Ethanol-Induced Microaggregate Formation in Pig and Rabbit Blood

Elmér, Olle; Göransson, Göran; Saku, Motonori; Bengmark, S

doi:10.1055/s-0038-1649235

Cited by 13 publications

(13 citation statements)

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“…In each experiment PRP was adjusted with PPP so that the final PRP-ethanol mixture in the cuvette contained 350 x 109 platelets/1. Screen Filtration Pressure (SFP) was measured as described earlier [5] after adding 40% ethanol to PRP or PPP. Platelet aggregation was induced by ADP (Sigma Chemicals Co., St. Louis, Mo, USA) added to PRP to a final concentration of 0.2-1/2M.…”

Section: Methodsmentioning

confidence: 99%

“…Alcohol ingestion in pigs results in circulating microaggregates [1] and trapping of large platelet aggregates in portal venules [7]. Microaggregates are formed when whole blood is mixed with alcohol [5]. In man, alcohol ingestion is associated with a prolonged bleeding time [61 and when platelet rich plasma (PRP) is incubated with alcohol ADP induced platelet aggregation is reduced [10,19,21].…”

Section: Introductionmentioning

confidence: 99%

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Effects of ethanol on platelet aggregation: An in vitro study

et al. 1983

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Alcohol 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.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of ethanol on platelet aggregation: An in vitro study

et al. 1983

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“…Platelets were counted in a Buerkner chamber using a phasecontrast microscope. Plasma alcohol concentrations were measured by gas chromatography as described earlier [28]. Serum osmolality was determined with an osmometer (Roebling, Svenska Labex, Stockholm, Sweden).…”

Section: Introductionmentioning

confidence: 99%

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

Elmér

Göransson

Zoucas

1984

Pathophysiol Haemos Thromb

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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.

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“…Even though the volume seems large the resulting blood alcohol concentration will, during the experiment, reach only the level (70 mmol/1) necessary to induce microaggregate formation in vitro [8] and in vivo [1] without reaching the level (150 mmol/1) reported as fatal [12]. Saline was given to control animals to obtain a corresponding gastric distension and stimulation as any type of feeding might have on the splanchnic circulation [2],…”

Section: Discussionmentioning

confidence: 99%

“…Urine output was measured hourly. Ethanol was determined with gas chromatography as described earlier [8], For statistical evaluation the Student's t test for paired observations was used.…”

Section: Metabolic and Liver Function Testsmentioning

confidence: 99%

Acute Portal Hypertension after Gastric Administration of Ethanol in the Pig

Elmér¹,

Bengmark²,

Göransson³

et al. 1982

Eur Surg Res

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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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Ethanol-Induced Microaggregate Formation in Pig and Rabbit Blood

Cited by 13 publications

References 0 publications

Effects of ethanol on platelet aggregation: An in vitro study

Effects of ethanol on platelet aggregation: An in vitro study

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

Acute Portal Hypertension after Gastric Administration of Ethanol in the Pig

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