Platelets haemostasis

Haemostasis is the mechanism activated after damage to the blood vessel wall that ensures that blood loss is restricted. Blood platelets are are activated and adhere to elements on the damaged lumenal surface of the vessel, eventually forming a platelet plug that stops the leakage of blood. Fibrinolytic mechanisms later produce lysis of the platelet mass when repair of the vessel has occurred. 

Nemmar, A. et al. (2007) Enhanced peripheral fhrombogenidty after lung inflammation is mediated by platelet-leukocyte activation role of P-selectin. Journal of Thrombosis and Haemostasis,... 

Haemostasis is achieved by the interplay between platelets, proteins within the plasma (the clotting factors) and endothelial cells. The endothelial cells lining the... 

Pathophysiologically, primary haemostatic defects, characteristically due to malfunction of vascular endothelial or platelets, are exemplified by von Willebrand disease and agents such as aspirin and non-steriodal anti-inflammatory drugs (NSAID) where there is a prolonged bleeding time or abnormality in closure using the laboratory equivalent of platelet function analyse the PEA-100. In contrast, secondary bleeding, follows a period of haemostasis... 

Third, there is a need to determine the underlying cause since this may be on an inherited basis described as thrombophilia where all family members need to be investigated. Experience and access to a superior haemostasis laboratory is needed. Defects may extend from hyperhomocysteinaemia through sticky platelet syndrome to mutations of factors V and II or reduced levels of the naturally occurring anticoagulants. Treatments differ and more than one abnormality in what is known as genetic coexpression may co-exist. Correspondence acquired lesions may reflect environmental influences. 

Drugs like salicylates, dipyridamole, phenylbutazone decrease the ability of platelets to aggregate, and thus impairing the haemostasis if warfarin induced bleeding occurs. 

Toxicity associated with NSAID therapy is largely due to inhibition of COX-1, whereas therapeutic benefit derives from inhibition of COX-2. Selective COX-2 inhibitors cause less gastric or renal toxicity than non-selective NSAIDs. Also, because only COX-1 is present in platelets, selective COX-2 inhibitors will have no effect on haemostasis. There is increasing evidence, however, that the physiological and... 

Both e-aminocaproic acid and tranexamic acid may improve haemostasis by a combination of inhibition of fibrinolysis, reduced release of tPA, and preservation of platelet function. Tranexamic acid is more potent and has the same low toxicity as -aminocaproic acid and the latter is now seldom used and is no longer registered for clinical use in many countries. 

Wan, T.C., Zabe, M., Dean, W.L., 2003, Plasma membrane Ca2+-ATPase isoform 4b is phosphorylated on tyrosine 1176 in activated human platelets. Thrombosis and haemostasis 89, 122-131. 

I 5 Matsuo T, Matsuo M, Kario K, et al, Characteristics of heparin-induced platelet aggregates in chronic hemodialysis with long-term heparin use. Haemostasis 2000 30 249-257. 

Michelson AD, Catteneo M, Eikelboom JW, et al. Aspirin resistance position paper of the working group on aspirin resistance, platelet physiology subcommittee of the scientific and standardization committee, International society on thrombosis and haemostasis. J Thromb Haemost 2005 3 1309-131 I. 

Herrmann KS (1983) Platelet aggregation induced in the hamster cheek pouch by a photochemical process with excited fluorescein isothiocyanate-dextran. Micovasc Res 26 238-249 Just M, Tripier D, Seiffge D (1991b) Antithrombotic effects of recombinant hirudin in different animal models. Haemostasis 21 (Suppl l) 80-87 Matsuno H, Uematsu T, Nagashima S, Nakashima M (1991) Photochemically induced thrombosis model in rat femoral artery and evaluation of effects of heparin and tissue-type plasminogen activator with use of this model. J Pharmacol Methods 25 303-317... 

Cook NS, Zerwes H-G, Tapparelli C et al. (1993) Platelet aggregation and fibrinogen binding in human, rhesus monkey, guinea-pig, hamster and rat blood activation by ADP and thrombin receptor peptide and inhibition by glycoprotein Ilb/IIIa antagonists. Thromb Haemostasis 70 531-539... 

Cox D, Motoyama Y, Seki J et al. (1992) Pentamadine a nonpeptide GPIIb/IIIa antagonist - in vitro studies on platelets from humans and other species. Thromb Haemostasis 68 731-736... 

McNicol A, Israels SJ. 1999. Platelet dense granules Structure, function and implications for haemostasis. Thromb Res 95 ... 

Plasma phase (secondary haemostasis - clotting). In which blood clots develop within a minute or two. Traumatised vessels and platelets liberate activating factors, which initiate the clotting process. 

Fox JEB. The platelet cytoskeleton. Thromb Haanost 70 884-893,1993b Fox JEB. Platelet activation New aspects. Haemostasis 26 102-131,1996. 

Whhe JG. Platelet Uhrastructure. In. Haemostasis and Thrombosis, 2nd. ed. Eds AL Bloom DP Thomas. Churhill Livingstone (UK) pp 20-46,1987c. 

Conflicting results have been reported about the absorption of EPA and DHA either as an ethyl ester (EE) or in a triglyceride (TG) formula. Based on a randomized double-blind study on the effects of EE and TG on plasma fatty acids, platelet function and haemostasis, it has been concluded that TG and EE fish oils are well incorporated... 

Nurdoi AT Platelet membrane glycoproteins and their clinical aspects. Thromb Haemostasis 6-29, 1987. 

Ruggeri ZM Mechanisms initiating platelet thrombus formation. Thromb Haemostasis 78 611-616, 1997. 

Ordinas A, Diaz-Ricart M, Bastida E, Escolar G, Castillo R, Tandon NN, Jamieson GA The role of subendothelial laminin and platelet laminin receptors in haemostasis. Nouvelle Revue Francaise D Hematologie 34 61-65,1992. 

Menard M, Meyers KM, Prieur DJ. Primary and secondary lysosomes in megakaryocytes and platelets of cattle with the Chediak-Higashi syndrome. Throm Haemostasis 1990 64 156-160... 

Sinakos Z, Cam JP. Platelet aggregation in mammalians (human, rat, rabbit, guinea-pig, horse, dog) a comparative study. Thrombosis and Haemostasis 1967 17 99-111... 

Platelets support haemostasis in three ways first by sticking to exposed collagen to form a physical barrier at the site of vessel injury second by accelerating the activation of coagulation proteins and finally by release of storage granule contents promotes vasoconstriction and wound healing. 

By means of the complex process of haemostasis, the organism seeks to protect itself spontaneously against bleeding and the corresponding loss of blood. Three components are available to this end (J.) blood vessels themselves (= vascular haemostasis), (2.) platelets and endothelial cells (= cellular haemostasis), and (J.) blood-clotting factors (= plasmic blood coagulation). 

Vinazzer H. Clinical and experimental studies on the action of ethamsylate on haemostasis and on platelet functions. Thromb Res 1980 19(6) 783-91. 

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