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Animal platelets adhesion

In practice, some anticoagulation agents such as heparin or antiplatelet agents, e.g. nitric oxide (NO) are delivered to sensor sites in order to reduce the risk of thrombus formation. Nitric oxide (NO), which is a potent inhibitor of platelet adhesion and activation as well as a promoter of wound healing in tissue, has been incorporated in various polymer metrics including PVC (poly(vinyl-chloride)), PDMS (poly-dimethyl-siloxane) and PU (poly-urethanes). Those NO release polymers have been tested in animals as outer protection coatings and have shown promising effects for the analytical response characteristics of the sensor devices [137],... [Pg.312]

Dietary intake of n-6 fatty acids such as linoleic acid, and n-3 fatty acids, such as the fish oils eicosapentanoic acid and docosahexaenoic acid, lowers plasma cholesterol and antagonizes platelet activation, but the fish oils are much more potent in this regard [26]. In particular, n-3 fatty acids competitively inhibit thromboxane synthesis in platelets but not prostacyclin synthesis in endothelial cells. These fatty acids have also been shown to have other potentially anti-atherogenic effects, such as inhibition of monocyte cytokine synthesis, smooth muscle cell proliferation, and monocyte adhesion to endothelial cells. While dietary intake of n-3 fatty acid-rich fish oils appears to be atheroprotective, human and animal dietary studies with the n-6 fatty acid linoleic acid have yielded conflicting results in terms of effects on both plasma lipoproteins and atherosclerosis. Indeed, excess amounts of both n-3 and n-6 fatty acids may actually promote oxidation, inflammation, and possibly atherogenesis (M. Toberek, 1998). In this context, enzymatic and non-enzymatic oxidation of linoleic acid in the sn-2 position of LDL phospholipids to 9- and 13-hydroxy derivatives is a key event in LDL oxidation (Section 6.2). [Pg.596]

While EETs regulate ischemic damage in animal models of ischemia-reperfusion, they may also help resolve thrombotic blockage of arteries in vivo. EETs prevent platelet aggregation independent of effects on TXA2 biosynthesis [97, 212], EETs induce membrane hyperpolarization and reduce Ca entry into platelets to inhibit platelet activation, cytoskeletal rearrangement, aggregation, and adhesion to endothehal cells [214,215],... [Pg.892]

The effects of oral L-arginine on vascular health and disease have been examined both in human beings and various animal models. In a recent review, Preli et al. (2002) summarized the results of oral l-arginine supplementation on athersclerotic lesion formation, as well as markers of endothelial function (e.g. macrophage function, platelet aggregation and adhesion, and in vitro vascular ring studies). [Pg.687]

The embolic agents most commonly used for splenic ablation are Gelfoam pledgets and polyvinyl alcohol particles. Yoshioka et al. [105] also showed excellent increases in platelet counts when coils were placed within the intrasplenic branches, and Hickman et al. [108] successfully used Gel-foam, polyvinyl alcohol particles, and coils alone or in combination for preoperative embolization. In animal studies, additional materials that have been used for this purpose are absolute ethanol [121,122], microfibrillar collagen [123], tissue adhesives [124], balloon catheters [125], silicone particles [126], and... [Pg.214]

Implantation of a polymer device into a vessel or tissue causes a complex inflammatory response inducing adhesive interactions between vascular cells (blood and tissue cells). During stenting, the endothelial layer is partially or completely destroyed. In animal experiments of vascular injury, denudation of endothelial cells results in platelet deposition followed by neointima formation [188-190]. In addition, complete coverage of endothelial cells is associated with attenuation or even stop of the growth of neointima from smooth... [Pg.455]


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See also in sourсe #XX -- [ Pg.382 , Pg.383 , Pg.387 , Pg.388 , Pg.389 ]




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