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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tocopherols and tocotrienols (vitamin E) and ascorbic acid (vitamin C) as well as the carotenoids react with free radicals, notably peroxyl radicals, and with singlet molecular oxygen (1O2), this being the basis of their function as antioxidants. RRR-alpha-tocopherol is the major peroxyl radical scavenger in biological lipid phases such as membranes or low-density lipoproteins (LDL). L-Ascorbate is present in aqueous compartments (e.g. cytosol, plasma, and other body fluids) and can reduce the tocopheroxyl radical; it also has a number of metabolically important cofactor functions in enzyme reactions, notably hydroxylations. Upon oxidation, these micronutrients need to be regenerated in the biological setting, hence the need for further coupling to nonradical reducing systems such as glutathione/glutathione disulfide, dihydrolipoate/lipoate, or NADPH/NADP+ and NADH/NAD+. Carotenoids, notably beta-carotene and lycopene as well as oxycarotenoids (e.g. zeaxanthin and lutein), exert antioxidant functions in lipid phases by free-radical or 1O2 quenching. There are pronounced differences in tissue carotenoid patterns, extending also to the distribution between the all-trans and various cis isomers of the respective carotenoids. Antioxidant functions are associated with lowering DNA damage, malignant transformation, and other parameters of cell damage in vitro as well as epidemiologically with lowered incidence of certain types of cancer and degenerative diseases, such as ischemic heart disease and cataract. They are of importance in the process of aging. Reactive oxygen species occur in tissues and cells and can damage DNA, proteins, carbohydrates, and lipids. These potentially deleterious reactions are controlled in part by antioxidants that eliminate prooxidants and scavenge free radicals. Their ability as antioxidants to quench radicals and 1O2 may explain some anticancer properties of the carotenoids independent of their provitamin A activity, but other functions may play a role as well. Tocopherols are the most abundant and efficient scavengers of peroxyl radicals in biological membranes. The water-soluble antioxidant vitamin C can reduce tocopheroxyl radicals directly or indirectly and thus support the antioxidant activity of vitamin E; such functions can be performed also by other appropriate reducing compounds such as glutathione (GSH) or dihydrolipoate. The biological efficacy of the antioxidants is also determined by their biokinetics.
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PMID:Antioxidant functions of vitamins. Vitamins E and C, beta-carotene, and other carotenoids. 144 60

Three weeks' dietary supplementation with a moderate dose of vitamin E (45 IU DL-alpha-tocopherol acetate daily), in eight healthy volunteers significantly increased the serum vitamin E level from 12.3 +/- 3.3 to 16.2 +/- 3.7 mg/L (means +/- SD) and significantly decreased neutrophil chemotaxis from 15 +/- 3 to 4 +/- 1 micron/h (means +/- standard error of the means). Generation of leukotriene B4 was not influenced by vitamin E, suggesting that the decrease in neutrophil chemotaxis was not due to blockage of the lipoxygenase pathway. Neither was the plasma malondialdehyde concentration influenced by vitamin E, contradicting the possibility of an antioxidant effect of vitamin E. As one early event in neutrophil chemotaxis is an increase in intracellular calcium concentration resulting from increased membrane permeability, it is possible that vitamin E influenced chemotaxis by a stabilizing effect on the neutrophil membrane, rather than by its antioxidant effect. Vitamin E supplementation could thus be beneficial in pathological conditions with activated neutrophils, such as ischaemic heart disease.
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PMID:Effects of dietary supplementation with vitamin E on human neutrophil chemotaxis and generation of LTB4. 166 72

