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M Koltai

Publications and source records attributed to M Koltai.

113 records · Page 7Linked to original sources
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Is malondialdehyde a marker of the effect of oxygen free radicals in rat heart tissue?

We tested the effect of exogenous purine derived free radicals and H2O2 vs ischemia and reperfusion on the thiobarbituric-acid (TBA)-reactive material and malondialdehyde (MDA) formation in isolated rat hearts using the thiobarbituric acid test and high performance lipid chromatography (HPLC). We could not detect increased thiobarbituric-acid-reactive material or MDA production during 6 mM H2O2 infusion, during free radical generation by purine-derived free radicals, or using ischemia and reperfusion. Increased thiobarbituric-acid-reactive material and MDA tissue levels were detected only during infusion of 12 mM H2O2 (p less than 0.001). We conclude that the generally used thiobarbituric acid assay for MDA is susceptible to artifacts and unsuited as an indirect measure for low-to-medium-levels of oxygen free radicals. Using HPLC assay, which accurately measures MDA, no evidence was found that MDA is a primary and direct lipid peroxidation product of exogenous or endogenous reactive oxygen species.

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Effect of a linoleic acid-rich diet on the acute phase of coronary occlusion in conscious rats: influence of indomethacin and aspirin.

We studied the effect of a long-term diet rich in linoleic acid (LAR diet) on the acute phase of experimental myocardial infarction. Male Sprague-Dawley CFY rats were fed a diet containing 12% sunflower seed oil or standard laboratory chow for 3 months. Gas-chromatographic determination of the fatty acid content in total heart phospholipids showed an increase in the n-6/n-3 fatty acid ratio, resulting from an elevated arachidonic acid content of the membrane. In parallel experiments in conscious animals, the left anterior descending coronary artery was ligated by a previously implanted silk loop. Long-term LAR diet increased the survival rate from 19 to 81% and reduced the occurrence of arrhythmias during the first 20 min after coronary ligation. Oral administration of 10 mg/kg indomethacin 1 hr prior to coronary ligation abolished the protective effect of the LAR diet, while 200 mg/kg aspirin did not. The prevention by indomethacin of the beneficial effect suggest the involvement of an increased prostaglandin synthesis in the protection offered by the diet. The ineffectiveness of aspirin in this respect is discussed. These results provide evidence that a long-term LAR diet may be of therapeutic value in the management of myocardial infarction.

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Experimental myocardial infarction in adjuvant arthritis rats.

We studied the influence of various inflammatory reactions on the survival rate and occurrence of arrhythmias in the acute phase of experimental myocardial infarction in conscious male Sprague--Dawley CFY rats. Chronic disseminated inflammatory disease was induced by subplantar injection of Freund complete adjuvant, while chronic local inflammatory lesion was produced by carrageenan granuloma pouch method. An acute inflammatory response in the rat paw was evoked by carrageenan. Myocardial infarction was provoked by tightening a previously implanted silk loop around the left anterior descending coronary artery 14 days after the induction of adjuvant disease, and 7 days or 4 h after the production of granuloma pouch or foot edema. Carrageenan paw swelling was induced in rats showing expressed primary and slight secondary lesions due to Freund adjuvant. Adjuvant arthritis, but not granuloma pouch or acute paw edema, protected the rat against the fatal complications of coronary ligation. This effect was characterized by a significant increase in the survival rate from 30% to 63%, and a reduction in the occurrence of various types of dysrhythmias. Carrageenan paw edema was also less expressed and of shorter duration in rats with adjuvant disease. The level of cardiolopin was considerably increased in the arthritic group, while the other phospholipids showed no change. We conclude that chronic disseminated inflammation markedly alters the reactivity of conscious rats to experimental myocardial infarction. The alterations observed may be related to an increased energy supply and/or to accumulation of some endogenous antiinflammatory substances during adjuvant arthritis.

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Actinomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia.

Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.

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