Background: Light to moderate alcohol consumption is associated with a reduced risk of coronary heart disease. Stimulation of fibrinolysis has been suggested as one of the mechanisms involved. The present study analyses the effect of regular alcohol consumption on various parameters of fibrinolysis. The question whether the alcohol-induced plasma increase of plasminogen activator inhibitor (PAI-1) may originate from thrombocytes was also addressed.
Methods: Six healthy male volunteers consumed three glasses of red wine daily during two periods of a week, with a week of abstinence from alcohol in between. PAI-1 antigen and activity levels, t-PA antigen and activity levels and plasmin antiplasmin (PAP) complexes were measured on days 1, 3, 8, 15, 17 and 22 of the experiment period. On the first day, PAI-1 antigen and activity before and after alcohol consumption was also measured in platelet-rich plasma (prp).
Results: Although some slight shifts in the various parameters could be noticed during the drinking periods, all favouring impairment rather than stimulation, no significant effect of regular moderate alcohol use could be observed on fibrinolysis. Alcohol did not trigger a release of PAI-1 from platelets.
Conclusions: Regular moderate alcohol consumption has no significant effect on fibrinolysis. The alcohol-induced increase of plasma PAI-1 does not originate from thrombocytes. The cardioprotective effect of moderate alcohol consumption cannot be explained by a beneficial influence on fibrinolysis.