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

Although there is general agreement that chronic ingestion of alcohol poses great risks for normal cardiovascular functions and peripheral-vascular homeostasis, a direct cause and effect between the real phenomena of alcohol-induced headache and risk of brain injury and stroke is not appreciated. "Binge drinking" of alcohol is associated with an ever-growing number of strokes and sudden death. It is becoming clear that alcohol ingestion can result in profoundly different actions on the cerebral circulation (e.g., vasodilation, vasoconstriction-spasm, vessel rupture), depending upon dose and physiologic state of host. Using rats, it has been demonstrated that acute, high doses of ethanol can result in stroke-like events concomitant with alterations in brain bioenergetics. We review recent in vivo findings obtained with 31P-NMR spectroscopy, optical reflectance spectroscopy, and direct in vivo microcirculatory studies on the intact brain. Alcohol-induced hemorrhagic stroke is preceded by a rapid fall in brain intracellular free magnesium ions ([Mg2+]i) followed by cerebrovasospasm and reductions in phosphocreatine (PCr)/ATP ratio, intracellular pH, and the cytosolic phosphorylation potential (CPP) with concomitant rises in deoxyhemoglobin (DH), mitochondrial reduced cytochrome oxidase aa3 (rCOaa3), blood volume, and intracellular inorganic phosphate (Pi). Using osmotic mini-pumps implanted in the third cerebral ventricle, containing 30% ethanol, it was found that brain [Mg2+]i is reduced 30% after 14 days; brain PCr fell 15%, whereas the CPP fell 40%. Such animals became susceptible to stroke from nonlethal doses of ethanol. Human subjects with mild head injury have been found to exhibit early deficits in serum ionized Mg (IMg2+); the greater the degree of early head injury (30 min-8 h), the greater and more profound the deficit in serum IMg2+ and the greater the ionized Ca (ICa2+) to IMg2+ ratio. Patients with histories of alcohol abuse or ingestion of alcohol prior to head injury exhibited greater deficits in IMg2+ (and higher ICa2+/IMg2+ ratios) and, unlike the subjects without alcohol, did not leave the hospital for at least several days. Women, for some unknown reason, exhibit a much higher incidence of morbidity and mortality from subarachnoid hemorrhage (SAH) than men. Data on 105 men and women with different types of stroke indicate that, on the average, a 20% deficit in serum IMg2+ is seen; total Mg (TMg) or blood pH is usually near normal. Women with SAH, however, exhibit much lower IMg2+ and higher ICa2+/IMg2+ ratios; the presence of ethanol in the blood is associated with even more depression in IMg2+ in SAH in women. It is possible that prior alcohol ingestion is, in large measure, responsible for a great deal of this unexplained higher incidence of SAH in women. It has recently been reported that the cyclical changes in estrogenic hormones appear to control the serum IMg2+ level in young women. A surge in estrogenic levels prior to SAH could thus precipitate, in part, the SAH. In other human studies, it has been shown that migraines and headache, dizziness, and hangover, which accompany ethanol ingestion, are associated with rapid deficits in serum IMg2+ but not in TMg. The former, and the alcohol-associated headache, can be ameliorated with IV administration of MgSO4. Premenstrual tension-headache (PTH) and its exacerbation by alcohol in women is also accompanied by deficits in IMg2+, and elevation in serum ICa2+/IMg2+; IV MgSO4 corrects the PTH and the serum deficit in IMg2+. Animal experiments show that IV Mg2+ can prevent alcohol-induced hemorrhagic stroke and the subsequent fall in brain [Mg2+]i, [PCr], pHi, and CPP. Other recent data indicate that alcohol-induced cellular loss of [Mg2+]i is associated with cellular Ca2+ overload and generation of oxygen-derived free radicals; chronic pretreatment with vitamin E prevents alcohol-induced vascular injury and pathology in the brain. (ABSTRACT TRUNCATED)
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PMID:Association of alcohol in brain injury, headaches, and stroke with brain-tissue and serum levels of ionized magnesium: a review of recent findings and mechanisms of action. 1054 55

