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L Bara

Publications and source records attributed to L Bara.

81 records · Page 5Linked to original sources
PubMed1977

[Study of the bleeding mechanism during fibrinolysis induced by streptokinase in the rabbit (author's transl)].

Our aim in this work has been to obtain precisions on the bleeding mechanism during fibrinolysis induced by streptokinase in the rabbit. Haemostasis was studied in vivo by the method oh Honour and Russell. The injection of 40 000 u/kg of streptokinase in 10 minutes induces rapidly fibrinolysis, which lasts for approximately one hour which is not accompanied by changes either in coagulation factors, or in platelet function. In vivo : . the adhesion of platelets to the vascular lesion is normal; . platelet aggregation is normal as is the formation of intravascular thrombi; . on the other hand the intra mural platelet thrombus is unstable. The embolization of the intravascular thrombi is responsible for new hemorrhages which can be correlated with the intensity of fibrinolysis. Thus, even in the absence of fibrinogenolysis, of fibrinogen degradation products FPD, of abnormal thrombin generation and of altered platelet function, the fibrinolytic activity induced by streptokinase could alone be responsible for bleeding episodes, occuring during thrombolytic treatment by streptokinase in man.

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PubMedDate not supplied

Mechanisms for the antithrombotic activity in man of low molecular weight heparins (LMWHs).

Although LMWH have been widely used for several years, the mechanisms of their anti-thrombotic action are not well understood. This is due in part to the misconception that in vitro coagulation results can be extrapolated to the in vivo antithrombotic condition. Thus, the mode of action of heparins on thrombin generation in plasma after addition of increasing amounts of unfractionated heparin (UH) or LMWH has been investigated in several studies, but a distinction has to be made between the effects on the intrinsic and the extrinsic system. The same applies for experiments conducted with platelet-poor plasma (PPP) and platelet-rich plasma (PRP). These experiments show that inhibition of prothrombin activation in PPP is more pronounced in the intrinsic system than in the extrinsic system for both types of heparin. This inhibition has been attributed mainly to their antithrombin activity which reduces factor V and factor VIII activation and its related positive feedback on thrombin formation. The comparison of the effects of low doses of LMWH and UH in citrated PRP indicate that LMWH are more active than UH because they are more resistant to platelet neutralization by platelet factor 4. Moreover, in vitro study will neglect the role of pharmacokinetic parameters which are important determinants of the antithrombotic activity of heparins. Another important difference between in vitro and in vivo studies lies in the fact that sc injection of both heparins will release tissue factor pathway inhibitor (TFPI) in the blood. We have used native whole blood for in vitro and ex vivo experiments. This offers the advantage of studying heparin activity in the presence of platelets and calcium. In this condition the inhibition of pro-thrombin and factor VII activation during blood coagulation in a glass tube (intrinsic system) was judged by measuring residual prothrombin and factor VIIa in serum obtained 2 to 4 hours after clotting. At prophylactic doses, LMWHs in contrast to UH significantly inhibit prothrombin activation. Although thrombin inhibition seems essential for the antithrombotic activity of both heparins, reduction of thrombosis is a global effect to which "both anti-IIa and anti-Xa activity contribute but to a different exent" (C. Hemker et al.). It should be noted that the clearance half-life of anti-Xa activity is significantly longer than that of anti-IIa. The efficacy of a single daily injection of LMWH in the prophylaxis of thrombosis is not logical in light of the short half-life of anti-IIa activity.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMedDate not supplied

[Effect of flurbiprofen on platelet functions. Study of its interference with the synthesis of platelet thromboxane and production of prostacyclin by the rabbit aorta].

The effect of flurbiprofen has been studied on the platelet aggregation of a human platelet rich plasma in the presence of 3 different inducers: ADP, collagen and arachidonic acid. Flurbiprofen is a potent inhibitor of platelet aggregation as compared to aspirin (160 to 2200 more potent). This inhibition was also found using isolated platelets stimulated by arachidonic acid where the suppression of the thromboxane synthesis was accompanied by the inhibition of 14C-serotonin release as well as of aggregation. The administration of flurbiprofen to rabbits, 1 and 3 mg/kg during 3 days was followed by an inhibition of the collagen-induced platelet reactivity. The aortic prostacyclin synthesis as studied by its biological activity was also inhibited at 3 mg/kg (p less than 0,01) but less significantly at 1 mg/kg. The more potent action of flurbiprofen compared to that of aspirin as well as its rapid reversibility would allow the use of this drug for the inhibition of some of the platelet functions.

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