Ethanol Inhibition of Thrombus Formation on Collagen-Coated Glass

Abstract

SummaryEpi-fluorescent video microscopy was used to evaluate the effect of ethanol on platelet mural thrombus formation. Whole blood, treated with ethanol, was perfused over collagen coated glass in a parallel-plate flow chamber at a shear rate of 1,000/s. Digital image processing and photodiode measurements were used to analyze the dynamics of thrombus growth on this surface. Ethanol concentrations as low as 0.02% v/v were found to inhibit 45 + 33% (± S.D.) of normal platelet accumulation on the slide while 0.2% v/v ethanol effected an 82 ± 15% inhibition of mural thrombus formation. While platelet adhesion to the collagen surface appeared unaffected by ethanol concentrations up to 0.1% v/v, 0.2% v/v ethanol had an effect on adhesion as well as aggregation. These results imply that low ethanol concentrations inhibit the formation of mural thrombi in a model of a damaged blood vessel at physiological shear rates. This inhibition would not be detected in systems which measure bulk aggregation, e.g. in aggregometric determinations.

Rapid Intake of Alcohol (Binge Drinking) Inhibits Platelet Adhesion to Fibrinogen Under Flow

“…Striking, platelet adhesion to collagen was not altered by alcohol intake. This contradicts a previous flow chamber model (Owens et al, 1990), in which adhesion to a collagen surface was inhibited at alcohol concentrations exceeding 1.0%. The blood alcohol concentrations in our test (1.25%) slightly exceeded this level, but we did not observe decreased adhesion.…”

Relationships between alcoholic beverages and cardiovascular risk factor levels in middle-aged men, the PRIME study

“…Red wine contains phenolic compounds which have been shown to reduce LDL oxidation [30,34,35]. Wine has also been shown to increase fibrinolysis [53,54] and to decrease platelet aggregation [55], possibly because of the small amounts of acetylsalicylic acid present [56], although this hypothesis has been questioned [57] and the antiplatelet effect of wine has been attributed to alcohol rather than other substances [52]. Also, as stated previously, beer consumption could be associated with a higher frequency of hyponatremia due to the low solute content of beer [50].…”

Patterns of alcohol consumption in middle-aged men from France and Northern Ireland. The PRIME Study

“…Although some authors have found that the protective effect of wine is superior to that of other alcoholic beverages (Rosenberg et al, 1981;Renaud & De Lorgeril, 1992;Goldberg, 1995), those results have not been con®rmed in other studies (Hennekens et al, 1979;Marques-Vidal et al, 1995). The mechanisms by which moderate alcoholic beverages consumption decreases coronary artery disease include the increase of high density lipoprotein levels (Gaziano et al, 1993;Marques-Vidal et al, 1995;Parker et al, 1996;Paunio et al, 1996), the modi®cation of hemostatic parameters (Sumi et al, 1988;Owens et al, 1990;Hendricks et al, 1994;Pellegrini et al, 1996) and the inhibition of lipoprotein oxidation by phenolic components present in red wine (Anonymous, 1993;Frankel et al, 1993;Kinsella et al, 1993;Sera®ni et al, 1994;Me Ârillon et al, 1997). However, although there is de®nitely a biological effect of alcohol, differences in consumption patterns and in lifestyle can also partly account for the relationship between alcohol consumption and coronary artery disease.…”