Observational data suggest that diets rich in fruits and vegetables and with high serum levels of antioxidants are associated with decreased incidence and mortality of stroke. We studied the effects of alpha-tocopherol and beta-carotene supplementation. The incidence and mortality of stroke were examined in 28 519 male cigarette smokers aged 50 to 69 years without history of stroke who participated in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study). The daily supplementation was 50 mg alpha-tocopherol, 20 mg beta-carotene, both, or placebo. The median follow-up was 6.0 years. A total of 1057 men suffered from incident stroke: 85 men had subarachnoid hemorrhage; 112, intracerebral hemorrhage; 807, cerebral infarction; and 53, unspecified stroke. Deaths due to stroke within 3 months numbered 38, 50, 65, and 7, respectively (total 160). alpha-Tocopherol supplementation increased the risk of subarachnoid hemorrhage 50% (95% CI -3% to 132%, P=0.07) but decreased that of cerebral infarction 14% (95% CI -25% to -1%, P=0.03), whereas beta-carotene supplementation increased the risk of intracerebral hemorrhage 62% (95% CI 10% to 136%, P=0.01). alpha-Tocopherol supplementation also increased the risk of fatal subarachnoid hemorrhage 181% (95% CI 37% to 479%, P=0.01). The overall net effects of either supplementation on the incidence and mortality from total stroke were nonsignificant. alpha-Tocopherol supplementation increases the risk of fatal hemorrhagic strokes but prevents cerebral infarction. The effects may be due to the antiplatelet actions of alpha-tocopherol. beta-Carotene supplementation increases the risk of intracerebral hemorrhage, but no obvious mechanism is available.
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PMID:Controlled trial of alpha-tocopherol and beta-carotene supplements on stroke incidence and mortality in male smokers. 1063 23

Nuclear factor kappa B (NF-kappaB) is a protein transcription factor that is required for maximal transcription of a wide array of pro-inflammatory mediators that are involved in the pathogenesis of stroke. The purpose of this review article is to describe what is known about the molecular biology of NF NF-kappaB and to review current understanding of the interaction between reactive oxygen species (ROS) in NF-kappaB. ROS seem to play a duel role by participating in the NF-kappaB activation cascade and by directly modulating DNA binding affinity. Exogenous and endogenous antioxidants are effective in blocking activation of NF-kappaB and preventing the consequences of pro-inflammatory gene expression. Phase II enzymes either directly or indirectly play a major in vivo role in minimizing oxidative stress by scavenging peroxides, peroxide breakdown products and dicarbonyls and in regeneration of lipid peroxidation chain-breaker, vitamin E. Dietary phase II enzyme inducers have been demonstrated to increase phase II enzyme activities in a variety of tissues. These data, together, suggest that phase II enzyme inducers could have therapeutic value for ameliorating inflammatory conditions.
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PMID:Redox regulation of nuclear factor kappa B: therapeutic potential for attenuating inflammatory responses. 1066 5

Free radical are highly reactive chemical species with an unpaired electron in an atomic or molecular orbital. In biological systems, the most important free radicals are superoxide anion and hydrogen peroxide; in the presence of transition metals such as iron, copper and manganese both these free radicals produce hydroxyl radicals. Free radicals attack proteins, nuclei acids and membranes containing large quantities of polyunsaturated fatty acids. Because of their toxicity, the organism has developed ways to deactivate them. The superoxide dismutase enzyme (SOD) catalyzes dismutation of the superoxide radical into hydrogen peroxide and oxygen hydrogen peroxide is in turn reduced to water and oxygen by peroxidase glutathione and catalase enzymes. The production of radicals in the brain is due to catecholamine metabolism such as dopamine and norepinephrine and is increased by the presence of transition metals and by a deficiency of antioxidant agents such as vitamin E. Two main groups of dementia exist in older age: the multi-infarctual dementias, caused by cerebrovascular disorders and the primary degenerative disorders such as Alzheimer, where no vascular disease is evident. Free radicals play an important role in Parkinson's disease, in Alzheimer's disease and in stroke. The value of SOD and CAT activity following the above mentioned degenerative diseases differ among the various studies carried out. In Alzheimer's disease, the value of SOD activity probably increases in the neuropathologically involved areas. In stroke, the SOD value does not vary either in the ischemic area or in the peri-infarctual one during the first 24 hrs after lesion, while the CAT value decreases.
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PMID:Free radicals: important cause of pathologies refer to ageing. 1070 16

