Actions of alcohol and ischaemic brain infarction
|Organizations:||University of Oulu, Faculty of Medicine, Department of Neurology
|Online Access:||PDF Full Text (PDF, 0.9 MB)|
|Persistent link:|| http://urn.fi/urn:isbn:9514257227
|Publish Date:|| 2000-07-27
|Thesis type:||Doctoral Dissertation
|Defence Note:||Academic Dissertation to be presented with the assent of the Faculty of Medicine, University of Oulu, for public discussion in Auditorium 8 of the University Hospital of Oulu, on September 1st, 2000, at 12 noon.
Docent Riitta Lassila
Professor Jack Neiman
Alcohol drinking may exercise both beneficial and untoward effects on the haemostatic and fibrinolytic systems. It may also predispose individuals to arterial thrombosis and trigger embolism in the brain. The aim here is to examine these problems.
Methods used for evaluating platelet function were platelet aggregation and associated thromboxane B2 release, shear-induced platelet aggregation, and measurement of urinary prostaglandins. Changes in fibrinolytic system were evaluated by measuring plasminogen activator inhibitor type 1. The combined effects of alcohol drinking, physical exercise, eating a meal and circadian rhythms in healthy volunteers were examined in three experimental studies. Case-control studies were used for assessing the mechanism and etiology of ischaemic brain infarction triggered during alcohol intoxication.
Alcohol drinking did not potentiate the effects of physical exercise on platelet function. Sleeping while under acute intoxication resulted in a significant activation of platelets, as shown by increased urinary excretion of a thromboxane metabolite. On the other hand, ingestion of a moderate dose of red wine seemed to attenuate platelet aggregation measured ex vivo, irrespective of whether the wine was consumed with a meal or alone. However, both red wine and a larger acute dose of alcohol in fruit juice inhibited fibrinolytic activity.
In a case-control study, platelet count and function were evaluated in 426 consecutive patients hospitalized on account of acute brain infarction. Compared with the hospital-based controls, a higher than normal platelet count was observed immediately after admission. Heavy drinkers showed both higher and lower than normal platelet counts more often than the other patients with brain infarction. The changes in platelet function among the heavy drinkers reflected their recent drinking habits.
Another case-control study indicated that recent heavy drinking of alcohol was an independent risk factor for cardiogenic embolism to the brain. Recent heavy drinking also seemed to predispose subjects to some other types of ischaemic brain infarction such as artery to artery embolism due to large-artery atherosclerosis and cryptogenic stroke, but these observations need to be confirmed in larger studies.
In conclusion, the results show some untoward effects of acute heavy drinking of alcohol, which could contribute to the onset of brain infarction either as triggering or as predisposing factors. On the other hand, drinking of a moderate dose of red wine did not have any clear untoward effect on healthy human volunteers.
Acta Universitatis Ouluensis. D, Medica
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