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Effects of Antithrombotic and Results of Drug Screening
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
The term “activation” is not very clearly defined. Does activation exist in advance of adhesion, or is it only its consequence? Logically, low degree activation might result in an increased reactivity to stimuli, but on the contrary a high degree might bring about a refractory state. ASA was generally considered as a drug effective on processes taking place later on in the process of thrombogenesis, i.e., on aggregation and release. This is based on its lack of effect on platelet survival and on the systemic release of some platelet constituents (beta-thromboglobulin, PF 4). On the other hand, some studies suggest that ASA might also influence some parameters usually serving as indicators of activation such as shape change. In the study of Simrock et al.13 single doses of 7 to 15 mg/kg were necessary in man to attain this effect lasting about 8 to 12 h.
Disorders in tHemostasis System and Changes in the Rheological Properties of the Blood in Ischemic Heart Disease and Diabetes Mellitus Patients
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
We determined a growth in the content of beta-thromboglobulin up to 38.7 ng/ml (in healthy persons 29.2 ng/ml) and the activity of the thrombocyte factor IV to 18.9 s (up to 14.9 s in healthy persons). Beta-thromboglobulin and thrombocyte factor IV are released from the alpha granules of the thrombocytes and are markers of the reaction of freeing of the thrombocytes. A growth in their content in IHD indicates intravascular activity of the thrombocytes and an increase in the reaction of their freeing.
Disseminated Intravascular Coagulation
Published in Rodger L. Bick, Disseminated Intravascular Coagulation and Related Syndromes, 2019
Increased platelet turnover and decreased survival will usually be seen in patients with disseminated intravascular coagulation;253, 254 however, since thrombocytopenia is often present this method of following patients may be of questionable significance especially in the severely thrombocytopenic patient. However, it has been found that simple methods using COULTER®* electronic counting techniques have proven highly successful in monitoring efficacy of therapy in the patient with acute or chronic DIC provided the platelet count is greater than 80,000/cmm.255 Platelet factor 4 levels and beta-thromboglobulin levels are newer assay techniques that are markers of overall platelet reactivity and release. As such, several recent reports have suggested that either of these modalities may be highly useful in aiding in the diagnosis of disseminated intravascular coagulation as well as in monitoring efficacy of therapy with respect to blunting or causing cessation of the intravascular clotting process.256–260 Both assays are now readily available for the clinical laboratory and each has its attendant advantages and disadvantages. Both platelet factor 4 and beta-thromboglobulin are elevated in the vast majority of instances of disseminated intravascular coagulation. However, it should be readily appreciated that neither of these modalities are diagnostic of DIC as they may be elevated in a wide variety of intravascular coagulation disorders including pulmonary emboli, acute myocardial infarction, deep venous thrombosis, and in many disorders associated with microvascular disease such as diabetes and autoimmune disorders.261, 262
Platelets after burn injury – hemostasis and beyond
Published in Platelets, 2022
B. Z. Johnson, A. W. Stevenson, L. W. Barrett, M. W Fear, F. M. Wood, M. D. Linden
Ex vivo measurement of platelet activation can be performed with a range of tools targeting different aspects of activation. One of the earliest measurements of platelet activation was aggregometry, whereby platelet-rich plasma is exposed to agonists under sheer in order to induce platelet aggregation [45]. The rate and amplitude of aggregation is measured by turbidometry. Platelet-derived thromboxane metabolites, sCD62P (P-selectin), sCD40L and beta-thromboglobulin (β-TG) measured in plasma can provide further evidence of platelet activation in vivo [70–73]. β-TG is released from platelet alpha granules during exocytosis, while CD62P and CD40L are bound to alpha granule membranes which fuse with platelet surface membrane during granule exocytosis, before they are cleaved and released from the platelet surface as soluble proteins. CD63 is similarly associated with the membrane of platelet dense granules, and expression is increased with activation-dependent granule exocytosis [74].
Neurological complications associated with left ventricular assist device therapy
Published in Expert Review of Cardiovascular Therapy, 2018
Kevin Goodwin, Austin Kluis, Tamas Alexy, Ranjit John, Rochus Voeller
It is probable that platelet activation and damage is also caused by the excessive shear forces of the CF-LVAD which may increase the risk of stroke. Induction of platelet activation by mechanical trauma results in the characteristic enhancement in aggregation and adherence to exogenous surfaces. The markers of platelet damage and activation, platelet factor 4 (PF4) and beta-Thromboglobulin (Beta-TG), have been shown to be elevated in CF-LVAD patients and may play a role in the development of thromboembolic events. Furthermore, it has been demonstrated that platelets exposed to high shear forces by CF-LVADs are hyporesponsive to aspirin, which could potentiate clotting. However, a significant association has not yet been found between decreased platelet responsiveness to aspirin and thromboembolic events [19].
Platelet function in disseminated intravascular coagulation: A systematic review
Published in Platelets, 2018
Mathies Appel Laursen, Julie Brogaard Larsen, Anne-Mette Hvas
Levels of beta-thromboglobulin is a potent platelet activation marker, but any renal impairment must be taken into account as beta-thromboglobulin is catabolized in the kidneys, and levels may therefore be falsely elevated (35,38). Renal impairment is common in DIC due to fibrin deposition in the small vessels of the kidney (39). This could explain the significantly higher levels of beta-thromboglobulin in one study of cancer patients developing DIC, which also found a significant correlation between plasma creatinine and beta-thromboglobulin levels (27). Remarkably, Stefanidis et al. still found significantly higher beta-thromboglobulin levels in DIC than in non-DIC when adjusting for serum-creatinine (35). In addition, beta-thromboglobulin levels rise quickly during systemic inflammation (40). The results of the included studies indicate that the beta-thromboglobulin level is a potential marker for DIC (27,35).