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

We examined the prevalence of high ethanol intake, hypertension, and other risk factors for intracerebral hemorrhage in a case-control study of 24 young and middle-aged patients with intracerebral hemorrhage. We recorded ethanol consumption, history of hypertension, liver disease, cigarette smoking, and mild or severe coagulation disorder in each case of intracerebral hemorrhage and in 48 control patients matched by sex and age. In univariate matched analyses, the frequencies of high ethanol intake (p = 0.009), hypertension (p = 0.05), and coagulation disorder (p = 0.05) were higher in the cases than in the controls. After controlling for possible confounding factors, we found that high ethanol intake and hypertension were the only independent risk factors for intracerebral hemorrhage (p = 0.02 and p = 0.05, respectively). The hemorrhagic lesion found in cases with a high ethanol intake tended to be located in the cerebral lobes (p = 0.01), contrasting with the typical basal ganglia location of hypertensive hematomas (p = 0.009). We conclude that chronic, high ethanol intake should be considered as an important risk factor for lobar hematomas in young and middle-aged people.
Stroke 1990 Nov
PMID:High ethanol consumption as risk factor for intracerebral hemorrhage in young and middle-aged people. 223 44

The cystic duct and gallbladder were ablated in eight patients with acute gallbladder disease who had been treated with minicholecystostomy instead of cholecystectomy because of multiple risk factors. First, endoluminal transcatheter radio-frequency electrocoagulation of the cystic duct was performed under fluoroscopic control, which resulted in complete occlusion in all eight patients. Next, the mucosa of the isolated gallbladder was sclerosed with 95% ethanol and 3% sodium tetradecyl sulfate in one to four sessions; no analgesics were required. The gallbladder volumes of all patients, estimated by means of ultrasound, were 1.5-22 cm3 (average, less than 10 cm3) after a mean follow-up period of 5 months. One patient died of a cerebrovascular accident 15 months after sclerotherapy. In all surviving patients, the gallbladder fistulas are dry and obliterated. These early clinical data indicate that electrocoagulation permits reliable, safe obliteration of the human cystic duct. The authors believe that sclerotherapy of the isolated gallbladder is feasible without toxic effects but that their treatment needs adjustment to achieve complete ablation of the gallbladder mucosa in a shorter period and in all patients.
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PMID:Ablation of the cystic duct and gallbladder: clinical observations. 238 27

The laterofrontal (LF) cirri on isolated gill filaments of Mytilus edulis, prepared in natural seawater, are active and initially beat with an average frequency of about 8 Hz (with a range of 6-14 Hz). However, the lateral (L) cilia on these filaments are arrested in a position at the end of their recovery stroke. Perfusion of the filament with artificial seawater (ASW), with or without 1% ethanol, has little or no biological effect on the activity of the LF cirri, although a transitory decrease in frequency often accompanies the perfusion process. The L cilia remain arrested during perfusion with ASW. The exposure of the gill to low levels of 5-hydroxytryptamine (5HT) (10(-8) less than 5HT less than 10(-7) M) has no effect on the activity of the LF cirri but stimulates the L cilia to beat. Exposure to higher concentrations of 5HT (greater than 10(-7) M) elevates the beat frequency of the L cilia and simultaneously inhibits the activity of the LF cirri, leading to their arrest in a position at the end of the effective stroke. This arrest of the LF cirri occurs as the L cilia attain a 5HT-induced beat frequency between 12 to 14 Hz. The influence of 5HT on the L cilia and the LF cirri can be reversibly mimicked or enhanced by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). A concentration of 0.5 mM IBMX mimics low 5HT concentrations (about 10(-7) M) by stimulating the L cilia to beat without affecting the beat frequency of the LF cirri. A combination of 10(-7) M 5HT and 0.5 mM IBMX in ASW mimics high (greater than 10(-6) M) 5HT concentrations by arresting the LF cirri and increasing the beat frequency of the L cilia. Under these conditions, the threshold of the LF cirri arrest response is again found to occur as the L cilia attain a beat frequency of 12-14 Hz. These results suggest that the mechanisms of LF cirri arrest and L cilia activation are mediated by 5HT-induced changes in intracellular cyclic AMP levels.
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PMID:The antagonistic effects of 5-hydroxytryptamine and methylxanthine on the gill cilia of Mytilus edulis. 241 3

