Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of vitamin E, betamethasone and mannitol upon a series of pathological free radical reactions within hypoxic brain tissue was evaluated by the chemiluminescence method. Hypoxia was induced by arterial hypoxemia (PaO2 17-22 mmHg) with normocapnia (PaCO2 28-38 mmHg) and normotension (MABP 100-140 mmHg). 4% O2-96% N2 mixed gas was used to obtain the lowered PaO2. In the untreated group, increased chemiluminescence was measured in the hypoxic state and the early stage of the initial post-hypoxic state. In the groups administered vitamin E, betamethasone, mannitol and a combination of them reduced chemiluminescence was detected. To explore the reaction stage at which the drugs act in lipid peroxidation, chemiluminescence spectra was analyzed using the brain homogenate with the drugs added. Intensity peaks of the spectra were around at 480, 520-530, 570, 620-640, 680-700 nm before addition of the drugs. All the intensity peaks diminished after addition of vitamin E and betamethasone, but very little decrease occurred after mannitol. The lowered chemiluminescence value may indicate the free radical scavenging action of vitamin E, betamethasone and mannitol in vivo. Chemiluminescence spectrum analysis shows that vitamin E and betamethasone act on the late chain reaction following hydroperoxide and mannitol acts on the early reaction--generation of active oxygens.
Stroke
PMID:Chemiluminescence in hypoxic brain--the second report: cerebral protective effect of mannitol, vitamin E and glucocorticoid. 392 29

The biochemical, clinical, and genetic features were examined in the proband (homozygote) and heterozygotes (n = 17) affected with familial apolipoprotein A-I and C-III deficiency, variant II (previously described as apolipoprotein A-I absence). The proband was a 45-year-old white female with mild corneal opacification and significant three-vessel coronary artery disease (CAD), who died shortly after bypass surgery. Autopsy findings included significant atherosclerosis in the coronary and pulmonary arteries and the abdominal aorta as well as extracellular stromal lipid deposition in the cornea. No reticuloendothelial lipid deposits in the liver, bone marrow, or spleen were noted (unlike Tangier disease). Laboratory features included marked high density lipoprotein (HDL) deficiency and undetectable plasma apolipoproteins (apo) A-I and C-III. The percentage of plasma cholesterol in the unesterified form was normal at 30%. The activity and mass of lecithin:cholesterol acyltransferase (LCAT) were 42% and 36% of normal, respectively, and the cholesterol esterification rate was 43% of normal. Deficiencies of plasma vitamin E and essential fatty acid (linoleic, C18:2) were also noted. Evaluation of plasma lipoproteins and apolipoproteins in 37 kindred members revealed 17 heterozygotes with HDL cholesterol values below the 10th percentile of normal. Of these, all had apoA-I levels more than one standard deviation below the normal mean, and 37.5% had a similar decrease in apoC-III values. Mean (+/- SD) plasma HDL cholesterol, apoA-I, and apoC-III values (mg/dl) in heterozygotes were 54.0%, 62.4%, and 79.2% of normal, respectively. No evidence of CAD was observed in 10 heterozygotes 40 years of age or less; however, CAD was detected in 3 of 7 heterozygotes over 40 years of age, one of whom died at age 56 years of complications of myocardial infarction and stroke. The inheritance pattern in this kindred was autosomal codominant. ApoA-I isolated from a heterozygote had an isoelectric focusing pattern and amino acid composition similar to normal. Utilizing DNA isolated from two obligate heterozygotes, no abnormalities in the apoA-I or apoC-III genes were detected by Southern blot analysis utilizing specific probes following restriction enzyme digestion. The data indicate that familial apolipoprotein A-I and C-III deficiency, variant II, is similar to variant I (described by Norum et al. 1982. N. Engl. J. Med. 306: 1513-1519), but differs at the clinical level (lack of xanthomas), the biochemical level (lack of detectable apoA-I, lower apoA-II level), and at the gene level.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Familial apolipoprotein A-I and C-III deficiency, variant II. 393 6

