Blood Coagulation after Long Distance Running: Antithrombin III Prevents Fibrin Formation

1990 ◽  
Vol 63 (03) ◽  
pp. 430-434 ◽  
Author(s):  
Peter Bärtsch ◽  
André Haeberli ◽  
P Werner Straub

SummaryPhysical exercise causes shortening of activated partial thromboplastin time (aPTT) and euglobulin clot lysis time. To investigate whether this activation of coagulation and fibrinolysis leads to in vivo thrombin or plasmin action after long distance running, 19 well trained male runners (36-65 years) were examined 5 to 53 min after termination of a 100 km race and 5 days later after at least 1 day without physical exercise. Compared to the control examination aPTT was decreased (30.2 ± 2.8 vs 35.3 ± 3.0 sec) and the following parameters were increased after the race: betathromboglobulin (40 ± 16 vs 23 ± 7 ng/ml), thrombin-antithrombin III (TAT) complexes (5.5 ± 3.4 vs 2.3 ± 0.7 pg/1), the fibrin(ogen) degradation products fragment E (57 ± 15 vs 35 ± 7 ng/ml) and B(3 15-42 (8.5 ± 2.5 vs 6.5 ± 2.5 ng/ml) (all p values <0.001). Platelet count, platelet factor 4, fibrinoepetide A (FPA) and haematocrit did not change significantly. Increased TAT complexes and unchanged FPA suggest that the generated thrombin was fully inactivated by antithrombin III (AT III) and did therefore not give rise to fibrin formation. The small increase of fibrin(ogen) degradation products indicates a minor in vivo activity of the fibrinolytic system. This investigation demonstrates the importance of AT III in the regulation of haemostasis in activated blood coagulation.

1987 ◽  
Author(s):  
P Bartsch ◽  
A Haeberli ◽  
P W Straub

Physical exercise leads to a shortening of activated partial thrcnboplastin time (PIT) and euglobulin lysis time (ELT). Whether this activation causes in-vivo thrombin and plasmin action remains controversial however. 19 well trained long distance runners were examined 25 min (range 5-53) after termination of a 100 km race (post-race values) run in 577 min (457-755) and 5 days later after at least one day without physical exercise (control values). FPA, platelet factors and fibrin (ogen) split products (fragment E and BB 15-42) were measured with radioimnunoassays. ELT was assessed before and after venous occlusion (VO). The table gives mean values ±SD:Thrombin time, platelet count, platelet factor 4 and haematocrit did not change significantly. FPA was normal in all post-race samples and did not correlate significantly with the time lag between arrival and blood sampling, indicating that activation of blood coagulation in exhaustive physical exercise of long duration does not lead to in-vivo fibrin formation. Activation of fibrinolysis, however, results in circulating plasmin activity as demonstrated by the elevation of the fibrin (ogen) degradation products fragment E and BB 15-42. Since the polyclonal antibodies used in the latter assay crossreact with BB 1-42, these results alone do not allow to jjdge whether plasmin degrades fibrin or fibrinogen. However, lack of fibrin formation suggests fibrinogenolysis rather than fibrinolysis.


1975 ◽  
Author(s):  
I. Rákóczi ◽  
B. Garadnay ◽  
L. Arnold ◽  
I. Gáti

It is known that antithrombin III (AT III) is the main inhibitor of blood coagulation. It inactivates thrombin and activated × factor. Heparin increases the AT III activity in vitro as well as in vivo. The authors have studied the AT III activity in sera of 30 pregnant women, at term, before labour started (2–24 hrs) and 30 as well as 60 min after the birth of placenta and daily for five days after delivery. The AT III activity was determined using the modified method of Gerendas. Out of the 30 women 15 were given 5000 IU heparin subcutaneously 1½—2 hours before delivery. In the 15 women with no heparin treatment AT III activity of serum significantly decreased after birth of placenta compared with the predelivery value and became normal on the fifth postpartum day. Heparin given subcutaneously prevented development of this decrease.


