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

Immediate circulatory reactions to acute intragastric ethanol administration were studied by a catheterization technique in spontaneously breathing dogs. Diluted ethanol was given in a dosage of 1 g/kg in test group I (n = 11), and 2/kg in group II (n = 10). The control group (m = 14) received only water. The highest blood ethanol concentration was 0.90 +/- 0.07 mg/ml (mean +/- SE) in group I, and 1.97 +/- 0.10 mg/ml in group II. Heart rate and cardiac output increased (p less than 0.,001), but stroke volume, mean aortic blood pressure and right atrial blood pressure remained practically unchanged. Systemic vascular resistance decreased. Mean pulmonary arterial blood pressure increased markedly in both test groups (p less than 0.001) while pulmonary arterial wedge pressure did not change. The pulmonary arterial resistance increased (p less than 0.01). Changes in respiratory rate or volume and arterial pO2 were negligible in group I, but respiratory minute volume decreased in group II. In conclusion, ethanol in concentrations 0.5 to 2.0 mg/ml increased resistance in the pulmonary arterial tree, indicating pulmonary arterial vasoconstriction, but reduced systemic vascular resistance, thus putting a concept of peripheral vasodilation in favour.
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PMID:Influence of ethanol on systemic and pulmonary hemodynamics in anesthetized dogs. 662 4

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

This study evaluates the hypothesis that ethanol alone, or in diluents for drugs used to protect hypoxic mice, is responsible in part for an increased tolerance to hypoxia (4-5% oxygen). The change in hypoxic tolerance following i.v. or i.p. administration of ethanol, diazepam, nimodipine and various diluent components was measured. Diazepam (50 mg/kg i.v.) increased hypoxic tolerance to 700 +/- 47% (n = 11) of saline control, its diluent increased hypoxic tolerance to 468 +/- 60% (n = 10) of saline control but the ethanol component of the diluent accounted for almost half of this diluent effect. Nimodipine (2 mg/kg i.p.), a calcium antagonist, increased tolerance to 180 +/- 18% of control (n = 19) and nimodipine diluent showed an even greater increase to 226 +/- 25% of control (n = 15). In this case essentially all of the protective effect of nimodipine diluent (81.3%) is accounted for by ethanol. Dose response curves indicate the maximum ethanol induced increase in hypoxic tolerance was approximately 335% of control at a dose of 2.4 g/kg. Buffers, etc. in the diluents evidently add to the protective effect of ethanol. Our data clearly indicate ethanol is the important component of some treatments which protect mice from hypoxia. The pharmacological activity of ethanol, even when used in a diluent, should not be ignored in evaluating therapeutic intervention for protection from hypoxia.
Stroke
PMID:The role of ethanol in diluents of drugs that protect mice from hypoxia. 665 66

This study was undertaken to investigate to what extent the cardiodepression of acute alcohol intoxication is dose-dependent and to assess the validity of isovolumetric and afterload parameters in the latter condition. Isovolumetric and ejection phase parameters were measured in-situ in the intact heart of the guinea pig. The diastolic and systolic pressure-volume-relationships were calculated on the basis of direct measurements obtained at control conditions and during acuta alcohol intoxication at blood alcohol concentrations (BAC) of 160 and 280 mg/100 ml, respectively. Cardiodepression was dose-dependent; left ventricular isovolumetric pressure fell 13% at a BAC of 280 mg/100 ml, maximal rate of pressure rise (dp/dt max) decreased 33%. The changes in afterload parameters were less consistent: there was an increase in left ventricular isovolumetric pressure and dp/dt max in the group with BAC of 160 mg/100 ml, but both of these parameters decreased at BAC levels of 280 mg/100 ml. Stroke volume and preload decreased comparably in both groups. The divergent pattern of induced hemodynamic alterations may be due to peripheral effects of ethanol and/or counter-regulatory adrenergic mechanisms. The mortality rate associated with BAC of 160 mg/100 ml was 55% and that of 280 mg/100 ml was 75%.
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PMID:[Left ventricular hemodynamics in acute alcohol intoxication in guinea pigs]. 668 33

The acute cardiac effects of ethanol (1 g/kg orally within 60 minutes) were examined in 22 healthy volunteers (11 men and 11 women) by M-mode echocardiography and systolic time intervals for three hours after beginning ingestion. Each subject also took part in a control study, in which the same volume of juice was substituted for ethanol. Heart rate increased by 15% and cardiac output by 17% during ethanol intake, while total peripheral resistance decreased by 15%. Left ventricular end-diastolic diameter was shortened by 2% during the declining phase of blood ethanol concentration; stroke volume and circumferential wall stress were simultaneously decreased by 7% and 5%, respectively. No ethanol-related changes were noted in echocardiographic indices of left ventricular function, neither were any sex differences observed in the cardiovascular changes after ethanol ingestion. Each of the systolic time intervals was significantly altered even during the control experiment. The responses of each of these intervals to ethanol differed significantly from those in the control test as well. Notably, the pre-ejection period/ejection time ratio rose after ethanol, this change, according to simultaneous echocardiographic data, resulting from reduced preload instead of impaired contractility, as maintained in previous investigations. It is concluded that alcohol in modest doses is capable of altering each of the extramyocardial influences on left ventricular function--heart rate, preload, and afterload--but does not impair myocardial performance, at least in normal subjects.
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PMID:Acute cardiovascular effects of ethanol A controlled non-invasive study. 682 40

