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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the relations between reported alcohol use and the incidence of hospitalization for several types of cerebrovascular disease. Daily consumption of three or more drinks, but not lighter drinking, was related to higher hospitalization rates for hemorrhagic cerebrovascular disease, especially intracerebral hemorrhage. Age, blood pressure, and black race were other independent predictors of hemorrhagic events; higher blood pressure appeared to be a partial mediator of the relation between alcohol use and hemorrhagic events. Alcohol use was associated with lower hospitalization rates for occlusive cerebrovascular disease; an inverse relation was present in both sexes, whites and blacks, and for extracranial and intracerebral occlusive lesions. Other predictors of hospitalization for occlusive disease included age, blood pressure, smoking, blood glucose and total cholesterol concentrations, and baseline disease. Our data suggest that heavier drinking increases the risk of hemorrhagic cerebrovascular events, but that alcohol use may lessen the risk of occlusive lesions.
Stroke 1989 Jun
PMID:Alcohol use and subsequent cerebrovascular disease hospitalizations. 272 39

To examine the relationship between alcohol consumption and ischemic stroke risk, we used data from our case-control study of stroke risk. Eighty-nine patients admitted to the hospital with ischemic stroke documented by computed tomography of the head were matched to 178 controls. Alcohol use was defined by an estimate of customary use (heavy, moderate, light, or none). We found no consistent or significant association between any level of alcohol use and ischemic stroke risk (odds ratios: any, 1.3; heavy, 0.5; moderate, 1.5; and light, 1.5). We repeated the analysis of our study using a control group assembled according to the study criteria of another case-control study that reported a significant association in men with heavy alcohol use (odds ratio, 4.2). We demonstrated that the association in the prior study may be spurious due to methodological problems.
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PMID:Evidence against the association between alcohol use and ischemic stroke risk. 273 Feb 58

The influence of ethanol (alcohol) consumption on blood pressure during and after the development of hypertension was examined by using spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP). Normotensive Wistar-Kyoto (WKY) rats were also used for comparison. Substituting alcohol (5-20%) for drinking water at 1 month of age retarded the age-dependent rise of blood pressure in all three strains so that, at 7 months, blood pressure measured by a tail-cuff method was 24 mm Hg, 26 mm Hg, and 41 mm Hg lower in the alcohol-treated WKY rats, SHR, and SHRSP, respectively, than in untreated rats. Significant differences in blood pressure were seen in each strain after only 3 months. Withdrawal of alcohol at this stage caused an acute rise of blood pressure then a return to subnormal levels, which persisted for a further 3 months. Administration of 15% alcohol to adult WKY rats and SHR for 2 months had no significant effect on blood pressure. Increasing alcohol content to 20% for a further 2 months prevented rises of blood pressure in both strains. Thus, although continuous drinking of alcohol does not lower blood pressure, it appears to counteract the development of hypertension in rats.
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PMID:Antihypertensive effect of alcohol in spontaneously hypertensive rats. 273 9

To evaluate the effects of chronic ethanolism on responses to hemorrhagic shock (HS), 24 dogs were fed a diet mixed with 3 g/kg ethanol (ETOH) for 3 mo (group 1, n = 12) and 9 mo (group 2, n = 12); 12 dogs were fed a regular diet with no alcohol. Blood alcohol level 2-3 h after food consumption was 116 +/- 10 mg/100 ml. On the experimental day, both ETOH-treated and ETOH-free dogs were divided into two subgroups, one for HS [mean arterial pressure (MAP) of 30 mmHg for 2 h] and one for observation during anesthesia. Chronic ethanolism altered cardiocirculatory function (increased MAP, arterial lactate, and hematocrit and decreased cardiac output, stroke work, and pancreatic blood flow) regardless of the length of time ETOH was consumed. HS impaired cardiovascular performance regardless of ETOH consumption. However, coronary blood flow, myocardial oxygen delivery, extraction, and consumption were significantly higher in the ETOH-treated compared with ETOH-free dogs after 2 h of shock. Cardiocirculatory dysfunction after fluid resuscitation from shock in the ETOH group was not related to inadequate coronary perfusion, metabolic acidosis, or cardiac hypertrophy. An increased total myocardial tissue calcium content in the ETOH group suggests that ETOH-mediated changes in calcium homeostasis contribute to cardiac contractile dysfunction in the trauma subject who chronically consumes alcohol.
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PMID:Hemorrhagic shock complicated by chronic ethanolism. 275 Sep 37

