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

76 consecutive patients aged under 40 with ischaemic brain infarction verified by carotid angiography and/or serial brain scanning were studied. In at least 15 cases (20%) the onset of symptoms was preceded within 24 hours by a bout of alcohol drinking. Ethanol-related cases comprised 40%, 25%, and 13% of the patients in the age-groups 16-19, 20-29, and 30-39 years, respectively. Ethanol intoxication preceding the stroke was 2-3 times as common in male and 3-4 times as common in female patients as ethanol intoxication in the general Finnish population of the same ages and sex. Occasional ethanol intoxication seems to carry an increased risk of ischaemic brain infarction in young adults.
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PMID:Does ethanol intoxication promote brain infarction in young adults? 8 45

f2 bacteriophage in the presence of fetal calf serum (at a final concentration of 10%) was exposed to six commonly used disinfectants for times of 10, 20 and 30 sec. At the end of exposure times skim milk neutralized the disinfectant activity and residual virus was assayed using the plaque technique. The 6 disinfectants considered were Javex, sodium hydroxide, ethanol, Wescodyne, One Stroke Ves-Phene and Sonacide. A 0.25% (w/v) solution of sodium hydroxide and 1/50 Javex (1200 parts/10(6) chlorine) were the most effective of the six disinfectants considered since 10(5) f2 bacteriophage were inactivated in 30 seconds in each instance. Since a 0.25% (w/v) solution of sodium hydroxide had a pH of 12.5 this made it too caustic to use as a disinfectant in many practical situations. It was concluded therefore that Javex at some dilution less than 1/50 (greater than 1200 parts/10(6) chlorine) was the most practical of the six disinfectants to use. Ethanol (95%, v/v) inactivated 10(3) f2 bacteriophage in 30 seconds while 1/20 Wescodyne and undiluted Sonacide inactivated 10(1)-virus particles. Ves-Phene at a dilution of 1/50 was a completely ineffective virucide during the 30 sec exposure. The resistance of f2 bacteriophage to inactivation by these six disinfectants was compared with that of echovirus 11 and coxsackievirus B5. In all instances except exposure to undiluted Sonacide, f2 was comparable in resistance to inactivation and in many cases had greater resistance.
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PMID:The relative resistance of f2 bacteriophage to inactivation by disinfectants. 45 39

The effects of acute ethanol administration on acid-base balance and hemodynamic parameters were studied in a canine model. Ten mongrel dogs, anesthetized and maintained on a volume ventilator, underwent splenic artery ligation 30 minutes prior to study. Group A (N = 5) served as controls. Thirty minutes after drug administration, the animals underwent a 20-cc/kg hemorrhage over 15 minutes. Thirty minutes postphlebotomy, resuscitation was performed with the same volume of homologous blood. Acid-base and hemodynamic parameters were monitored over 3.5 hours. Ethanol levels peaked 60 minutes following administration at 207 +/- 13 mg%. During the entire study, no differences were observed in heart rate, pulmonary capillary wedge pressure, systemic vascular resistance index, pO2, or pCO2, between the two groups. Following hemorrhage, statistically significant decreases in pH, mean arterial pressure (MAP), cardiac index (CI), and left ventricular stroke work index (LVSWI) developed in group A compared to controls. Maximal disparity developed in pH (7.21 +/- 0.05 to 7.33 +/- 0.02, P < 0.01), MAP (67 +/- 11 v 110 +/- 9 torr, P < 0.01), CI (1.69 +/- 0.24 compared to 2.72 +/- 0.19 L/min/M2, and LVSWI (18.7 +/- 1.2 compared to 44.9 +/- 4.8 gr-meter/M2/beat, P < 0.01) at 60, 45, 30, and 75 minutes postphlebotomy. In this study, ethanol directly or indirectly caused an increased metabolic acidosis and myocardial depression in the post-hemorrhage period.
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PMID:Protracted metabolic acidosis: the impact of acute ethanol in hemorrhagic shock. 140 53