We used a gerbil model of cerebral ischemia to study the effects of ion channel blockers on neuronal death resulting from enhanced glutamate release and calcium ion influx. The common carotid arteries of gerbils were occluded for 5 minutes and injected intraperitoneally immediately after ischemia with an alkylene iminopropylene derivative (glutamate blocker) or a piperazinyl ethanol derivative (calcium blocker) given at high or low doses. Two vehicle groups received saline or 0.2% methyl cellulose solution. Seven days later, the gerbils were perfusion-fixed and their brains were processed for histologic study. The number of neurons per millimeter (neuronal density) of the CA1 region was calculated, and the neuronal density in each group was statistically compared using the Mann-Whitney U test. Compared with a control group not subjected to carotid ligation, neurons of the two vehicle groups and the low-dose calcium blocker group were almost nonexistent in the CA1 region. Neuronal densities of the glutamate blocker group and the high-dose calcium blocker group were similar and were found to be within normal limits by statistical analysis. Our study shows that detrimental membrane phenomena and the incidence of delayed neuronal death may be counteracted by the systemic administration of these ion channel blockers after ischemic insult.
Stroke 1988 Aug
PMID:Prevention of delayed neuronal death in gerbil hippocampus by ion channel blockers. 245 32

Afterload reduction is an accepted therapeutic modality for the treatment of congestive heart failure caused by chronic aortic regurgitation. However, the role of vasodilator therapy in acute aortic incompetence has not been established. To investigate this, left ventricular volume overload was produced in 18 dogs by constructing a valved conduit from the descending thoracic aorta to the left ventricular apex. The time course of aortic, pulmonary and conduit flows was analyzed in eight control studies and established stability of the experimental model. In the remaining 10 dogs, intravenous nitroglycerin, titrated to reduce mean aortic blood pressure by 40%, and placebo (ethanol) were each infused for 20 min periods. Compared with placebo, nitroglycerin significantly reduced aortic flow (3,945 +/- 324 to 3,397 +/- 362 ml/min, p less than 0.01), regurgitant flow (1,304 +/- 131 to 764 +/- 90 ml/min, p less than 0.001), septal-lateral end-diastolic diameter (47.5 +/- 1.8 to 46.5 +/- 1.8 mm, p less than 0.001), left ventricular end-diastolic pressure (6.9 +/- 0.8 to 6.0 +/- 0.6 mm Hg, p less than 0.05), left ventricular stroke work (19.0 +/- 2.6 to 10.8 +/- 1.7 g-m/beat, p less than 0.001) and systemic vascular resistance (2,253 +/- 173 to 1,433 +/- 117 dyne-s/cm5, p less than 0.001). In contrast, pulmonary flow, left anterior descending coronary flow and subendocardial pH did not change during infusion of either nitroglycerin or placebo. These data indicate that by decreasing preload and afterload, and by preserving coronary flow and tissue pH, nitroglycerin effectively reduced ventricular and regurgitant volumes in the setting of acute volume overload.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of nitroglycerin in an experimental model of acute aortic regurgitation. 249 44

An extensive search of the English-language literature identified 62 epidemiologic studies that examined the relation between moderate alcohol consumption and risk of stroke. Moderate drinking (less than 60 g ethanol/day) and ischemic stroke have a complex association that might be explained by interaction with race; a J-shaped association has been found in predominantly white populations, while little (if any) association has been found among Japanese. By contrast, moderate drinking increases risk of both intracerebral and subarachnoid hemorrhage in diverse populations. There is insufficient epidemiologic evidence to conclude whether recent alcohol use affects risk of either ischemic or hemorrhagic stroke. These distinctive associations help explain contradictory reports on the relation between moderate alcohol consumption and risk of "stroke." The high prevalence of alcohol use throughout the world suggests opportunities for primary prevention and the importance of continued research in this area.
Stroke 1989 Dec
PMID:Moderate alcohol consumption and stroke. The epidemiologic evidence. 268 94

The alcoholism is no hereditary but genetic factors can be involved and racial differences in alcohol susceptibility depend on break down rate of ethanol. The alcohol adaptation and tolerance and physical dependence appearance with symptoms and signs display after abstinence on people suffers with chronic intoxication, it would be related to changes caused by alcohol over molecules of neuronal membranes, especially proteins and receptors. An account is achieved about the various neurologic manifestations related to alcoholism, nutritional in origin or unknown pathogenesis. The results obtained looking over the admission along 1988 in Neurological Service ("La Paz" Hospital) allowed to take into account three groups of alcoholic patients (miscellaneous, abstinence syndrome-encephalopathy-dementia-neuropathy, and stroke). It is analysed the results and it is afforded some conclusions about.
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PMID:[Neurologic effects of alcoholism]. 270 Feb 94

