significantly ( P <.001), that of plasminogen decreased significantly ( P <.005), while FDP showed a higher value ( P <.01). The significance of the fibrinolytic system in acute tonsillitis is discussed.

The Resistance of Soluble Derivatives of Fibrinogen and the Sensitivity of Its Insoluble Forms to Fibrinolytic Degradation in Blood

1974 ◽  
Vol 32 (02/03) ◽  
pp. 582-591 ◽  
Author(s):  
Victor Gurewich ◽  
Andrzej Nowak ◽  
Izabella Lipinska ◽  
Boguslaw Lipinski
Keyword(s):  
Fibrinolytic Activity ◽  
Degradation Products ◽  
Venous Occlusion ◽  
Protamine Sulfate ◽  
Electrophoretic Method ◽  
Soluble Fibrin ◽  
Fibrin Degradation Products ◽  
Fibrin Monomer ◽  
Derivatives Of

SummaryThe effect of naturally induced fibrinolytic activity on fibrinogen and certain soluble and insoluble derivatives was studied. Experiments were performed on blood removed after venous occlusion of the arm and immediately after death. A previously described electrophoretic method was used by which the heterogeneity of fibrinogen can be demonstrated directly in intact plasma. It was shown that fibrinogen, soluble fibrin monomer (FM) complexes and fibrin degradation products are resistant to degradation by naturally-induced fibrinolytic activity. By contrast, rapid lysis of fibrin, protamine sulfate (PS) precipitated fibrinogen, and PS and ethanol induced gels of FM occurred. The observations are believed relevant to our understanding of the pathway of fibrinogen and FM catabolism and the interpretation of the origin of serum FDP.

Sustained Fibrinolysis After Administration of t-PA Despite Its Short Half-Life in the Circulation

1987 ◽  
Vol 57 (01) ◽  
pp. 035-040 ◽  
Author(s):  
Paul R Eisenberg ◽  
Laurence A Sherman ◽  
Alan J Tiefenbrunn ◽  
Philip A Ludbrook ◽  
Burton E Sobel ◽  
...  
Keyword(s):  
Half Life ◽  
Fibrinolytic Activity ◽  
Degradation Products ◽  
Clinical Success ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Fibrin Degradation Products ◽  
Short Half Life ◽  
Type Plasminogen Activator ◽  
The Difference

SummaryTo characterize the duration of the fibrinolytic response to tissue-type plasminogen activator (t-PA) and streptokinase (SK) in patients with acute myocardial infarction we serially assayed crosslinked fibrin degradation products (XL-FDP) and Bβ15-42 fibrinopeptide. Use of specific monoclonal antibodies permitted quantification and differentiation of fibrin from fibrinogen degradation products. Marked elevations of XL-FDP occurred within 1 hour after administration of t-PA (n = 13) or SK (n = 35) to >1000 ng/ml in 79% of the patients. All patients given t-PA exhibited elevations of XL-FDP >1000 ng/ml, most exhibited values >5000 ng/ml (79% of patients). In contrast 6 of the patients given SK failed to exhibit XL-FDP >1000 ng/ml. XL-FDP >5000 ng/ml occurred in only 14%. The difference in the response to t-PA compared to SK was particularly striking 7 hours or more after administration of activator at which time XL-FDP were markedly elevated in patients given t-PA (5821 ± 1683 ng/ ml) compared with decreasing values in patients given SK (2924 ± 1186 ng/ml) (p <0.01). Levels of Bβ315-42 were significantly higher after t-PA compared with SK beginning 3 hours after treatment, consistent with a greater intensity of fibrinolytic response to t-PA. Marked elevations of this short lived degradation product of fibrin (t1/2 = 10-20 minutes) in the samples drawn late after administration of t-PA (44.3 ±12.8 nM) but not after SK (11.7 ± 4.5 nM) confirmed prolonged fibrinolytic activity of plasmin after t-PA. There was no discernible relationship between the extent of fibrinolysis as assessed by XL-FDP and Bβ 15-42 and the total dose of t-PA administered or the duration of the infusion. Elevations of XL-FDP invariably occurred after SK, and were not significantly different in patients with or without recanalization. Thus “clinical success” of coronary thrombolysis appears to depend on a favorable balance between thrombosis and fibrinolysis rather than the intensity of fibrinolysis alone. The prolonged fibrinolytic activity after t-PA appears to reflect the enhanced binding of this activator to fibrin and is likely to result in more sustained and hence more effective fibrinolysis with t-PA compared to SK despite the short half-life of t-PA (t1/2 = 6 minutes) in the circulation.

Relationship between Plasma Fibrinolytic Activity and Serum Fibrinogen Degradation Products (FDP) Tested by Various Methods

1971 ◽  
Vol 26 (01) ◽  
pp. 083-087 ◽  
Author(s):  
B Lipiński ◽  
A Nowak ◽  
A Odrzywolska ◽  
J Dosiak
Keyword(s):  
Healthy Subjects ◽  
Fibrinolytic Activity ◽  
Degradation Products ◽  
Clot Lysis ◽  
Proteolytic Degradation ◽  
Fibrinogen Degradation Products ◽  
Lysis Time ◽  
Euglobulin Clot Lysis Time ◽  
Fibrinogen Content ◽  
Clot Lysis Time

SummaryIt was found in the present work that the level of serum fibrinogen degradation products (FDP) determined by the immunoassay method correlated well with the staphylococcal clumping titer in serum (correlation coefficient r = 0.68). The content of FDP in serum of 30 healthy subjects and patients with various diseases did not correlate, however, neither with blood fibrinolytic activity estimated by the euglobulin clot lysis time, nor with fibrinogen content and plasma anticlotting activity. It is concluded, that FDP appear in circulation as a result of local proteolytic degradation of intravascularly deposited fibrin without generalized activation of fibrinolysis.

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