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Platelet adhesion, inhibition

Vascular Tone Immune Surveillance Cellular Adhesion Vascular Permeability Neurotransm ission Bronchodilation Platelet Adhesion Inhibition Renal Function Antioxidant Leukocyte Adhesion Inhibition Protection Against TNF Toxicity Enzyme Function Inhibition DNA Damage Induction Lipid Peroxidation Induction Increased Susceptibility to Radiation Alkylating Agents Toxic Metals Antioxidant Stores Depletion... [Pg.352]

Degrades ADP (an aggregating agent of platelets) to AMP -t P Inhibits platelet adhesion and aggregation by elevating levels of cGMP... [Pg.607]

Decorsin 4 400 Macrobdella decora Inhibits platelet adhesion... [Pg.342]

The important in vivo role of platelet cGMP-PK I for the inhibition of platelet adhesion to vascular endothelium has been further demonstrated by recent studies... [Pg.236]

SNVP is a lipophilic N-substituted valeryl analog of SNAP. It caused prolonged nitric oxide mediated vasodilatation in rats [70, 71]. In vivo, SNVP prevented the hyper-aggregability of circulating platelets caused by angioplasty of rabbit carotid arteries. Here, only minor effects on blood pressure were observed, whereas platelet adhesion was strongly inhibited [71]. [Pg.243]

Cyclo(Met-Tyr) and cyclo(Met-Trp) produced a marked inhibitory effect toward platelet adhesion induced by both ADP and thrombin. A moderate cytotoxic effect was displayed by cyclo(Met-Trp) against HeLa (55.85% inhibition), HT-29 (39.80% inhibition), and MCF-7 cancer cells (54.96% inhibition) whereas... [Pg.685]

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,... [Pg.95]

Abciximab is a Fab fragment of a murine-human monoclonal antibody that binds to the integrin GPIIb/IIIa receptor on activated platelets and inhibits fibrinogen, von Willebrand factor, and other adhesion molecules from binding to activated platelets, thus preventing their aggregation. See Chapter 34 for additional details. [Pg.1200]

Chronic diseases such as atherosclerosis are also propagated by oxidative stress (73). The sequence of events leading to arterial occlusion is complex and not fully understood. However, both platelet adhesion and macrophage activation participate in the formation of atherosclerotic plaques in the environment of elevated serum cholesterol (74). Oxidative chemistry can profoundly affect several steps in the formation of atheroma (75), including recruitment of immune cells such as macrophages, and as during ischemia-reperfusion, the antioxidant nature of NO can inhibit this process (76). [Pg.356]

Inhibitor of platelet vWF receptors Inhibits the link of vWF with their platelet receptor GPIb inhibiting platelet adhesion... [Pg.39]

Collagen-GPVI inhibitors Inhibit platelet adhesion to subendothelium... [Pg.39]

Cilostazol is a PDE3 inhibitor and also is a drug with multiple mechanisms of action (23,24), some of which are directly platelet-related, and others of which exert their effects indirectly via endothelial cells (Figs, 4 and 5), As a PDE inhibitor, it increases the concentration of cyclic nucleotides within platelets and inhibits platelet aggregation in response to shear forces (via ADP) and a variety of agonists. Like other inhibitors of platelet activation, it blocks the expression and release of P-selectin, a key adhesion molecule on the membrane of platelet alpha granules that externalizes with activation, and plays an important role in the interactions between platelets, endothelial cells, and leukocytes, The effect of cilostazol on P-selectin expression appears to be additive to those of aspirin and clopidogrel (25). [Pg.72]

Blood-compatible polymer materials are required to inhibit both platelet adhesion and coagulation just as the endothelial on the polymer surface. It is known that there are many investigations in the design and the synthesis of socalled antithrombogenic materials. The immobilization of biologically active substances such as heparin [74, 75], urokinase [76], and prostaglandins [77-81] is one of the practical approaches. [Pg.137]


See other pages where Platelet adhesion, inhibition is mentioned: [Pg.857]    [Pg.145]    [Pg.73]    [Pg.342]    [Pg.25]    [Pg.163]    [Pg.238]    [Pg.239]    [Pg.242]    [Pg.243]    [Pg.243]    [Pg.247]    [Pg.309]    [Pg.313]    [Pg.181]    [Pg.134]    [Pg.160]    [Pg.685]    [Pg.148]    [Pg.123]    [Pg.239]    [Pg.129]    [Pg.115]    [Pg.123]    [Pg.232]    [Pg.401]    [Pg.1]    [Pg.96]    [Pg.117]    [Pg.127]    [Pg.71]    [Pg.4]    [Pg.38]    [Pg.41]    [Pg.137]   
See also in sourсe #XX -- [ Pg.146 ]




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