The nervous system is particularly susceptible to the harmful effects of alcohol. These include Wernicke-Korsakoff syndrome, which is related to thiamine deficiency secondary to chronic alcohol abuse. Other neurotoxic effects of alcohol with cognitive impairments include delirium tremens, alcoholic seizures or "rum fits," and alcoholic neuropathies. It has become recognized in recent years that alcohol and its metabolites directly damage the nervous system even in the absence of nutritional deficiencies. Cerebral blood flow (CBF) measurements provide a noninvasive indirect monitor of cerebral metabolic activity. It has been shown conclusively that CBF measured by the 133Xe inhalation method is decreased in chronic alcoholism, correlating well with the amount of alcohol consumed. With abstinence, CBF returns toward normal levels provided the neurotoxic effects of chronic alcoholism are of recent onset. Clinical and pathological studies show significant loss of brain volume with ventricular dilatation after alcohol abuse even among young "social" drinkers. This toxic effect of alcohol is accompanied by varying degrees of cognitive impairments ranging from slight memory loss to frank dementia. Both the decrease in brain volume and the cognitive impairments, which occur with or without nutritional deficiency, are to a large extent reversible with abstinence and nutritional supplementation. Alcohol appears to accelerate age-related declines in CBF while nutritional deficiencies enhance the neurotoxic effects of alcohol. Measurements of local CBF (LCBF) and partition coefficients (L lambda) in deep cerebral structures, including the hypothalamus, thalamus, forebrain nuclei, and limbic system, can be achieved utilizing three-dimensional methods after inhalation of stable xenon as a contrast medium combined with serial computed tomographic imaging of the brain. Among chronic alcoholics, there are significant and diffuse reductions in cortical and subcortical gray matter CBF that are especially remarkable in hypothalamus and substantia innominata, which includes the nucleus basalis of Meynert, a major source of cholinergic input to neocortex and hippocampus. Reductions in LCBF are measurable in cognitively impaired patients with and without Wernicke-Korsakoff syndrome. Reductions of CBF include white matter and are more severe in patients with Wernicke-Korsakoff syndrome. Both types of encephalopathy improve with treatment, but recovery is usually more rapid and complete if nutritional deficiency is absent. Alcohol also appears to be a risk factor for stroke, possibly by depleting neuronal reserves and unfavorably influencing cardiovascular risks.
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PMID:Cerebral hemodynamic and metabolic effects of chronic alcoholism. 270 68

Clinical studies using 31P and 1H MRS with a whole body 2.0 T MRI/MRS system are described. In most cases, techniques to quantitate absolute molar concentrations of metabolites in various organs were used. In the brain, AIDS, chronic stroke, and white matter lesions were associated with alterations of brain 31P metabolites. Epilepsy was associated with increased pH in the seizure focus. In the heart, dilated cardiomyopathy was associated with increased PDE/ATP while PCr/ATP was unchanged. In the liver, alcoholic hepatitis and cirrhosis were associated with diminished hepatic ATP while alcoholic hepatitis had increased pH and cirrhosis had decreased pH. This allowed differentiation of normal liver, alcoholic hepatitis, and alcoholic cirrhosis without biopsy. In the prostate, malignancy was associated with increased PME/ATP and decreased PCr/ATP. The PME/PCr was greatly increased in malignant prostate with no overlap in normals. Other cancers outside the brain had increased PME and effective treatment was often associated with diminished PME. 1H MRS of the brain was performed using ISIS and outer volume suppression pulses for volume localization. Excellent high resolution 1H water-suppressed spectra were obtained at echo times as short as 30 ms, showing well resolved peaks for lactate, N-acetylaspartate, glutamate, choline, creatinine, and inositol. 1H MRS demonstrated that the uptake of ethanol by the brain was slower than the rise of ethanol in blood. 31P spectroscopic imaging of the brain with resolution of 2.25 x 2.25 x 2.5 cm produced metabolic images and high resolution spectra from desired regions of interest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical magnetic resonance spectroscopy of brain, heart, liver, kidney, and cancer. A quantitative approach. 270 9

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.
Alcohol
PMID:Effect of varying concentration of ethanol on systemic hemodynamics and regional circulation. 271 21


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