Ethanol-inhibited platelet prostaglandin synthesis in vitro.

Stuart, M J

doi:10.15288/jsa.1979.40.1

Cited by 39 publications

(17 citation statements)

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“…The present results are in concordance with earlier results from animal experiments where alcohol in similar concentrations caused a prolongation of the bleeding time, an increase in blood loss after a standardized liver resection [ 12] and platelet refractoriness in vitro [11], Impairment of human platelet function by alcohol in vitro has been demon strated recently [33,34]. The mechanism by which alcohol affects platelet function re mains unknown.…”

Section: Discussionsupporting

confidence: 92%

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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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Section: Discussionsupporting

confidence: 92%

“…The mechanism by which alcohol affects platelet function re mains unknown. In vitro, alcohol impairs platelet prostaglandin synthesis but this inhi bition is too small to be the primary cause for the platelet dysfunction [33]. Acidosis affects platelet function [35] and acidosis may result from the metabolism of alcohol.…”

Section: Discussionmentioning

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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“…As a consequence, platelet ADP is reduced, and as endogenous ADP is the mediator of collagen-induced aggregation, aggregation by collagen is reduced. This is also supported by reports [19,21] indicating that the first observed effect of alcohol on ADP-induced aggregation is a reduction of the second wave which depends on release of endogenous ADP.…”

Section: Discussionsupporting

confidence: 83%

“…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%

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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“…Ethyl alcohol was demonstrated to impair platelet function in vivo [2,7,14] and in vitro [1,14], Results by Stuart [30] indicated that ethanol inhibited in vitro prostaglandin synthesis in human platelets. In vitro experiments using rat, rabbit and pig thrombocytes indicated that the effect of ethanol on platelets could be mediated to some extent by the red cell [2,8].…”

Section: Discussionmentioning

confidence: 99%

Effect of Acute Ethanol Intoxication on Primary Haemostasis, Coagulation Factors and Fibrinolytic Activity

Zoucas¹,

Bergqvist²,

Göransson³

et al. 1982

Eur Surg Res

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The effect of ethanol intoxication on haemostasis was studied by transection of mesenteric microvessels and liver resection in the rat. Plasma concentrations of alcohol were within the range of those found in ethanol intoxication in man. Bleeding time and blood loss were increased 1 h after ethanol administration, regardless of the utilized technique. A significant positive correlation existed between bleeding time following liver resection and bleeding time after simultaneous transection of a mesenteric arteriole and venule. Coagulation mechanisms, assayed by whole blood clotting time, APT time, one-stage prothrombin time, recalcification time, thrombin time, Owren’s P & P test and determination of plasma factor V and fibrinogen levels, were not significantly changed in ethanol-intoxicated animals. Administration of alcohol did not affect fibrinolytic activity, while it inhibited significantly ADP and collagen-induced platelet aggregation in the rat.

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Ethanol-inhibited platelet prostaglandin synthesis in vitro.

Cited by 39 publications

References 0 publications

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

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

Effects of ethanol on platelet aggregation: An in vitro study

Effect of Acute Ethanol Intoxication on Primary Haemostasis, Coagulation Factors and Fibrinolytic Activity

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