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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty pigs were randomly assigned to a blind treatment with vitamin E or placebo. Ten animals each received 0.5 g d-alpha tocopherol intravenously before ischemia (group 1) or before reperfusion (group 2). Ten control pigs were treated with a lipid emulsion as placebo. The left anterior descending coronary artery was distally ligated for 45 min followed by 3 days of reperfusion. Infarct size was determined as ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was assessed by sonomicrometry. Myocardial and plasma concentrations of vitamin E were determined by high-performance liquid chromatography. Global hemodynamic parameters and estimated left ventricular oxygen consumption did not differ among the three groups. Intravenous treatment with vitamin E raised the plasma levels of this vitamin from 1 +/- 0.3 mg/l (control group) to 21 +/- 6 mg/l before ischemia, to 4 +/- 2 mg/l before reperfusion and to 2 +/- 0.6 mg/l at the end of the experiments in group 1. In group 2, vitamin E plasma levels increased from 1 +/- 0.3 mg/l to 24 +/- 13 mg/l before reperfusion and to 2 +/- 0.6 mg/l after 3 days of reperfusion. At the end of the experiments, myocardial vitamin E concentrations amounted to 4.2 +/- 0.7 ng/mg fresh weight (control group), 9.7 +/- 2.1 ng/mg (group 1), and to 8.7 +/- 1.4 ng/mg (group 2). The increase in vitamin E plasma concentration was not associated with a cardioprotective effect. Infarct sizes of the three groups (group 1: 68 +/- 12%, group 2: 66 +/- 15%, control group: 69 +/- 8%) were almost identical.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute treatment with vitamin E does not protect the regionally ischemic, reperfused porcine heart. 202 85

From in vitro studies involving multilamellar liposomes or other artificial systems, several groups of workers have deduced that Trolox (a water-soluble analogue of vitamin E) and ascorbate are synergistic antioxidants. Here, we demonstrate that while Trolox and ascorbate individually protect cultured hepatocytes against oxyradicals generated either with xanthine oxidase plus hypoxanthine or with hydrogen peroxide, the two antioxidants do not appear to be synergistic when used in equimolar combinations. Also, in a rat model of hepatic ischemia-reperfusion, we observed that infusion of Trolox or ascorbate (7.5-10 mumol/kg body weight) into the postischemic liver reduced the reperfusion injury by 76 or 67%, respectively. However, when both compounds were used together (each at the same dose as used separately), the organ salvage amounted to only 79%. Therefore, there is no evidence of synergism between Trolox and ascorbate in our in vitro and especially in vivo systems.
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PMID:Trolox and ascorbate: are they synergistic in protecting liver cells in vitro and in vivo? 203 21

We examined the effects of dietary deficiency of vitamin E and selenium on the ischemia-reperfusion model of renal injury in the rat. Deficient diets imposed for six weeks on three-week-old weanling rats led to no significant differences in body weights, serum creatinine, GFR, RBF, TmPAH or urinary total protein excretory rates prior to ischemia. Twenty-four hours after one hour of ischemia, animals on the deficient diet demonstrated more markedly impaired GFR, RBF, TmPAH and urine to plasma creatinine concentrations and an increased renal failure index. Tubular damage was more severe injury in the deficient animals. Lipid peroxidation, 15 minutes after the release of the ischemic clamp, was increased in the deficient animals. We confirmed the effects of our dietary manipulation in impairing the oxidant scavenging system in the deficient animals since glutathione peroxidase activity was reduced to less than 5% in the basal state, and this striking reduction persisted following ischemia. Plasma vitamin E concentrations were also markedly depressed in the deficient diets. This dietary deficiency also worsened the course of acute renal injury and was accompanied by 50% mortality compared to 0% mortality in the control animals. Thus, dietary deficiency of vitamin E and selenium led to greater structural and functional renal impairment and increased lipid peroxidation following ischemia. These data provide support for the role of reactive oxygen species in mediating ischemia-reperfusion injury.
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PMID:Dietary deficiency of antioxidants exacerbates ischemic injury in the rat kidney. 207 54