1982 ◽  
Vol 48 (02) ◽  
pp. 166-168 ◽  
Author(s):  
F Violi ◽  
C Alessandri ◽  
S Frattaroli ◽  
A Ghiselli ◽  
F Balsano

SummaryA double blind study was performed on 20 atherosclerotic patients. A placebo was administered to one group of 10 patients (group A) and ticlopidine (500 mg/day) was administered to another group of 10 patients (group B) for one month. ADP and collagen-induced platelet aggregation (PA), platelet malondial-deyde (MDA) produced by thrombin stimulation and plasma beta-thromboglobulin (βTG) levels, prothrombin time, activated partial thromboplastin time (APTT) fibrinogen, antithrombin (AT) III, fibrin(ogen) degradation products, alpha2-antiplasmin and plasminogen were evaluated in both groups before and after treatment. No changes in PA, MDA and βTG were seen in group A. Group B showed a significant decrease of PA, βTG and a significant increase of MDA. No changes on blood coagulation data were seen in either group. This study suggests that ticlopidine is able to inhibit platelet function in vivo.


1981 ◽  
Author(s):  
A Stemberger ◽  
F Straßer ◽  
G Blüimel ◽  
B v Hundel shausen ◽  
S Jelen ◽  
...  

Blood coagulation and fibrinolysis was carefully monitored in patients suffering from traumatic-haemorrhagic shock. Parameters like antithrombin III (AT III),factor X (IIa), plasminogen,fibrin degradation products, antiplasmin and fibronectin were measured. It could be demonstrated that a severe haemorrhagic shock correlated with an activated blood coagulation and stabilisation of circulation was followed by normalisation of blood coagulation.However in patients developping septic complications new disorders in blood coagulation were observed. The appearance of endotoxins was measured by a recently developped limulus amoebocyte lysate (LAL). Best results were obtained by diluting heat treated heparinized plasma samples followed by an incubation step with the X a substrate S-2222. Detection of less than 0.2 ng endotoxin/ml plasma could be achieved. The available data of 30 patients with traumatic-haemorrhagic and bacteriotoxic shock showed that the appearance of endotoxin mostly correlated with a decrease of AT III and fibronectin.In conclusion, AT III, fibronectin and endotoxin may serve as sensitive markers in the early diagnosis of sepsis.


Critical Care ◽  
2008 ◽  
Vol 12 (Suppl 2) ◽  
pp. P209
Author(s):  
A Hanke ◽  
A Staib ◽  
K Görlinger ◽  
M Perrey ◽  
D Dirkmann ◽  
...  

1984 ◽  
Vol 51 (02) ◽  
pp. 232-235 ◽  
Author(s):  
D C Triantaphyllopoulos

SummaryTwenty-one rabbits were infused with 20μg/kg/hr of E. coli endotoxin for 6 hr. Eight of the animals were preinjected immediately before the infusion of endotoxin, with a bolus dose of human AT III calculated to increase the antithrombin content of the plasma by about 4 units/ml. All eight animals which were preinjected with AT III survived, while 5 of the 13 control rabbits infused with endotoxin alone died. The changes in coagulation parameters from the baseline values, between the 8 control rabbits which survived and the 8 animals which were preinjected with AT III were compared. The concentration of the preinjected human AT III declined significantly faster (P: <0.01) than that of the native rabbit AT III. AT III prevented the decline of F.XII throughout the infusion of the endotoxin. However, the decline in F.V, fibrinogen, prothrombin and platelets was not affected (P: >0.5) by the injection of AT III.


Author(s):  
Stein Gerrit Paul Menting ◽  
Brian Hanley ◽  
Marije Titia Elferink-Gemser ◽  
Florentina Johanna Hettinga

1985 ◽  
Vol 53 (4) ◽  
pp. 371-373
Author(s):  
J. Strnad

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