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Over-activation of the fibrinolytic system may result in proteolytic destruction of fibrinogen. However, the effect of the degradation products formed during fibrinogenolysis on fibrinolytic process and plasminogen/plasmin properties remains unclear. To investigate this effect and its mechanism, the ability of fibrinogen fragments E and D to act on plasminogen and tPA binding, proenzyme activation, fibrin clot lysis and plasmin inhibition by plasma α2-antiplasmin, were studied. It was found that early product fragment EE binds to plasminogen and tissue-type plasminogen activator and enhances plasminogen conversion into plasmin. C-terminal lysine residues of all 3 chains pair and 16 or 23 amino acid residues of Aα- chain are essential for this process. C-terminal lysines of fragment E Aα- and γ-chains and lysine-binding site of tPA kringle 2 are responsible for the interaction between these proteins. Binding of fragment E to plasminogen is provided by N-terminal Aα1–19 and C-terminal Bβ120–122 regions. Late plasmic fibrinogen degradation product fragment EL loses the ability to potentiate plasmin generation but can bind proenzyme and its activator. Fragment D has no binding properties towards plasminogen and tPA. None of fibrinogen fragments protects plasmin from α2-antiplasmin inhibition. It is concluded that at over-activation of the fibrinolytic system and subsequent fibrinogenolysis, the products of fibrinogen degradation, can bind plasminogen and tPA and potentiate generation of plasmin, which will be neutralized under the normal level of the plasmin inhibitor.
The experiment was performed on 30 cows, including 10 animals infected with the BVD-MD virus. The following parameters were determined: prothrombin time, thrombin time, activated partial thromboplastin time, fibrinogen and D-dimer concentrations, antithrombin III activity, and blood platelet counts. The obtained results indicated that the BVD-MD virus lowered blood platelet counts and led to dysfunctions in plasma coagulation and fibrinolytic systems. The observed changes in the examined haemostatic indicators suggest that BVD-MD infections could lead to the development of disseminated intravascular coagulopathy that has adverse consequences for the animals' health.
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N-methylnicotinamide inhibits arterial thrombosis in hypertensive rats

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There are few findings indicating that nicotinamide may potentially influence intravascular thrombosis. Interestingly, N-methylnicotinamide, one of the metabolites of nicotinamide - could be more potent than its parent compound. In the present study we have investigated the influence of N-methylnicotinamide on arterial thrombosis in normotensive and renovascular hypertensive rats. The contribution of platelets, coagulation and fibrinolytic systems in the mode of N-methylnicotinamide action was also determined. Furthermore, we examined the role of nitric oxide/prostacyclin in the mechanisms of N-methylnicotinamide action. N-methylnicotinamide, but not nicotinamide, administered intravenously into renovascular hypertensive rats developing electrically induced arterial thrombosis caused dose-dependent decrease of thrombus weight, collagen-induced platelet aggregation and plasma antigen/activity of plasminogen activator inhibitor - 1, without changing of occlusion time, routine coagulation parameters and plasma activity of tissue plasminogen activator. Indomethacin - an inhibitor of prostacyclin synthesis, completely abolished the antithrombotic and antiplatelet effect of N-methylnicotinamide, and the plasma level of 6-keto-PGF1alpha, prostacyclin metabolite, increased simultaneously with the inhibition of thrombus formation. Our study shows that N-methylnicotinamide via production/release of prostacyclin inhibits arterial thrombosis development. The antithrombotic effect of N-methylnicotinamide is accompanied by platelet inhibition and enhanced fibrinolysis, due to the decrease production of plasminogen activator inhibitor - 1.
The purpose of the present research is compare the effects of coagulation factors in non-athletes gilrs after exhaustive anaerobic activity sessions in the morning and evening. Present study was semi-emprical that was done on 12 non-athlete female students in range of 18-24 years. Exercise protocol was RAST test, that in which each person passed amain 35 meters of distance for 6 times and rest 10 seconds between each stage. Blood sampling was performed Once in the morning (8 am) and a later week in evening (5 pm) in two stages (before and after). Datas were analyzed with Kolmogorov Smirnov test, Levine's test and two-way ANOVA level (p < 0/05 ). The results showed that there was not significative difference between the effects of an anaerobic activity in the morning and in the evening on hematocrit, platelet, partial time Thromboplastin (PTT), Prothrombin time (PT) and fibrinogen in non-athletic subjects. Findings showed that training for normal persons, non-athletes and patients, especially patients with clotting problems, and cardiovascular disease will be suggeste, each activity to be act with caution at morning and during the day.
The purpose of the present research is compare the effects of coagulation factors in nonathletes gilrs after exhaustive anaerobic activity .Present study was semi-emprical that was done on 12 non-athlete female students in range of 18-24 years. Exercise protocol was RAST test, that in which each person passed amain 35 meters of distance for 6 times and rest 10 seconds between each stage.Blood sampling was performed in two stages (before and after).Datas were analyzed with Kolmogorov Smirnov test, Levine's test and two-way ANOVA level (p < 0/05 ). The results showed that anaerobic exercise had a significant influence on partial time Thromboplastin (PTT), and fibrinogen in non-athletic subjects.But there was not significative difference on Prothrombin time (PT), platelet and hematocrit.Findings suggested that a meeting of anaerobic exercise on blood coagulation factor, effectiveness and changes in some of the invoices for training program Drafradghyrfal is important.
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