Cerebrospinal fluid (CSF) pleocytosis after seizure activity has been anecdotally reported for many years, but it has not been well documented. We reviewed the records of all adult patients admitted to Grady Memorial Hospital from November 1979 through October 1980 with the diagnosis of seizure. Of 102 patients whose CSF was examined, 35 (34%) had pleocytosis; in 31 (30%) there was no explanation for the pleocytosis despite laboratory and radiologic tests to rule out established causes. For those patients without an identifiable cause of pleocytosis the mean number of white cells was 72/cu mm with a median of 10 and a range from 3 to 464. A predominance of polymorphonuclear leukocytes (PMNs) was found in 57% of the initial CSF examinations. Eighty-six percent of patients with seizures due to ethanol withdrawal had a PMN predominance in their CSF, and 88% of patients with seizures due to a recent or remote cerebrovascular accident had a mononuclear cell predominance. The pleocytosis was usually transient; normalization of the CSF was associated with the rapid recovery of the patient. We conclude that an abnormal CSF leukocyte count may be entirely attributable to seizure activity, although the mechanism is unknown. Before assigning this cause, however, a thorough search is imperative to rule out treatable disorders that may cause CSF pleocytosis.
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PMID:Cerebrospinal fluid pleocytosis after seizures. 682 99

Ethyl alcohol produced graded contractile responses in rat cerebral arterioles and venules in vivo and in isolated canine basilar and middle cerebral arteries at a concentration range (10 to 500 milligrams per deciliter) which parallels that needed for its graded effects of euphoria, mental haziness, muscular incoordination, stupor, and coma in humans. Two specific calcium antagonists, nimodipine and verapamil, prevented or reversed the alcohol-induced cerebrovasospasm and thus may prove valuable in treating the hypertension and stroke observed in heavy users of alcohol.
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PMID:Alcohol-induced spasms of cerebral blood vessels: relation to cerebrovascular accidents and sudden death. 683 78

Cardiac effects of ethanol ingestion (1.75 g/kg within 3 hours) were examined in 8 healthy males by echocardiography and systolic time intervals in a controlled study. Heart rate (HR) was increased by 15% (p less than 0.05) during intoxication when blood ethanol (mean +/- SD) was 33.7 +/- 4.1 mmol/l. Left ventricular (LV) end-diastolic dimension was simultaneously shortened by 4% (p less than 0.01) and LV end-systolic dimension by 3% (p less than 0.05). Stroke volume was reduced by 12% (p less than 0.05). Most subjects experienced hangover symptoms 12 hours after the beginning of ethanol intake; blood ethanol was 8.8 +/- 4.0 mmol/l. At this time, HR was raised by 17% (p less than 0.05), ejection fraction by 7% (p less than 0.05), and circumferential fiber shortening velocity by 19% (p less than 0.01); total peripheral resistance was decreased by 17% (p less than 0.001). The resultant increase in cardiac output amounted to 22% (p less than 0.01). In short, the main effect of ethanol at modest blood concentrations was to reduce LV preload without detectably impairing myocardial performance. Hangover was characterized by vasodilation as well as intensified LV myocardial and pump performances.
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PMID:Drunkenness, hangover, and the heart. 683 36

To evaluate the hemodynamic changes related to alcohol flush, the effects of ethanol intake (0.5 g/kg) were studied by echocardiography and systolic time intervals in 10 Finnish and 9 Japanese healthy volunteers. In 5 Japanese subjects, post-drink facial flush was associated with elevated blood acetaldehyde (peak levels 20-83 mumol/l) and marked cardiocirculatory stimulation. Heart rate was increased directly post ingestion by 65% (p less than 0.01), stroke index by 23% (p less than 0.05), and cardiac index by 106% (p less than 0.05). Diastolic blood pressure was simultaneously decreased by 23% (p less than 0.05), peripheral vascular resistance by 54% (p less than 0.01), and circumferential wall stress by 22% (p less than 0.05); ejection fraction was raised by 26% (p less than 0.01). The other Japanese and the Finnish subjects had no detectable acetaldehyde in blood after ethanol ingestion. The average hemodynamic alterations in them were similar in direction to the changes presented above, but quantitatively 6-10 times smaller (p less than 0.005 for each of these variables). Thus, in Orientals with genetically defective acetaldehyde oxidation, ingestion of even small amounts of alcohol evokes intense enhancement of left ventricular function, probably because of acetaldehyde-induced catecholamine release and peripheral vasodilation.
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PMID:Alcohol and the heart. Intense hemodynamic changes associated with alcohol flush in orientals. 683 37


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