| Popis: |
Epidemiological studies have demonstrated an inverse correlation between moderate wine and alcohol consumption and morbidity and mortality from coronary heart disease (CHD). This protective effect has been associated with an increase in the plasma level of high density lipoprotein (HDL)-cholesterol, as it is well known that plasma HDL is inversely correlated with CHD. In addition, it has become evident that blood platelets contribute to the rate of development of atherosclerosis and CHD through several mechanisms. Recent studies have shown HDL-cholesterol levels can explain only 50% of the protective effect of alcoholic beverages. The other 50% may be partly related to decreased platelet activity. The antiplatelet activity of wine is explained not only by ethanol but also by the polyphenolic components with which red wines are richly endowed. Several studies carried out in humans and animals have shown that wine phenolics could exert their effects by reducing prostanoid synthesis from arachidonate. In addition, it has been suggested that wine phenolics could reduce platelet activity mediated by nitric oxide. Moreover, wine phenolics increase vitamin E levels while decreasing the oxidation of platelets submitted to oxidative stress. However, a rebound phenomenon of hyperaggregability is observed after acute alcohol consumption but not after wine consumption. This protection afforded by wine has been duplicated in animals with grape phenolics added to alcohol. This rebound phenomenon could explain ischemic strokes or sudden deaths known to occur after episodes of drunkenness. It appears that wine and wine phenolics in particular could significantly inhibit platelet aggregation and that this could explain, at least in part, the protective effect of red wine against atherosclerosis and coronary heart disease. |
