Blood platelet activation

Bodin S, Tronchere H, Payrastre B. 2003. Lipid rafts are critical membrane domains in blood platelet activation processes. Biochim Biophys Acta 1610 247-257. 

Ginkgo. Because this herb can inhibit blood platelet activity, it should be used cautiously with blood-thinning drugs such as warfarin, heparin, or even aspirin. 

Blood)platelet activating/actor a physiologically active ether lipid (alkoxylipid) that was first isolated from blood leukocytes. PAF is formed in many animal tissues as the result of an external stimulus and has the character of a hormone (so-called mediator). The chemical structure of PAF was elucidated in 1979 as a mixture of l-0-alkyl-2-0-acetyl-sn-glycero-3-phos-phocholines. PAF effects the aggregation of blood... 

Holub, B.J. (1991) Effect of dietary omega-3-fatty acids on blood platelet activity, in Health Effects of Dietary Batty Acids (ed. G.J. Nelson), American Oil Chemists Society, pp. 122-128. 

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

The formation of a platelet aggregate requires the recruitment of additional platelets from the blood stream to the injured vessel wall. This process is executed through a variety of diffusible mediators which act through G-protein-coupled receptors. The main mediators involved in this process are adenosine diphosphate (ADP), thromboxane A2 (TXA2), and thrombin (factor Ila). These mediators of the second phase of platelet activation are formed in different ways. While ADP is secreted from platelets by exocytosis, the release of TXA2 follows its new formation in activated platelets. Thrombin can be formed on the surface of activated platelets (see Fig. 2). 

Collagen is a major component of connective tissue that becomes exposed at the subendothelium of injured blood vessels. It contributes to platelet adhesion and also plays a role in platelet activation by binding to several receptors on platelets such as integrin a 2(3 1 or glycoprotein VI (GP VI). 

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. 

Enterochromaffin cells are interspersed with mucosal cells mainly in the stomach and small intestine. In the blood, serotonin is present at high concentrations in platelets, which take up serotonin from the plasma by an active transport process. Serotonin is released on platelet activation. In the central nervous system, serotonin serves as a transmitter. The main serotonin-containing neurons are those clustered in form of the Raphe nuclei. Serotonin exerts its biological effects through the activation of specific receptors. Most of them are G-protein coupled receptors (GPCRs) and belong to the 5-HTr, 5-HT2-, 5-HT4-, 5-HTs-, 5-HT6-, 5-HT7-receptor subfamilies. The 5-HT3-receptor is a ligand-operated ion channel. 

Blood platelets are key players in the blood-clotting mechanism. These tiny fragments of cytoplasm are shed into the circulation from the surface of megakaryocytes located in the bone marrow. When the lining of a blood vessel is injured, activated platelets release clotting factors, adhere to each other and to damaged surfaces, and send out numerous filopodia. The shape changes that occur in activated platelets are the result of actin polymerization. Before activation, there are no microfilaments because profilin binds to G-actin and prevents its polymerization. After activation, profilin dissociates from G-actin, and bundles and networks of F-actin filaments rapidly appear within the platelet. 

Kroll MH, Schafer Al Biochemical mechanisms of platelet activation. Blood 1989 74 1181. 

Platelet-activating factor A mediator of platelet aggregation and inflammation that is produced in response to stimuli, such as white blood cells. 

Schafer A, Schulz C, Eigenthaler M, et al. Novel role of the membrane-bound chemokine fractalkine in platelet activation and adhesion. Blood 2004 103(2) 407—412. 

Many of the coagulation factors measured by global coagulation tests have limited stability, and the time and temperature of storage of sample will affect their measurements. Concepts of analyte stability and half-life in plasma extend to markers measured by immunoassay. Markers of platelet activation are affected by artifactual activation in vitro upon collection of the blood specimen. This section will highlight some of the nonanalytical variables that, if uncontrolled, can lead to spurious results and thus affect the interpretation of laboratory data. 

Various additive mixtures have been proposed for inclusion in blood collection tubes to prevent in vitro platelet activation. One formulation involves the use of a mixture of acid-citrate-dextrose (ACD, 1 5 dilution), 30 p-M acetylsalicylic acid... 

In vitro platelet activation is dependent on the anticoagulant that is used for blood collection. In one study it was demonstrated that PF4 levels in platelet-poor plasma isolated after incubation without any stimuli for 1 hour at 37°C were as follows conventional heparin, 1180 ng/ml hirudin, 469 ng/ml citrate, 440 ng/ml and EDTA, 217 ng/ml (110). EDTA appears to suppress platelet degranulation. PF4 levels obtained with a low-molecular-weight heparin preparation called Frag-min were, however, comparable to those obtained with hirudin (110). 

Kuhne T., Homstein A., Semple J., et al. Flow cytometric evaluation of platelet activation in blood collected into EDTA vs. Diatube-H, a sodium citrate solution supplemented with theophylline, adenosine and dipyridamole. Am J Hematol 1995 50,40-5. 

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