Observational studies have shown an inverse relationship between consumption of fruits and vegetables high in beta-carotene, vitamins C and E, and ischemic heart disease (IHD) and stroke. In large observational studies, beta- carotene reduced the risk of IHD events in men, particularly in smokers. In contrast, four large randomized trials did not reveal a reduction in cardiovascular events with beta-carotene use, and may, in fact, increase IHD and total mortality in male smokers. There have been only a few large observational studies and one randomized trial with vitamin C, which have shown no beneficial or deleterious impact of this vitamin on cardiovascular events. Most large observational studies have shown an inverse relationship between vitamin E and IHD. However, a meta-analysis of the four randomized trials done in Europe and America involving a total of 51,000 participants allocated to vitamin E or placebo for 1.4 to 6 years, did not demonstrate a reduction in cardiovascular and IHD mortality and nonfatal myocardial infarction. Currently, there are no data to support the use of these vitamins to reduce the risk of cardiovascular events. Trials are in progress to determine whether a longer duration of administration of vitamin E or the association of vitamin E with cofactors may reduce cardiovascular events.
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PMID:Beta-carotene, vitamin C, and vitamin E and cardiovascular diseases. 1095 62

A recent large-scale, open-label, randomized, controlled trial in 11, 324 myocardial infarction (MI) survivors has shown low-dose fish oil, but not vitamin E, to reduce significantly the cumulative rate of all-cause death, nonfatal MI, and nonfatal stroke. Neither intervention significantly reduced the other primary endpoint, the cumulate rate of cardiovascular death, nonfatal MI, and nonfatal stroke. Analysis of secondary endpoints indicated that the benefits of the 875 mg fish oil capsules containing 850 to 882 mg eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) as ethyl esters was in reducing mortality and not in a reduction of nonfatal MI. It was a safe intervention. The internal validity and external validity of the data was examined and the findings placed in clinical perspective. Important questions remain about the benefits of increased plant sources of n-3 polyunsaturated fatty acids (PUFA) for those who cannot obtain or consume fish. Also the benefits of diet versus fish oil supplementation haven't been determined precisely. Although it seems reasonable to increase sources of n-3 PUFA in the diet for those at high risk of coronary heart disease, current data do not support a policy of promoting fish oil capsules for secondary prevention of coronary heart disease.
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PMID:The Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardio (GISSI)-Prevenzione Trial on fish oil and vitamin E supplementation in myocardial infarction survivors. 1098 Sep 13

Dietary antioxidants and folic acid may play a role in the pathophysiology of coronary disease and stroke. We review patient-oriented evidence on the effectiveness of supplementation with antioxidants and/or folic acid in the prevention of myocardial infarction and stroke. Observational data suggest cardiovascular benefit of vitamin E supplementation, but results of controlled clinical trials are inconsistent regarding the effect on nonfatal myocardial infarction. Moreover, studies have not shown a protective effect of vitamin E against fatal myocardial infarction and have not addressed stroke. For vitamin C and folic acid supplementation, observational data are inconsistent and controlled clinical trials are lacking. Thus, the available evidence is insufficient to recommend the routine use of vitamin E, vitamin C or folate supplements for the prevention of myocardial infarction or stroke. The evidence argues against the use of beta carotene supplements for this purpose. The costs and risks associated with these supplements are low, however, and physicians may choose to recommend vitamin E, folate and/or vitamin C supplementation pending conclusive evidence from clinical trials.
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PMID:Update on vitamin supplements for the prevention of coronary disease and stroke. 1101 58

