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Effect of ascorbic acid supplementation on certain oxidative stress parameters in the post reperfusion patients of myocardial infarction.
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Reperfusion injury causes oxidative stress thereby resulting in an imbalance between oxidant-antioxidant systems. In the present communication, the effect of ascorbic acid supplementation has been studied on certain oxidant and antioxidant parameters in the blood of the patients with myocardial
Improvement of sympathetic response to exercise by oral administration of ascorbic acid in patients after myocardial infarction.
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BACKGROUND
Recent studies indicated that excessive oxidative stress in an animal heart failure model injures both the sympathetic nerve endings and receptors, resulting in disturbance of norepinephrine release and sensitivity to norepinephrine. However, it has not been clarified whether this
Reassessment of changes in leucocyte and serum ascorbic acid after acute myocardial infarction.
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After an acute myocardial infarction, there is an apparent acute fall in leucocyte ascorbic acid associated with an acute rise in white blood cells and serum cortisol. The apparent fall in leucocyte ascorbic acid is the result of the granulocytosis which occurs after the infarction. Estimations of
Ascorbic acid prevents acute myocardial infarction induced by isoproterenol in rats: role of inducible nitric oxide synthase production.
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The goal of this study was to investigate whether sub-chronic anti-oxidant treatment with ascorbic acid (Vit C) is able to protect the heart against myocardial infarction. The effects of Vit C treatment on the histopatological changes and immunohistochemistry for p53, COX-2 and iNOS were evaluated
[Content of different forms of ascorbic acid in the tissues of rabbits with experimental myocardial infarct].
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It was established that experimental myocardial infarction leads to a decrease in the ascorbic acid content in the left heart ventricle in the ischemic are and to a negligible rise in the dehydroascorbic acid concentration within the first hours after artery ligation followed by its lowering at the
Effect of ascorbic acid on infarct size in experimental focal cerebral ischaemia and reperfusion in a primate model.
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Temporary occlusion of major cerebral blood vessels occasionally becomes necessary during surgical procedures. Ascorbic acid (Vitamin C) is an important non-enzymatic scavenger of free radicals and its protective effect on the brain in permanent focal cerebral ischaemia has been proven in a primate
Mortality and clinical course of patients with acute myocardial infarction treated with streptokinase and antioxidants: mannitol and ascorbic acid.
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There is increasing evidence that free radical scavengers limit reperfusion injury in animal experiments. We randomly administered 250 ml 20% mannitol infusion and 10.0 g ascorbic acid infusion, potent free radical scavengers to 42 patients with acute myocardial infarction receiving streptokinase. A
Acute Myocardial Infarction Following Administration of Polyethylene Glycol Electrolyte Solution with Ascorbic Acid (MoviPrep®) at Home: A Case Report.
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A male individual aged 82 years with hypertension who had a smoking history, but no history of cardiovascular events, developed acute myocardial infarction immediately after he took oral polyethylene glycol electrolyte solution with ascorbic acid as a pretreatment for a colonoscopy to examine
Correction of haemorheological disturbances in myocardial infarction by diquertin and ascorbic acid.
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In a model of the high blood viscosity syndrome, developed after myocardial infarction in rats, it was observed that a therapy of a combination of diquertin (20 mg/kg) and ascorbic acid (50 mg/kg) for a -period of 6 days, resulted in an improvement of haemorheological indices. The decrease in blood
Myocardial salvage with trolox and ascorbic acid for an acute evolving infarction.
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Both Trolox (a water-soluble analogue of alpha-tocopherol) and ascorbic acid were more effective than superoxide dismutase or catalase in protecting myocyte cell cultures from free radical attack (induced by hypoxanthine and xanthine oxidase). In a canine model of two hours of left anterior
Inhibitory effects of a phosphate diester of alpha-tocopherol and ascorbic acid (EPC-K1) on myocardial infarction in rats.
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The inhibitory effect of a phosphate diester of alpha-tocopherol and ascorbic acid (EPC-K1) was examined in myocardial infarction induced in rats, in comparison with a selective 5-lipoxygenase inhibitor, AA-861. EPC-K1 significantly reduced the infarct size at 24 and 48 h after ligation, whereas
Synergistic interactions of ferulic acid with ascorbic acid: its cardioprotective role during isoproterenol induced myocardial infarction in rats.
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Studies on the lipid peroxidation and antioxidant changes and their significance during myocardial injury have provided a new insight into the pathogenesis of heart disease. The heart failure subsequent to myocardial infarction may be associated with an antioxidant deficit as well as increased
Effect of antioxidant-rich foods on plasma ascorbic acid, cardiac enzyme, and lipid peroxide levels in patients hospitalized with acute myocardial infarction.
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OBJECTIVE
To determine whether a fat- and energy-reduced diet rich in antioxidant vitamins C and E, beta carotene, and soluble dietary fiber reduces free-radical stress and cardiac enzyme level and increases plasma ascorbic acid level 1 week after acute myocardial infarction.
METHODS
Randomized,
Studies of blood ascorbic acid levels in acute myocardial infarction.
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Fasting serum samples from 53 patients with an acute myocardial infarction were investigated for their vitamin C content during the first week of their illness. The vitamin C levels found were generally within the accepted normal limits. However, there were highly significant lower levels on the
Attenuation of abnormalities in the lipid metabolism during experimental myocardial infarction induced by isoproterenol in rats: beneficial effect of ferulic acid and ascorbic acid.
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The present study aims at evaluating the effect of the combination of ferulic acid and ascorbic acid on isoproterenol-induced abnormalities in lipid metabolism. The rats were divided into eight groups: Control, isoproterenol, ferulic acid alone, ascorbic acid alone, ferulic acid+ascorbic acid,
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