Ethanol has long been recognized as a toxic agent that has acute and chronic effects on cerebral and hepatic function. Over the past two decades important influences on the cardiovascular system have been either rediscovered or observed for the first time. The combined use of tobacco cigarettes and alcohol appears to increase the risk of many of these clinical abnormalities. While many individuals addicted to ethanol have subclinical abnormalities of the heart, somewhat less than a majority develop symptomatic cardiac problems. These include heart failure and arrhythmias. In addition to supraventricular arrhythmias that often normalize spontaneously, there is an increased incidence of sudden death that peaks at about 50 years of age in the alcoholic population. A significant degree of blood pressure elevation occurs in individuals who abuse alcohol. This appears to be transient and is normalized in most individuals during abstinence. The increased incidence of hemorrhagic and nonhemorrhagic stroke in middle age also appears to decline when alcohol abuse is interrupted. A preventive effect of mild to moderate drinking on coronary artery disease is, at present, equivocal, largely due to the question of appropriate controls.
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PMID:Alcohol and the cardiovascular system. 219 48

The effect of ethanol (0.5 g/kg, IV) at different concentrations (30%, 60%, and 90%) was studied in male cats using radioactive microspheres on systemic hemodynamics and regional circulation. Ethanol produced a significant fall in systolic, diastolic and mean blood pressure. A significant reduction in heart rate, left ventricular work, cardiac output and total peripheral resistance was also observed. No change occurred in stroke volume. A significant decrease in blood flow to left ventricle, right ventricle and interventricular septum was observed, but the vascular resistance of these regions was unaltered. Brain blood flow was not affected by various concentrations of ethanol. The vascular resistance significantly decreased in spinal cord, medulla, pons, midbrain, hypothalamus, thalamus, caudate nucleus, cerebellum and cortex. The average brain blood flow (ml/min/100 g) was 35.63 in control, 37.17 in 30%, 35.56 in 60% and 35.05 in 90% ethanol-treated cats. Spleen, liver, pancreas, gastrointestinal tract, skin, muscle and bone did not show any significant change in the blood flow, while vascular resistance following ethanol treatment. The blood passing through the arteriovenous shunts was significantly decreased by ethanol. It is concluded that ethanol produces marked cardiovascular changes which are not affected by varying the concentration of ethanol.
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PMID:Effect of varying concentration of ethanol on systemic hemodynamics and regional circulation. 271 21

The effects of ethanol ingestion on ADP-induced platelet aggregation and associated thromboxane formation were studied in the platelet-rich plasma of 10 healthy male volunteers, each serving as his own control. Ethanol caused a transient decrease in threshold concentration of ADP to produce irreversible aggregation. Over a wide range of ADP total platelet aggregation was increased. In the presence of irreversible aggregation, formation of thromboxane B2 rose from 303 +/- 56 to 950 +/- 212 fmol per 10(7) platelets (p less than 0.01). The effects lasted as long as ethanol was present in blood, did not significantly correlate to blood ethanol levels and exhibited great individual variation. It remains to be proved, whether these observations could contribute to the increased risk of ischemic brain infarction associated with acute ethanol ingestion.
Stroke
PMID:Acute ethanol ingestion increases platelet reactivity: is there a relationship to stroke? 396 61

The influence of chronic alcohol consumption on blood pressure was examined in normotensive Wistar/Kyoto rats (WKY) and in stroke-prone spontaneously hypertensive rats (SHR-SP). Ethanol, administered in drinking water from 5 weeks of age to produce moderate blood alcohol levels, substantially retarded the development of hypertension in SHR-SP and caused a mild reduction of blood pressure in WKY. Alcohol withdrawal caused an acute rise in blood pressure in both strains, followed by a reduction to the subnormal levels previously induced by alcohol treatment. This sustained antihypertensive effect of alcohol was not attributable to reductions of body weight or fluid intake.
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PMID:Retarded development of hypertension in stroke-prone spontaneously hypertensive rats following chronic alcohol consumption. 404 Aug 26