Myocardial ischemia is a disease process characterized by reduced coronary flow such that the supply of nutritive blood to heart muscle (myocardium) is insufficient for normal myocardial aerobic metabolism. Prompt reestablishment of coronary flow by invasive and noninvasive clinical procedures is the most direct and effective means of limiting myocardial damage in ischemic heart disease patients, although reperfusion carries with it an injury component which may reflect, at least to some degree, the toxic effects of partially reduced oxygen species and their participation in degenerative cellular processes such as membrane lipid peroxidation. Vitamin E, a lipophilic, chain-breaking antioxidant, is a prominent membrane constituent in heart muscle, where it modulates/regulates various aspects of heart muscle-cell metabolism and function. Vitamin E's beneficial effects against experimentally induced oxidative damage to the heart, along with inverse epidemiological correlations between plasma vitamin E level and either anginal pain or mortality due to ischemic heart disease, suggest that vitamin E might have protective and therapeutic roles against myocardial ischemic-reperfusion injury. Laboratory investigations aimed at addressing this possibility have demonstrated that vitamin E supplementation protects isolated hearts against ischemic-reperfusion injury, and relatively more inconsistent and limited data document cardioprotective effects of vitamin E in some animal models of myocardial ischemia-reperfusion, especially when administered prior to the ischemic period. Clinical attempts to establish whether vitamin E has therapeutic benefit in ischemic heart disease patients remain inconclusive, having relied upon a variety of nonuniformly controlled protocols and a single, rather subjective endpoint (anginal pain). Consequently, although laboratory data constitute a conceptual context for and indirect support of the idea that vitamin E could be a cardioprotectant against ischemic-reperfusion injury, compelling clinical evidence regarding vitamin E's therapeutic potential in the ischemic heart-disease patient is lacking. Elective coronary revascularization would appear to provide an attractive clinical setting for evaluating the therapeutic efficacy of vitamin E in the context of cardiac ischemia-reperfusion. Further biochemical work would still be required to define how vitamin E exerts any cardioprotective effect observed in these patients.
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PMID:Therapeutic potential of vitamin E against myocardial ischemic-reperfusion injury. 185 72

The effect of vitamin E on the ventricular fibrillation threshold was studied in an experimental model of acute myocardial ischemia. An anterior thoracotomy was performed on 23 anesthetized Wistar rats. The ventricular fibrillation threshold was measured. Vitamin E was then administered intravenously to an experimental group (n = 11) and a placebo to a control group (n = 12). The ventricular fibrillation threshold was measured again. Finally, the left anterior descending coronary artery was occluded, producing anteroapical myocardial ischemia. The ventricular fibrillation threshold was measured again. This threshold did not vary significantly when vitamin E or the placebo was administered before occluding the coronary artery but after the occlusion a threshold decrease in the placebo group was observed, whereas no such decrease was manifested in the vitamin E-treated group. The results suggest that vitamin E prevents ventricular fibrillation in acute myocardial ischemia in rats.
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PMID:Vitamin E and ventricular fibrillation threshold in myocardial ischemia. 261 72

Myocardial ischemia and reperfusion have been shown to result in damage to the phospholipid components of cardiac myocyte cell membranes as indicated by the tissue accumulation of unesterified fatty acids (UFA). A portion of this damage and subsequent dysfunction may be a consequence of free radical-induced membrane lipid peroxidative events. alpha-Tocopherol, a lipophilic antioxidant, was used in this study as an agent by which the extent of ischemia and reperfusion injury might be decreased. Increasing rat myocardial tissue levels of alpha-tocopherol by 51% was found to attenuate lipid perturbations as determined by the accumulation of tissue UFA in an isolated heart model of global ischemia and reperfusion. Nontreated hearts made ischemic for 25 min with 30 min of reflow had a significantly increased total UFA level of 5,961 +/- 799 nmol/mg protein (P less than 0.05) compared with control perfused hearts containing 3,116 +/- 463 nmol UFA/mg protein and with alpha-tocopherol-treated ischemic and reperfused hearts containing 3,066 +/- 365 nmol UFA/mg protein. Contractile dysfunction, excessive accumulation of tissue calcium, and release of lactate dehydrogenase after ischemia and reperfusion were also reduced, demonstrating protective effects in alpha-tocopherol-treated hearts. Thus alpha-tocopherol proved effective in the attenuation of ischemia and reperfusion damage. These results suggest that reducing lipid alterations may prove beneficial in protecting against membrane damage subsequent to ischemia and reperfusion.
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PMID:alpha-Tocopherol attenuates myocardial membrane-related alterations resulting from ischemia and reperfusion. 270 58

