Clot Retraction

With very simple equipment, it is possible to observe the inhibition of clot retraction in the presence of the offending drug. However there are limiting factors to the routine application of this procedure. Clot retraction requires the presence of platelets in sufficient numbers. Frequently, the recovery of a normal platelet level after a reaction takes 5-15 days, a time which might be sufficient to allow the antibodies to disappear. 

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Platelets can be activated by a variety of agents including the physiologic agonists ADP, thromboxane A2, epinephrine, collagen, and thrombin. Platelet activation is generally associated with a change in platelet shape (except for epinephrine-induced platelet activation) from discs to spiny spheres with pseudopodia. Platelet pseudopod formation is dependent on actin polymerization in the activated platelets. The interaction of actin filaments with myosin, mediated by calcium (9), facilitates platelet contractile activity (e.g., clot retraction). 

Studies with transgenic mice lacking the C-terminal Ala-Gly-Asp-Val sequence with recombinant human molecules lacking Ala-Gly-Asp-Val failed to support platelet aggregation but had normal clot retraction (Rooney et al, 1996, 1998). These and other results suggest either that different receptors are responsible for platelet aggregation and clot retraction or the binding sites may be more complex (Remijn et al., 2001). 

Rooney, M. M., Parise, L. V., and Lord, S. T. (1996). Dissecting clot retraction and platelet aggregation. Clot retraction does not require an intact fibrinogen gamma chain C terminus./. Biol. Chem. 271, 8553-8555. 

Blood coagulation Rabbit Oral Coagulation time, clot retraction, prothrombin time... 

The most dramatic illustration of a mass-specific illusion is the comparative heat dissipation of the human erythrocyte and platelet. In mammals, both of these cell types are anucleate and discoid in shape, but the longest dimension of the former is four times that of the latter. Yet heat production of a human erythrocyte was shown to be 10 fW, a sixth that of a human platelet (61 fW see Table 1). The relatively high metabolic activity of platelets is probably due to the need to maintain a considerable phosphagen (phosphocreatine) pool for actomyosin contraction at stimulation and clot retraction. Phosphocreatine is synthesized from creatine using ATP and acts as a demand on the ATP cycle to drive the coupled catabolic half-cycle. On the other hand, ATP requirements of the erythrocyte are relatively small, being mostly confined to active transport of ions at the plasma membrane. 

When blood clots, a plasma protein called fibrinogen is converted to fibrin, which forms a network of threads. Blood cells become enmeshed in this network and form the clot. The clear fluid formed as the clot retracts is the serum. When citrate, heparin, or some other anticoagulant is added to blood to prevent clotting and the cells are removed by centrifugation, the fluid remaining is plasma. Plasma differs from serum in that it contains fibrinogen and certain other coagulation factors not contained in serum. 

Lysis 30, Lysis 60 (Ly30, Ly60) Reduction of amplitude relative to maximum amplitude at 30 and 60 min after time of maximum amplitude. These parameters represent the influence of clot retraction and fibrinolysis. 

Viable, fertile, increased fetal mortality features of Glanzmann thrombasthenia in man, e.g. defective platelet aggregation, clot retraction, spontaneous bleeding, prolonged bleeding times dysfunctional osteoclasts, development of osteosclerosis with age (Hodivala-Dilke et al. 1999 McHugh et al. 2000). 

On the other hand, evidence is accumulating which seems to indicate that fibrin plays a passive role in clot retraction and is simply carried along by actively contracting elements of platelet origin (Discombe, 1950 Bloom, 1955 Sokal, 1960 Castaldi et al., 1962 Rodman et al., 1963). 

Tephorine and Diparcol, both synthetic antihistamines known to inhibit clot retraction (Bounameaux, 1957 Hugues, 1959), only partially inhibit ATPase activity and superprecipitation of thrombosthenin. Finally, monoiodoacetate, a powerful inhibitor of clot retraction, inhibits neither phenomenon. 

The findings reported above may be summarized as follows Inhibitors of the ATPase activity of thrombosthenin always are inhibitors of superprecipitation, whereas they do not necessarily affect manifestations of the contractile activity of the whole platelet, such as clot retraction, to the same extent. 

The second even more striking manifestation of contractile activity is clot retraction. Here again, the major problem consists in explaining how the contractile material can come in contact with the fibrin fibers. In the presence of fibrin, and different from VM in a fibrin-free system. 

The situation may be summarized as follows Most likely, thrombosthenin is the effector of clot retraction activity there remain, however, a series of puzzling observations, which still await explanation. Until then, clot retraction is still as good a playground for speculation as it has been for the past 100 years. 

Budtz-Olsen, 0. E. (1951). Clot Retraction. Blackwell, Oxford. 

Cohen 1. "The mechanism of clot retraction. In Platelet Membrane Glyo(qnoteins, JN George, AT Nurden, DR Phillips, eds. New York Plenum Press, 1985, pp 299-323. 

Rcxxiey MM PariseLV, Lord ST. Dissecting clot retraction and platelet aggr ation. JBiol Chem 1996 271 8553-8555. 

A platelet function disorder, termed thrombasthenia, has been described in a Thoroughbred foal (Miura et al. 1987). The disorder is characterized by bleeding tendencies, absence of clot retraction, and lack of aggregation in response to ADP, collagen, and thrombin. 

Type I Glanzmann s thrombasthenia has been described in a female Great Pyrenees (Boudreaux et al. 1996a). Platelets have minimal aggregation in resporrse to ADP, collagen, thrombin, and PAF, and clot retraction is severely impaired. Surface expression of glycoprotein Ilbllla is markedly reduced. Therefore, this disorder closely resembles human type I Glanzmann s thrombasthenia. 

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