We previously published results of investigations which indicated that the combination of mannitol, which acts as a free radical scavenger, and perfluorochemicals (PFC), which have a strong oxygen-carrying capacity, can be therapeutic in cases of brain infarction. The present experiment tested the hypothesis that the effectiveness of such treatment could be increased by an optimal combination of such scavengers and other chemicals. Fifty-two dogs were used, employing the "canine model of a completely ischemic brain regulated with the perfusion method." A total of six drugs with free radical scavenger capacities were tested: mannitol, vitamin E, vitamin C, Nizofenone (Y-9197), dexamethasone (DEXA) and suloctidil (MY-103). These drugs were administered intravenously 15 minutes prior to the production of ischemia, when cerebral blood flow was reduced to one-tenth its normal volume. After one hour, recirculation was allowed and the recovery of electrical activity of the brain observed for three hours. Judged by the degree of recovery of brain electrical activity, five drugs were considered to have protective effect against brain ischemia: mannitol, vitamin E, MY-103, DEXA and Y-9197. Among these five drugs, mannitol, vitamin E and DEXA are known to be safe and easily used clinically. The combined administration of these three drugs, together with PFC, was also investigated. It was found that the speed and degree of recovery of brain electrical activity were greater when these drugs were given together than when one was administered alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke
PMID:The protective effect of combined administration of anti-oxidants and perfluorochemicals on cerebral ischemia. 608 1

The platelet survival time was shortened in stroke-prone spontaneously hypertensive rats (SHRSP) at 10 weeks of age on feeding the regular diet but it was normalized on administering the vitamin E-supplemented diet. Platelet survival time was normal in stroke-resistant spontaneously hypertensive rats (SHRSR) at 10 weeks of age on feeding the regular diet but it was shortened when supplying the vitamin E-free diet. The maximal uptake of 75Se-selenomethionine by platelets was increased in SHRSP at 10 weeks of age on feeding the regular diet. It was further increased in SHRSP on feeding the vitamin E-free diet. On the other hand, the increased maximal uptake of 75Se-selenomethionine by platelets was normalized in SHRSP on feeding both the vitamin E-supplemented diet and the vitamin E-supplemented diet after administering the vitamin E-free diet. Therefore, we concluded that the deficiency of vitamin E brought about the shortening of platelet survival time and enhanced platelet production.
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PMID:The effect of vitamin E on platelet kinetics of stroke-prone spontaneously hypertensive rats (SHRSP). 709 71

One hundred patients with transient ischemic attacks, minor strokes, or residual ischemic neurologic deficits were enrolled in a double-blind, randomized study comparing the effects of aspirin plus vitamin E [0.4 g (400 IU)/d; n = 52] with aspirin alone (325 mg; n = 48). The patients received study medication for 2 y or until they reached a termination point. Preliminary results show a significant reduction in the incidence of ischemic events in patients in the vitamin E plus aspirin group compared with patients taking only aspirin. There was no significant difference in the incidence of hemorrhagic stroke although both patients who developed it were taking vitamin E. Platelet adhesion was also measured in a randomized subgroup of both study populations by using collagen III as the adhesive surface. There was a highly significant reduction in platelet adhesiveness in patients who were taking vitamin E plus aspirin compared with those taking aspirin only. Measurement of alpha-tocopherol concentrations confirmed compliance of the patients with the medication schedule, showing a near doubling of serum concentrations of alpha-tocopherol. We concluded that the combination of vitamin E and a platelet antiaggregating agent (eg, aspirin) significantly enhances the efficacy of the preventive treatment regimen in patients with transient ischemic attacks and other ischemic cerebrovascular problems.
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PMID:Vitamin E plus aspirin compared with aspirin alone in patients with transient ischemic attacks. 749 35

Vitamin E in the reduced, alpha-tocopherol form shows very modest anticlotting activity. By contrast, vitamin E quinone is a potent anticoagulant. This observation may have significance for field trials in which vitamin E is observed to exhibit beneficial effects on ischemic heart disease and stroke. Vitamin E quinone is a potent inhibitor of the vitamin K-dependent carboxylase that controls blood clotting. A newly discovered mechanism for the inhibition requires attachment of the active site thiol groups of the carboxylase to one or more methyl groups on vitamin E quinone. The results from a series of model reactions support this interpretation of the anticlotting activity associated with vitamin E.
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PMID:On the mechanism of the anticlotting action of vitamin E quinone. 766 63