Low density lipoprotein (LDL) oxidation is considered an important step in the atherogenic process. Oxidatively modified particles induce the expression of adhesion molecules, stimulate the production of inflammatory cytokines and impair endothelial function. The measurement of oxidised LDLs in vivo is very difficult, therefore most investigators rely on the measurement of in vitro oxidability of these particles to evaluate their deleterious effects. Supplementation with water and lipid soluble anti-oxidant vitamins, especially vitamin C and E, significantly increase the resistance to LDL oxidation. Vitamin E supplementation also improves endothelium-dependent vasodilation in hypercholesterolaemic and subjects who smoke cigarettes. Epidemiological studies have not consistently demonstrated a protective effect of vitamin E consumption as food or supplements on coronary events or stroke. Likewise, only one of five large prospective trials has shown a beneficial effect of vitamin E supplementation on cardiovascular events or mortality. One report showed that supplemented haemodialysed patients had a lower incidence of cardiovascular events. Thus, presently, there is not enough evidence to widely recommend the use of vitamin E supplements for vascular protection.
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PMID:Therapeutic potential of vitamin E in heart disease. 1106 Aug 25

In-vitro studies and animal model studies provide an ever-growing body of evidence, direct and indirect, that oxidation of low-density lipoprotein and/or related oxidative mechanisms play a role in atherogenesis. However, two recent, very large, carefully conducted clinical intervention trials using adequate doses of vitamin E demonstrated no effect on a composite end-point of non-fatal infarction, stroke or death from cardiovascular causes. Why the unexpected negative results? Possibly because the animal intervention evidence on which these trials were based deals primarily with very early lesions (fatty streaks). That evidence does not necessarily provide a basis for predicting what antioxidant intervention will do in patients with advanced lesions, particularly when the end-points used relate to unstable plaques and fatal thrombosis, events for which we have no adequate animal models. Nor does it necessarily follow that the same antioxidants used successfully in animals will be effective in humans. The strength of the evidence for the oxidative modification hypothesis is such that negative clinical trials with one particular antioxidant, in patients with very advanced coronary heart disease and lasting only 3-5 years, should not be taken as refutation of the hypothesis. Perhaps different kinds of human trials are needed, trials in which the development of new lesions is measured, in order to test whether antioxidants can decrease the rate of initiation and early progression of atherosclerosis as they do in animals. The answer to the title query is 'Probably, but it is too soon to say'.
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PMID:Is there a potential therapeutic role for vitamin E or other antioxidants in atherosclerosis? 1108 33

30 patients with CT proven infarct presenting within 24 hours of the acute event were included in the study with 20 age and sex matched controls. On day 1 and day 15 of stroke, levels of plasma lipid peroxide (oxidant) and plasma alpha-tocopherol and beta carotene (antioxidant) were estimated. The patients were randomly assigned to two groups, one group receiving 300 mg/day of vitamin E for 15 days. Neurological examination was conducted according to Mathew scale on day 1 and day 15 and rehabilitation assessment was done at day 15 and at 6 weeks according to Barthel Index. On day 1, the mean value of plasma lipid peroxidation in controls was 4.97 +/- 1.44 nmol/ml and in stroke patients 5.89 +/- 1.56 nmol/ml (p < 0.05). The plasma beta-carotene in controls was 2.35 +/- 1.09 mg/L while in stroke patients was 1.07 +/- 0.55 mg/L (p < 0.001) and plasma alpha-tocopherol in control 9.74 +/- 2.76 micrograms/ml as compared to 7.57 +/- 2.92 micrograms/ml in stroke patients (p < 0.02). Initially the plasma lipid peroxide levels are high and antioxidant levels are low in patients of ischemic stroke. Exogenous vitamin E supplementation does not have any significant effect on early neurological outcome but it does bring about significant changes in subsequent recovery and rehabilitation of patients of stroke.
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PMID:Lipid peroxide, beta-carotene and alpha-tocopherol in ischaemic stroke and effect of exogenous vitamin E supplementation on outcome. 1122 81


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