Olle Elmér

Impairment of Primary Hemostasis and Platelet Function after Alcohol Ingestion in Man

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.

Acute portal hypertension after gastric administration of ethanol in the pig.

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.

Effects of ethanol on platelet aggregation: an in vitro study

SummaryAlcohol ingestion results in the formation of circulating microaggregates in the pig. To investigate the underlying mechanism, the effects of alcohol on platelet aggregation using a Born-aggregometer, was investigated. After incubating unstirred platelet rich plasma (PRP) with moderate concentrations of alcohol (175 mmol/l) the aggregation induced by collagen was reduced. This was probably due to platelet refractoriness caused by platelet ADP release. We could also demonstrate that high concentrations of alcohol (630 mmol/l) caused platelet release in stirred PRP. Release of ADP from red cells, after incubating unstirred whole blood with low concentrations of alcohol (17 mmol/l), was the probable explanation to the observed platelet refractoriness to ADP and collagen. Alcohol causing release of ADP from red cells is likely the cause of platelet aggregation in circulating blood and is probably the mechanism in formation of circulating platelet aggregates after alcohol ingestion.

Acute Alcohol Intoxication and Traumatic Shock

The reaction to a standardized soft tissue trauma was investigated in pigs pre-treated with gastric administration of saline or 40% ethanol. Circulating microaggregates in vena cava, vena portae and a

Circulating Microaggregates after Gastric Administration of Ethanol in the Pig

Earlier in vitro experiments have shown microaggregate formation in pig and rabbit blood after addition of ethanol. In this study ethanol was given to pigs resulting in ethanol concentrations of 30-40 mmol/l 2-4 h after administration. As would be expected ethanol concentration was higher in the portal vein than in the hepatic vein, caval vein or aorta. Microaggregates in circulating blood were measured with screen filtration pressure (SFP). SFP rose to more than double the initial value in ethanol-intoxicated pigs whereas it remained unchanged in controls. The ethanol-intoxicated pigs developed hemoconcentration and metabolic acidosis. Our results indicate that microaggregates probably made up of aggregated platelets are formed in pig blood during acute ethanol intoxication.

Influence of Physiological Saline, Dextran 70, Hydroxyethyl Starch, Degraded Gelatin, and Fat Emulsion Solutions on Screen Filtration Pressure

The effect of 0.9% NaCl solution, dextran 70, hydroxyethyl starch, degraded gelatin and fat emulsion on Hb, Hct, platelet count and screen filtration pressure has been studied in the rabbit. Dextran 70, hydroxyethyl starch and degraded gelatin caused hemodilution and decreased platelet count. Screen filtration pressure increased after infusion of degraded gelatin and tended to decrease after dextran 70 and hydroxyethyl starch. 0.9% NaCl and fat emulsion caused less pronounced changes. Intraportal infusion of 7 ml/kg body weight of the same solutions gave results which at present are difficult to interpret.