ETHANOL INHIBITS RABBIT PLATELET RESPONSES TO COLLAGEN IN VITRO BUT DOES NOT AFFECT RABBIT PLATELET ADHERENCE TO DE-ENDOTHELIALIZED A0RTAE IN VIVO

Abstract

Epidemiological studies indicate that moderate consumption of alcohol is associated with a reduced risk of coronary heart disease, but it is not known whether inhibition of platelet functions by ethanol is involved. We studied the effects of ethanol on rabbit platelet responses to collagen in vitro and in vivo. Addition of ethanol (4 mg/ml) to suspensions of washed platelets prelabelled with [14c]serotonin inhibited aggregation and secretion in response to low (0.4 μg/ml) concentrations of acid soluble collagen (14% secretion without ethanol, 3% secretion with ethanol). With a higher concentration of collagen (1.25 μg/ml), 4 mg/ml ethanol had no inhibitory effect. The inhibitory effect of ethanol on collagen-induced aggregation was also observed in citrated platelet-rich plasma (c-PRP) to which ethanol was added in vitro and in c-PRP from rabbits given ethanol acutely by gavage (3.5 g/kg) 30 min before blood sampling. The accumulation of [51cr]-labeled platelets on the subendothelium of rabbit aortae de-endothelialized with balloon catheters was measured in vivo in rabbits given ethanol (blood ethanol concentration at time of vessel wall injury: 4.1 ± 0.2 mg/ml, mean ± S.E., n=6). Ten min after de-endothelialization, there was no difference between the number of platelets adherent per square mm of injured aorta of control rabbits (39,400 ± 2,600, mean ± S.E., n=6) and intoxicated rabbits (36,800 ± 3,700, mean ± S.E., n=6). Thus, although ethanol inhibits platelet aggregation and secretion in response to collagen in vitro and ex vivo, it does not alter platelet adherence to the subendothelium, including its constituent collagen, in vivo. Therefore, it is unlikely that ethanol exerts its beneficial effects against coronary heart disease by altering the initial adherence of platelets to injured vessel walls.