The development of blood pressure was monitored by the tail-cuff method in normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) receiving ethanol (alcohol) in drinking water from weaning (approximately 1 month of age). Alcohol administration over a 3-month period attenuated the development of hypertension in SHRSP and also caused a small reduction of the initial blood pressure rise in WKY. This was accompanied by a reduction of fluid intake and an increase of circulating antidiuretic hormone (arginine vasopressin; AVP). Circulatory volume remained constant. Direct measurement of arterial blood pressure in conscious rats before and after autonomic blockade confirmed the antihypertensive effect of alcohol in SHRSP and indicated that it is at least partly dependent on altered activity of neural mechanisms. Sudden withdrawal of alcohol caused an immediate increase of fluid intake followed by a rise of blood pressure lasting several days in both WKY and SHRSP. This withdrawal hypertension could not be attributed to changes in plasma catecholamines or AVP.
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PMID:Effects of chronic alcohol consumption and alcohol withdrawal on blood pressure in stroke-prone spontaneously hypertensive rats. 276 25

The effects of prolonged infusions of ethanol on endothelium-dependent vasorelaxation induced by acetylcholine and adenosine triphosphate (ATP) and on endothelium-independent relaxation induced by papaverine were studied and compared in isolated perfused rat mesenteric artery preparations. Infusion of ethanol over 60 minutes at concentrations of 1.6, 4.7, 6.3, and 7.9 mg/ml caused concentration-related inhibition of norepinephrine-induced vasoconstriction. In preparations infused with 6.3 and 7.9 mg/ml, this effect reached a maximum after 10-20 minutes but had vanished by the end of the infusion; 1 hour after the end of the infusion, the effects of norepinephrine were potentiated by 71% and 108%, respectively. Acetylcholine-induced vasorelaxation (EC50 3.0 ng/ml in controls) was significantly reduced after 6.3 mg/ml ethanol infusion and totally abolished after 7.9 mg/ml ethanol infusion. ATP-induced vasorelaxation (EC50 180 ng/ml in controls) was also abolished after 7.9 mg/ml of ethanol infusion. By contrast, the vasorelaxant effects of papaverine were not affected by 7.9 mg/ml ethanol infusion. Light-microscopic examination revealed that the endothelial cells were present in ethanol-treated and in control mesenteric arterial beds. These observations indicate that ethanol suppresses endothelium-dependent vasorelaxation without apparent removal of the endothelial cells. The compromised relaxant capacity of the endothelium after ethanol and the resultant intensification of the vasoconstrictor response to norepinephrine may contribute to the development of vascular diseases such as hypertension and stroke.
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PMID:Alcohol suppresses endothelium-dependent relaxation in rat mesenteric vascular beds. 278 50

Alcohol use is a recognized risk factor for stroke. We hypothesized that alcohol use may increase the risk of stroke, independent of an effect on blood pressure, by causing cerebral vasoconstriction. To examine this, we used retinal vessels as a marker for cerebral vessels and analysed the cross-sectional associations between alcohol use and total retinal vessel width in 741 Japanese and 434 American white male telephone executives. Systolic and diastolic blood pressures were negatively associated with retinal vessel width in the Japanese (p less than 0.0001, 0.0001, respectively) but this association did not achieve statistical significance in the Americans (p less than 0.1, 0.3). Japanese drinkers had a larger mean retinal vessel width than Japanese abstainers, while American drinkers had a smaller retinal vessel width than abstainers. These associations between alcohol use and retinal vessel width were not significant within nationalities but the interaction between alcohol use and nationality was significant, independent of other stroke risk factors (p less than 0.04). Although these results do not support the initial hypothesis, they are consistent with known biological differences in alcohol metabolism between Japanese and American men and support different effects of alcohol use on retinal vessel calibre in these two nationalities.
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PMID:Alcohol use and retinal vessels: insights into the mechanism of alcohol-induced stroke. 280 66