In experimental hyperthyroidism, acceleration of lipid peroxidation occurs in heart and slow-oxidative muscles, suggesting the contribution of reactive oxygen species to the muscular injury caused by thyroid hormones. This article reviews various models of oxidative muscular injury and considers the relevance of the accompanying metabolic derangements to thyrotoxic myopathy and cardiomyopathy, which are the major complications of hyperthyroidism. The muscular injury models in which reactive oxygen species are supposed to play a role are ischemia/reperfusion syndrome, exercise-induced myopathy, heart and skeletal muscle diseases related to the nutritional deficiency of selenium and vitamin E and related disorders, and genetic muscular dystrophies. These models provide evidence that mitochondrial function and the glutathione-dependent antioxidant system are important for the maintenance of the structural and functional integrity of muscular tissues. Thyroid hormones have a profound effect on mitochondrial oxidative activity, synthesis and degradation of proteins and vitamin E, the sensitivity of the tissues to catecholamine, the differentiation of muscle fibers, and the levels of antioxidant enzymes. The large volume of circumstantial evidence presented here indicates that hyperthyroid muscular tissues undergo several biochemical changes that predispose them to free radical-mediated injury.
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PMID:Oxidative muscular injury and its relevance to hyperthyroidism. 218 67

Epilepsy complicates severe head trauma. Development of persistent seizures appears to correlate with the extent of trauma. Although early reports suggested that prophylactic administration of antiepileptic drugs would prevent epileptogenesis, controlled studies have failed to corroborate this assumption. Head trauma initiates a sequence of responses that includes altered blood flow and vasoregulation, disruption of the blood-brain barrier, increases in intracranial pressure, focal or diffuse ischemia, hemorrhage, inflammation, necrosis, and disruption of fiber tracts. The presence of an intracranial hematoma has a robust association with the development of post-traumatic epilepsy. Extravasation of blood is followed by hemolysis and deposition of heme-containing compounds into the neuropil, initiating a sequence of univalent redox reactions and generating various free radical species, including superoxides, hydroxyl radicals, peroxides, and perferryl ions. Free radicals initiate peroxidation reactions by hydrogen abstraction from methylene groups adjacent to double bonds of fatty acids and lipids within cellular membranes. Intrinsic enzymatic mechanisms for control of free radical reactions include activation of catalase, peroxidase, and superoxide dismutase. Steroids, proteins, and tocopherol also terminate peroxidative reactions. Tocopherol and selenium are effective in preventing tissue injury initiated by ferrous chloride and heme compounds. Treatment strategies for prevention or prophylaxis of post-traumatic epilepsy must await absolute knowledge of mechanisms. Antioxidants and chelators may be useful, given the speculation that peroxidative reactions may be an important component of brain injury responses. However, potential treatment strategies involving gamma-aminobutyric acid (GABA) agonists, NMDA receptor antagonists, and barbiturates need further scientific assessment.
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PMID:Post-traumatic epilepsy: cellular mechanisms and implications for treatment. 222 73

Opiate-receptor antagonists improve behavioral, electrophysiologic and/or histologic outcome in various experimental models of central nervous system ischemia. To address the potential mechanism(s) by which opiate-receptor antagonists may exert their protective actions in cerebral ischemia, metabolic and biochemical changes were measured in brain of rats pretreated with the opiate-receptor antagonist nalmefene or vehicle and subjected to 60 min of global ischemia followed by 2 hr of reperfusion. 31P and 1H magnetic resonance spectroscopy were used to follow the metabolic changes during ischemia and reperfusion, after which brain tissue was frozen in situ. Biochemical assays included free fatty acids, thromboxane B2, ascorbate, vitamin E and amino acids. Nalmefene-treated animals showed more rapid and complete recovery of cellular bioenergetic state (as indicated by the phosphocreatine to inorganic phosphate ratio), tissue acidosis and lactate levels during reperfusion than placebotreated controls. Ischemia/reperfusion caused significant increases of fatty free acids and thromboxane, associated with significant decreases of ascorbate and glutamate; nalmefene pretreatment limited each of these changes. The degree of metabolic improvement as reflected by recovery of high energy phosphates and reduction of lactic acidosis were highly correlated with changes in tissue levels of arachidonate and glutamate. Thus, the beneficial effects of opiate-receptor antagonists in cerebral ischemia may be due, in part, to an ability to enhance metabolic recovery with associated, reduction in phospholipid hydrolysis and excitotoxin release.
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PMID:Opiate-receptor antagonist improves metabolic recovery and limits neurochemical alterations associated with reperfusion after global brain ischemia in rats. 224 36