We investigated in rats fed a purified diet for 2 and 4 months whether wine drinking was associated with the rebound effect on thrombin-induced platelet aggregation observed after alcohol withdrawal. With 6% ethanol drinking or its equivalent in red or white wine, platelet aggregation was reduced similarly by 70% when the animals drank the alcoholic beverages up to the venipuncture. Depriving the rats of alcoholic beverages for 18 hours was associated with an increase in the platelet response of 124% in those receiving 6% ethanol, of 46% with white wine but a decrease of 59% in those with red wine. The protective effect of red wine on platelets could be reproduced by tannins (procyanidins) extracted from grape seeds or red wine and added to 6% ethanol, but not by glycerol or wine without alcohol. That was related to inhibition of the alcohol-induced lipid peroxidation as shown by the lowering of conjugated dienes, lipid peroxides, and the increase in vitamin E in plasma. Owing to tannins, the platelets of rats drinking red wine did not exhibit the rebound effect observed hours after alcohol drinking, eventually associated with sudden death and stroke in humans.
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PMID:Platelet rebound effect of alcohol withdrawal and wine drinking in rats. Relation to tannins and lipid peroxidation. 774 10

The potential role of natural antioxidants (vitamin C--ascorbic acid, vitamin E--tocopherols, carotenoids and selenium) in the prevention of cardiovascular diseases is reviewed. It is probable that free oxygen radicals and oxidatively modified particles of low-density lipoproteins (LDL) participate in the development of atherosclerotic lesions. A great number of experimental, cross-sectional, retrospective and prospective epidemiological studies found a substantial increase of the risk of ischemic heart disease and stroke in individuals and populations with low intake of antioxidants from diet. Extremely high cardiovascular mortality in Slovakia and other postcommunist countries could be only partially explained by "classical" risk factors (hypertension, hypercholesterolemia and smoking). In the communist European countries there was a high consumption of spirits, cigarettes and salt, polluted environment and low consumption of the chief source of antioxidants--fruits. In these countries emphasis should be given to the prevention of antioxidant deficiencies by the increase of fruit and vegetable consumption, and to the decrease in salt, spirit, cigarettes and saturated fat consumption.
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PMID:[The role of antioxidants in the prevention of cardiovascular diseases]. 781 21

We studied free radical, lipid peroxide (LPO) and antioxidant levels of blood in three cases with mitochondrial encephalomyopathy. Case 1 was a 17-year-old man with MELAS. Serum vitamin E levels were decreased and LPO levels were increased after stroke-like episodes in case 1. Case 2 was a 68-year-old woman with MELAS and a maternal elder aunt of case 1. She showed an elevated serum LPO levels (6.58 nmol/ml) in the absence of stroke-like episode and serum CoQ10 level was 0.54 microgram/ml before therapy. By CoQ10, idebenone and tocopherol nicotinate therapy, serum LPO levels decreased gradually in parallel with the decrease of lactate and pyruvate levels. Free radicals were measured in case 2 and controls by spin trapping method. Hydroxyl radical and C center radical were increased and H radical was normal in blood. But these free radicals in serum were all normal. Her serum antioxidants revealed an elevated percent inhibition of SOD and a decreased transfferin level. Case 3 was a 52-year-old woman with MERRF. She showed an elevation of serum LPO (12.8 nmol/ml). Her serum antioxidants revealed an elevated vitamin E and ceruloplasmin levels and percent inhibition of SOD.
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PMID:[Free radical, lipid peroxide and antioxidant in mitochondrial encephalomyopathy]. 795 20

Reactive oxygen species (ROS) such as the superoxide (O2.-) and the hydroxyl radical (OH.) are aggressive chemical compounds that can induce tissue injury, e.g. by peroxidation of polyunsaturated fatty acids in cell membranes or directly by DNA damage. Many pathological conditions are in part caused by ROS. There are various biological defense systems directed towards radicals: specific enzymes, e.g. superoxide dismutase or glutathione peroxidase; nonessential antioxidants, e.g. the plasma proteins and uric acid; and the essential antioxidants, e.g. vitamin C, vitamin E and carotenoids. This review focuses on various clinical conditions where ROS are of major pathogenetic significance: ageing, cancer, stroke, hematologic disorders, adult respiratory distress syndrome (ARDS) and organ preservation in transplantation medicine. Moreover, the complementary system of the vitamins C and E in defense against ROS is shortly discussed and the need for further studies about the effects of antioxidant treatment, such as interventional studies, proposed. The chronic exposure of the organism to ROS is an important factor for tissue injury in the process of ageing. Lipofuscin is a typical product of lipid peroxidation and inversely correlates with longevity of an organism. The ingestion of higher doses of antioxidative vitamins was recently shown to be protective for the development of cataracts, a degenerative disorder of the eye. The impairment of the immune system in elderly people might be prevented by a higher intake of multivitamin supplements. Whether supplementation with antioxidative vitamins can extend the life span in humans, as was shown in experimental animals, remains unanswered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antioxidant vitamins and disease--risk of a suboptimal supply]. 807 83


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