Early administration of vitamin E to low birth weight (less than 1500 g) infants results in alleviation of the symptoms of retinopathy of prematurity and a lowered incidence of intraventricular hemorrhage. If vitamin E is given to children with cholestatic liver disease (orally or parenterally) before 3 years of age, neurological symptoms such as areflexia, ataxia, and sensory neuropathy are prevented or reversed. Restitution of neurological function is more limited in children ages 5-17 years even after prolonged therapy. Vitamin E is also useful in prevention of neuropathy and retinopathy associated with abetalipoproteinemia and cystic fibrosis. Blood levels of tocopherol are often low in subjects with hemolytic anemias. Administration of vitamin E to G-6-P-D-deficient subjects increased hemoglobin levels, and decreased the number of irreversibly sickled cells in sickle-cell anemia subjects. Most trials have indicated that administration of vitamin E for 6 months or more to subjects with intermittent claudication results in longer walking distance and improved blood flow. Vitamin E reduces platelet aggregation, platelet adhesion to collagen, and platelet thromboxane production. Prostacyclin production is generally enhanced. The significance of these effects to thrombotic diseases. Epidemiological studies have indicated that subjects with higher blood levels of vitamin E have lower risk of death from ischemic heart disease and cancer, a lower risk of breast cancer, and a lower incidence of infections.
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PMID:Clinical uses of vitamin E. 391 44

Vitamin E, cholesterol and triglycerides were measured in blood sera of 167 patients (40-59 years old) with angina pectoris. An increase in concentration of vitamin E was observed only in patients with hyperlipidemia, whereas the vitamin content was similar to the control values in patients with hypertension, in smokers and in the persons free of risk factor. Distinct correlation was found only between vitamin E and the triglycerides contents (r = 0.42). These data corresponded to the results of a previous examination of 224 men and 435 women without ischemic heart disease: in men the content of vitamin E correlated with triglycerides (r = 0.50) and in women--with cholesterol (r = 0.34). The ratio of vitamin E/triglycerides appears to be a more adequate index of the vitamin content in men.
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PMID:[Vitamin E and serum lipids in ischemic heart disease]. 647 33

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

Dietary effects of polyunsaturated fatty acids (PUFA) omega-3 on lipid peroxidation (LPO) and antioxidant system were studied in 73 patients with ischemic heart disease, hyperlipoproteinemia (HLPE) type IIa, IIb, IV and essential hypertension. Eiconol-enriched antiatherosclerotic diet has more potent hypolipidemic, hypotensive and thrombolytic action in association with inhibition of LPO, enhances SOD activity, keeps red cell catalase within normal. Vitamin E concentrations were not changed. It is suggested that eiconol addition to antiatherosclerotic diet causes no LPO induction and is pathognomonic for HLPE, hypertension and IHD patients.
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PMID:[Dietary effects of PUFA omega-3 on lipid peroxidation and antioxidant system in patients with IHD, hyperlipoproteinemia and hypertension]. 781 30

Lipid peroxidation, presumably the result of free radical-mediated injury, has been shown to occur during myocardial ischemia and reperfusion. Since vitamin E is a very effective, naturally occurring, chain-breaking antioxidant, it was investigated whether a vitamin E-supplemented diet increased myocardial tolerance towards ischemia and reperfusion in pigs. In addition to a standard diet which contained 30 mg vitamin E/kg (approximately daily vitamin E intake 30 mg), ten pigs were fed with 10 g vitamin E (all-rac-alpha-tocopherol acetate, Merck AG, Darmstadt, Germany) daily for at least 4 weeks. Ten control pigs remained on the standard diet. In an open chest preparation, the left anterior descending coronary artery was distally ligated for 45 min followed by 3 d of reperfusion. Infarct size was determined as the ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was evaluated by sonomicrometry. Vitamin E concentrations in plasma and myocardium were measured by high-performance liquid chromatography. Global hemodynamic characteristics did not differ between the two groups. Oral pretreatment with vitamin E raised the plasma concentration of this vitamin from 1.1 +/- 0.3 to 5.0 +/- 1.0 mg/l and the myocardial content from 4.2 +/- 0.7 to 18.6 +/- 2.7 ng/mg fresh weight. Vitamin E treatment did not reduce infarct size, which amounted to 71.3 +/- 5% in the control group and to 71.7 +/- 8.2% in the treated animals. Furthermore, recovery of regional systolic shortening of the reperfused segment did not significantly differ in the two groups after 3 d of reperfusion; it measured 2 +/- 4% in the controls and 6 +/- 6% (p = 0.16) in the treated animals. Therefore, chronic, oral treatment with vitamin E which raised myocardial and plasma concentrations of this vitamin 4- to 5-fold did not increase myocardial tolerance towards ischemia and reperfusion in this animal model.
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PMID:Failure of chronic, high-dose, oral vitamin E treatment to protect the ischemic, reperfused porcine heart. 844 Nov 76


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