The influences of vitamin E deficiency on compression injury of the rat spinal cord associated with ischemia were investigated. Growing rats were divided into two groups and given a diet containing either 2 IU/100 g or less than 0.1 IU/100 g of alpha-tocopherol acetate, respectively, for 6-8 weeks before experiments. Motor disturbances induced by spinal cord injury were found to be enhanced by vitamin E deficiency. The spinal cord blood flow (SCBF) was reduced by compression and subsequently increased transiently and then decreased gradually in both groups, but the level was lower in the vitamin E-deficient group than in the control group. After injury, the vitamin E-deficient group showed lower recoveries than the control group in the amplitude and latency of spinal cord evoked potentials and greater pathological changes of the spinal cord, such as bleeding and edema. The increase in the level of TBA-reactive substances in the spinal cord after injury increased with decrease in the dietary level of vitamin E. These results suggest that vitamin E may have a protective effects against ischemic spinal cord injury by its antioxidant effect.
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PMID:Influence of dietary vitamin E deficiency on compression injury of rat spinal cord. 229 24

Free radical-mediated reperfusion injury has been established as an important mechanism leading to post-ischemic reperfusion myocardial damage. The present study was undertaken to determine the protective role of vitamin E, a membrane-bound free-radical scavenger, on ischemia-reperfusion myocardial injury. After 4 months of feeding a semipurified diet containing 0, 30, and 3000 ppm of R,R,R,-alpha-tocopherol acetate, rat hearts were subjected to Langendorff perfusion. Myocardial damage was judged by the release of creatine phosphokinase (CPK) after 45 min of global ischemia followed by 20 min of reperfusion. Effluent CPK was significantly lowered in the two tocopherol-supplemented groups, although increasing dietary vitamin E by 100-fold above requirement did not confer further protection. However, effluent prostacyclin, detected as the stable metabolite 6-keto-PGF1 alpha by radioimmunoassay, was potentiated by dietary vitamin E in a dose-dependent manner. Analysis of lipids in cardiac subcellular fractions showed considerable enrichment of tocopherol in these membranes by diets, but the levels of polyunsaturated fatty acids, phospholipids, and cholesterol were essentially unchanged by dietary treatment or ischemia-reperfusion. These data demonstrated that requirement level of tocopherol (30 ppm) in the diet is sufficient to protect against reperfusion injury of the myocardium and suggests that tocopherol is important in maintaining cardiac prostacyclin synthesis under conditions of oxygen stress.
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PMID:Effects of vitamin E on prostacyclin release and lipid composition of the ischemic rat heart. 231 Feb

The effect of alpha-tocopherol (vitamin E) on ischemic neuronal damage was studied in the gerbil. The animals were subjected to 5 min of cerebral ischemia by bilateral common carotid artery occlusion. Immediately after ischemia, alpha-tocopherol at a dose of 50 or 100 mg/kg was administered intravenously. Morphological changes in the CA1 sector of the hippocampus were evaluated after 7 days of survival. alpha-Tocopherol prevented ischemia-induced neuronal death. The average density of CA1 pyramidal neurons (cells/mm, mean +/- S.E.M.) was 252 +/- 8 (n = 8) in the sham-operated group, 50 +/- 20 (n = 8) in the ischemia group, and 140 +/- 35 (n = 8) and 182 +/- 36 (n = 8) in the groups treated with alpha-tocopherol at the doses of 50 and 100 mg/kg, respectively. The results suggest that free radical scavenging action of alpha-tocopherol played an important role in preventing the neuronal death.
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PMID:Protective effect of alpha-tocopherol on ischemic neuronal damage in the gerbil hippocampus. 233 5

The effect of dietary vitamin E on the fetal ischemic distress induced by clamping the uterotubal vessels of pregnant rats was studied. The fetal heart rate was measured by the pulsed doppler technique as an index of fetal distress induced by ischemia. On reperfusion after clamping the vessels for 9 min., the decreased fetal heart rate was restored to normal rapidly and completely in the E-supplemented group, but slowly and incompletely in the E-deficient and control groups. On reperfusion after ischemia, the amounts of lipid peroxides, measured as thiobarbituric acid (TBA)-reactive substances, were greatly increased in the fetal brain and liver and in the placenta in the E-deficient and control groups, but not in the E-supplemented group. The vitamin E concentrations in fetal tissues were less than 10% of those in the maternal tissues. But a diet containing a large amount of vitamin E induced significantly increased concentrations of vitamin E in fetal brain and liver. These results suggest that vitamin E may have a protective effect on fetal distress by decreasing lipid peroxides.
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PMID:[Effect of dietary level of vitamin E on protection of fetus against ischemic distress induced by clamping the uterotubal vessels of pregnant rats]. 237 15


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