The effect of alcohol ingestion on primary hemostasis was investigated in fasting healthy humans. Primary hemostasis was measured with the template bleeding time and platelet aggregation assayed with the turbidometric method. Blood was collected to study coagulation and fibrinolysis. 1 h after ingestion of 2 ml/kg body weight of 40% alcohol the plasma alcohol concentration was 19.3 ± 1.6 mmol/l. At this time there was a significant prolongation of the bleeding time accompanied by an impairment of platelet responsiveness to both collagen and ADP. A prolongation of the bleeding time and impairment of platelet function was also found 2 h after alcohol ingestion. Ingestion of this amount of alcohol did not affect parameters of coagulation or fibrinolysis. The data indicate that primary hemostasis is impaired in man after ingestion of moderate amounts of alcohol. This may explain the favorable effect of moderate alcohol consumption on ischemic heart disease but indicates an increased risk for patients with bleeding.

SummaryIncreased microaggregate formation was found after mixing ethanol with blood from pig and rabbit in vitro, measured with Swank’s Screen Filtration pressure method. Final ethanol concentrations were in the range found in ethanol-intoxication in man. No rise in SFP was noticed when plasma with 10,000 platelets/μl was used. It is therefore doubtful that altered plasma proteins caused the rise in SFP. It is suggested that if a direct effect of ethanol upon platelet aggregation exists in vivo, it may be of importance in acute ethanol intoxication and in chronic alcoholism.

SummaryPlatelet aggregation was measured by Born’s method. Plasma from Sprague-Dawley rats and inbred albino rabbits was used. 20% ethanol in 0.9%(w/v) NaCl was added to plasma at final concentrations of 56.5 mM, 85.9 mM 171.5 mM and 343.1 mM or to whole blood at final concentrations of 8.7 mM, 17.4 mM, 52.5 mM, 171.5 mM and 343.1 mM. Experiments using 0.9% NaCl volumes equivalent to the added ethanol volume were also conducted. Dose-response aggregation tests showed that a decrease in ADP-and collagen-induced aggregation existed when ethanol was mixed with rat or rabbit blood prior to the preparation of platelet-rich plasma. There was no effect on ADP-induced platelet aggregation when ethanol was mixed with rat or rabbit plasma. Collagen-induced aggregation was impaired only in rat plasma when ethanol concentration reached 343.1 mM. These results suggested that ethanol modified platelet function possibly via red cells.

A single gastric administration of 15 ml/kg of 40 % ethanol to anesthetized pigs resulted in an increased portal venous blood pressure which increased with increasing blood alcohol levels. For the first 2 h there was no significant alteration in liver blood flow, but 3 h after the administration of ethanol, when portal blood pressure reached its highest values, liver blood flow had decreased. This was probably caused by increased hepatic vascular resistance as shown in electron thin-section phase-contrast microscopy which at this time showed marked hepatocyte swelling, narrowing of the sinusoids and platelet aggregates in small portal branches.

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