Mechanism, platelet adhesion

Ruggeri ZM, Mendolicchio GL. 2007. Adhesion mechanisms in platelet function. Circ Res 100 1673-1685. 

Kim, et al., ( ) have utilized radioiodinated (I proteins to measure adsorption of individual proteins and protein mixtures on LTI carbon surfaces. Their results indicate a very rapid adsorption of albumin onto the LTI carbon surface, consistent with Kim s model of blood interactions via a platelet-adhesion mechanism (.8). Microcalorimetric and electrophoretic mobility studies of protein adsorption on LTI carbon surfaces have been done by Chiu, et al., ( 5). The extension of the adsorbed protein layers have been directly measured by Fenstermaker, et al., ( ) and Stromberg et al., 7) at NBS using ellipsometric methods. 

Several investigators have found that foreign surfaces, when exposed to blood, adsorb plasma proteins (21, 22). Platelet adhesion to this proteinated surface is the first observable event in thrombosis on the foreign surface. If we consider the proteinated surface as an acceptor in a platelet adhesion mechanism (23), the significance of the nature and composition of adsorbed protein is its role in platelet adhesion (24). 

Bleeding from injured blood vessels can be arrested by the activation of the hemostatic mechanism [24]. However, an artificial device surface placed in contact with blood can disturb the balance of this mechanism [24]. Excessive blood clotting with increased risk of embolization can occur due to the adhesion of platelets and lenkocytes to device surface and the formation of fibrin network following the... 

Bennett JS Mechanisms of platelet adhesion and aggregation an update. Hosp Pract (Off Ed) 1992 27 124. 

Dudek AZ, Nesmelova I, Mayo K, Verfaillie CM, Pitchford S, Slungaard A. Platelet factor 4 promotes adhesion of hematopoietic progenitor cells and binds IL-8 novel mechanisms for modulation of hematopoiesis. Blood 2003 101(12) 4687-4694. 

Fig. 9.1. A dysfunctional or injured endothelium is at the basis for initiation of and progression to atherosclerosis. Several mechanisms, such as adhesion molecules or liberation of von Willebrand factor (vWf, upper panel), determine a series of phenomena, including platelet activation and aggregation. This participation of platelets involves the implication of molecules like glycoprotein Ilb/IIIa, fibrinogen, and von Willebrand factor. The endothelium also acts as a source of signals that regulate local functions, including VSMCs (lower panel). A list of the most relevant messengers produced by a functional and a dysfunctonal endothelium is presented in the lower panel...

DETA/NO is a stable NO-donor with the longest NO generation half-life of approximately 20 h. Thrombelastography performed on rabbit blood showed that DETA NONOate-derived NO significantly decreased coagulation activity and platelet activation [48]. Monitoring by intravital microscopy showed that DETA/NO attenuated the platelets/endothelial cells adhesion response to endotoxins (e.g. lipopolysaccharides) in murine intestinal venules [49]. The main mechanism of the antiadhesive action of DETA/NO on platelets was activation of soluble guanylate cyclase [49]. 

Besides cholesterol efflux from arterial wall and its role in RCT, additional properties of HDL have been proposed for its protective anti-atherogenic activities. HDL protects vascular function by a number of potential alternative mechanisms, including inhibition of LDL oxidation [8,9], platelet aggregation and coagulation [10], and endothelial monocyte adhesion [11], as well as promotion of endothelial nitric oxide synthase (eNOS) [12], and prostacyclin synthesis [13-15]. The proposed alternate protective mechanisms for HDL are attractive but many of them lack validation under in vivo conditions. 

Mickelson JK, Lakkis NM, VillarrealLevy G, Hughes BJ, Smith CW. Leukocyte activation with platelet adhesion after coronary angioplasty a mechanism for recurrent disease. J Am Coll Cardiol 1996 28 345-353. 

Dipyridamole is a platelet adhesion inhibitor, although the mechanism of action has not been fully elucidated. The mechanism may relate to 1) Inhibition of red blood cell uptake of adenosine, itself an inhibitor of platelet reactivity, 2) phosphodiesterase inhibition leading to increased cyclic-3 , 5 -adenosine monophosphate within platelets and, 3) inhibition of thromboxane A2 formation,... 

Therapeutic irradiation is known to have multiple interactions with the vasculature of the irradiated tissue (12). Radiation has direct cytotoxic effects on the vascular endothelium, likely due to induction of oxidative injury. Radiation-induced injury stimulates inflammation and influx of inflammatory cells in addition to creating aprocoagulant state in the vascular space by the transcriptional induction of tissue factor with the subsequent activation of coagulation factors as well as von Willebrand factor and platelets. Experimental evidence suggests that the mechanism by which radiation initiates these responses is in part through the induction of cell-adhesion molecules including ICAM-1, E-selectin, and P-selectin and in part through local cytokine production and release (13). 

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