Reovirus 3 in the presence of foetal bovine serum was exposed to six disinfectants for times of 10, 20 and 30 sec. At the end of such exposure times the addition of skim milk terminated disinfectant activity, and residual virus was assayed using the plaque technique. The six disinfectants considered were Javex (a sodium hypochlorite disinfectant), sodium hydroxide, ethanol, Wescodyne, One Stroke Ves-Phene, and Sonacide. Ethanol (95% v/v) and 1/75 Javex (800 ppm chlorine) were the most effective virucides. Both of these agents inactivated 10(5) plaque forming units (PFU) in 30 sec. Undiluted Sonacide, 0.25% (w/v) sodium hydroxide and 1/200 Wescodyne each inactivated between 10(2) and 10(3) PFU in 30 sec. Javex at a dilution of 1/100 (600 ppm chlorine) was next in effectiveness, inactivating 10(1.5) PFU in 30 sec and was more effective than 1/50 Ves-Phene which inactivated 10(1) PFU in 30 sec. Ethanol in 70% (v/v) solution was totally ineffective in inactivating reovirus 3. Ethanol (95% v/v) after dilution in the test system was 76% (v/v) and ethanol (70% v/v) was really 56% (v/v).
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PMID:The effectiveness of six disinfectants in inactivation of reovirus 3. 652 63

Twenty-three healthy males, aged 23 to 62 years, were examined by M-mode echocardiography and systolic time intervals for 3 h after (1) ethanol 1 g/kg by mouth taken over 60 minutes; (2) atenolol 100 mg by mouth; (3) ethanol (1 g/kg) + atenolol (100 mg). The peak mean blood ethanol (+/- s.e.) was 112 +/- 4 mg/100 ml in test 1 and 104 +/- 7 mg/100 ml in test 3. During increasing blood ethanol, heart rate (HR), systolic blood pressure (BP), cardiac output (CO) and echocardiographic indices of left ventricular (LV) function were significantly augmented, while total peripheral resistance (TPR) decreased. During declining blood ethanol, systolic BP, LV end-diastolic and end-systolic diameters, stroke volume (SV) and circumferential wall stress were significantly reduced; echocardiographic indices of LV function were unaltered, but the pre-ejection period/LV ejection time ratio was increased. Atenolol decreased HR, systolic BP, SV, CO, and all estimates of LV function, but increased TPR. Ethanol + atenolol tended to cause smaller depressions in the indices of LV function than did atenolol alone, in spite of similar plasma atenolol concentrations (n = 6). It is concluded that ingestion of modest doses of ethanol evokes vasodilation and enhances LV function during increasing blood ethanol, and reduces LV preload and afterload during decreasing blood ethanol without impairing contractility. Social drinking and beta blockade seem not to have any harmful acute combined effects on the heart and circulation, at least in normal subjects.
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PMID:Acute effects of alcohol, beta blockade, and their combination on left ventricular function and hemodynamics in normal man. 662 23

One hundred consecutive patients (67 men, 33 women) aged from 15-55 with acute ischemic brain infarction verified by computed tomography and/or angiography and/or brain scanning were studied. In 40 cases the onset of symptoms was preceded within 24 hours by ethanol intoxication. Ethanol intoxication preceding brain infarction was 4-7 times as common in men and 6-15 times as common in women as ethanol intoxication in the general Finnish population of the same age and sex. Nineteen of the patients were heavy drinkers. Heavy drinking was twice as common in men and 5 times as common in women as heavy drinking in the general Finnish population of the same age and sex. Both occasional ethanol intoxication and regular heavy drinking seem to carry an increased risk of ischemic brain infarction. The ethanol-induced risk was highest in middle-aged women and young men.
Stroke
PMID:Ethanol intoxication: a risk factor for ischemic brain infarction. 665 51


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