Eicosanoid platelet effects

Srivastava KC. (1986). Isolation and effects of some ginger components of platelet aggregation and eicosanoid biosynthesis. Prostaglandins Leukot Med. 25(2-3) 187-98. 

ZO053 Srivastava, K. C. Isolation and effect of some ginger component of platelet aggregation and eicosanoid biosynthe- ZO065 sis. Prostaglandins Leukot Med 1986 ... 

Resveratrol has also been reported to offer protection against cardiovascular disease, such as coronary heart disease. The effects of resveratrol on factors implicated in the development of coronary heart disease - human platelet aggregation and the synthesis of eicosanoids (lipids) from arachidonate by platelets - were investigated and compared with the actions of other wine phenolics - catechin (1.39), epicatechin (7.18a), and quercetin (1.43) - and the antioxidants a-tocopherol (7.10a), hydroquinone and butylated hydroxytoluene. Resveratrol and quercetin demonstrated a dose-dependent inhibition of platelet aggregation, whereas the other compounds tested were inactive. Resveratrol also inhibited the synthesis of the eicosanoids in a dose-dependent manner, whereas the other phenolics were less effective of not effective at all. Removal of the alcohol from the wine did not diminish the effect on platelet aggregation (Pace-Asciak et al., 1995 Goldberg et al., 1995). 

Some, but not all, of the pharmacological effects of eicosanoids are mediated through alterations in the concentration of cyclic adenosine monophosphate (cyclic AMP). For example, prostaglandins Ej and E2 inhibit platelet aggregation by increasing the cyclic AMP concentration. Conversely,... 

The effects of onion and garlic on eicosanoid metabolism have mainly been studied by observing the effects of garlic and onion preparations on platelet aggregation and subsequent eicosanoid synthesis. 

Figure 12.10. Role of eicosanoids in thrombocyte (platelet) aggregation, and rationale of low-dose acetylsalicylic acid treatment. a Thrombocyte aggregation is suppressed by the intact vascular endothelium by a constant secretion of PGE and PGI. b Inhibition subsides at lesions. This sets off aggregation, which is sustained and amplified by the secretion of thromboxanes by the platelets themselves. Aggregation will also promote plasmatic coagulation (i.e., fibrin clot formation), b Effects of low dose application of acetylsalicylic acid. Endothelial cells are nucleated covalently inactivated cyclooxygenase molecules will be replaced by newly synthesized ones, so that the activity is not substantially diminished. In contrast, thrombocytes lack protein synthesis, so that the effect of repeated doses will be cumulative.

Each eicosanoid is associated with specific types of biological activity (Table 29.4). In some cases, the effects oppose one another. For example, thromboxanes are vasoconstrictors that trigger blood platelet aggregation, whereas prostacyclins are vasodilators that inhibit platelet aggregation. The levels of these two eicosanoids must be in the right balance for cells to function properly. 

Ricinoleic Acid Ricinoleic acid (RA) can increase mucosal permeability and cause cytotoxicity. It is also associated with the release of eicosanoids, a platelet-activating factor, and nitric oxide (NO). RA disrupts normal intestinal motility and a combination of these effects accounts for the laxative action of RA (167). Consistent with these findings, RA will increase nitric oxide synthatase activity in the rat ileum and colon (168), which likely accounts for the involvement... 

On the other hand, Mutanen et al. (128) found that canola oil and sunflower oil enhanced in vitro platelet aggregation. Similarly, McDonald et al. (113) found that both canola oil and sunflower oil increased prostacyclin production (an antiaggregating eicosanoid) and decreased thromboxane production (a proaggregating eicosanoid). Although the effect of canola oil on platelet activity and clot formation is not as well established as its favorable effect on plasma cholesterol and lipoprotein levels, there is evidence that it may impede clot formation. 

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