The effects of ethanol and pentobarbital on the function of isolated working hearts from control and ethanol-fed male Long-Evans rats were studied. Hearts from ethanol-fed animals (38% of calories; 10-12 months) exhibited functional tolerance to the cardiodepressive effects of 18-71 mM ethanol in the perfusing medium. Left ventricular systolic pressure, peak relaxation rate, isovolumic pressure indexes, peak aortic flow rate, cardiac output, and stroke work of the control hearts were depressed to a greater extent than were those indexes of the alcoholic rat hearts during exposure to ethanol in vitro. Differences in the functional responses of controls and alcoholics were not the result of differences in energetics; myocardial O2 consumption, O2 supply-to-utilization ratio, and external work efficiency changed similarly in both groups of hearts during perfusion with ethanol. Cross-tolerance of the alcoholic rat hearts to the in vitro cardiodepressive effects of pentobarbital was also apparent. Peak rate of left ventricular pressure development, peak aortic flow rate, isovolumic pressure indexes, and cardiac output of the control rat hearts were significantly lower than those indexes of the alcoholic rat hearts during perfusion with 0.5 mM pentobarbital. In addition, four of the seven control hearts could not be paced during pentobarbital perfusion using 3V electrical pulses; the pacing voltage had to be raised and right ventricular pacing used to maintain stable function of those hearts at a 321 beats/min pacing rate. Myocardial O2 consumption and O2 supply-to-utilization ratios of control and alcoholic rat hearts were similar, but external work efficiency was slightly higher in the alcoholics than in controls during pentobarbital perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res 1988 Aug
PMID:Tolerance to ethanol and cross-tolerance to pentobarbital by isolated hearts from chronic alcoholic rats. 305 74

This study examines the hypothesis that there may be a clinically important association between alcohol intake and stroke. Alcohol consumption and the haematological and biochemical markers of alcohol intake were studied in hospital admissions for stroke and compared with community based control subjects from an occupational screening survey. In males, moderate to heavy alcohol consumption (greater than 30 units per week) was associated with an increased relative risk of stroke. Light drinking (less than 30 units per week) was associated with reduced relative risk when compared to teetotallers. The relative risk of stroke in moderate and heavy consumers of alcohol compared with teetotallers was elevated 1.8 times. Similar patterns of risk were present for increasing levels of aspartate transaminase and uric acid. Relative risk was increased for all levels of gamma-glutamyl transferase above the lowest. There was a decrease in relative risk associated with increasing levels of mean erythrocyte cell volume though this did not achieve statistical significance. There were few heavy drinkers among the female cases or controls. We conclude that high alcohol intake may be a significant preventable risk factor particularly among male strokes.
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PMID:A community case-control study of alcohol consumption in stroke. 320 34

Alcohol-related minor accidents such as sprains and burns are common in sauna, but more serious accidents also take place--head contusions, heat stroke after passing out in sauna and drownings while swimming. The exact number of these accidents is not known, but in Finland (population 4.8 million) the consumption of alcohol has been estimated to be a contributing factor in some 20 to 25 sauna-related deaths every year. The scientific information on the interaction of sauna and alcohol on human physiology is totally lacking. Thus our discussion on the physiological and medical consequences of this interaction relies merely on presumptions. Ingestion of large amounts of alcohol while sauna bathing may affect the body's ability to maintain blood pressure. In particular, the risk of an orthostatic hypotensive reaction is increased with concomitant faintings and accidents. Alcohol intoxication and particularly the hangover phase exposes a person to cardiac arrhythmias, and sauna may further increase the arrhythmia-risk due to enhanced adrenergic activity. Sauna bathing and heavy drinking, and also sauna bathing during hangover phase undoubtedly create real health risks.
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PMID:The sauna and alcohol. 321 3


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