Publications by authors named "Vaona I"

To investigate the hypothesis that plasmatic changes of lipoperoxidative markers are associated with deep venous thrombosis (DVT), peripheral venous blood samples were obtained from 10 patients with venographically proven DVT before starting anticoagulant therapy, and 36+/-3 and 60+/-3 hours later. Values of myeloperoxidase (MPO), 4-hydroxynonenal (HNE) and malondialdehyde (MDA) were compared with those of 10 age-matched control subjects. Despite individual variations, mean plasma MPO level was higher in the DVT group (p < 0.

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Plasma activity of myeloperoxidase (MPO), malondialdehyde (MDA) and 4-hydroxynonenal (HNE) was measured prior to any treatment in 50 consecutive stroke patients with acute cerebral ischaemia, as well as in 14 healthy control subjects. Mann-Whitney-Wilcoxon test for unpaired data showed greater values of MPO (p < 0.01), MDA (p < 0.

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Opioid peptide gene expression was characterized in adult rat ventricular cardiac myocytes that had been cultured in the absence or the presence of phorbol 12-myristate 13-acetate. The phorbol ester induced a concentration- and time-dependent increase of prodynorphin mRNA, the maximal effect being reached after 4 h of treatment. The increase in mRNA expression was suppressed by incubation of cardiomyocytes with staurosporine, a putative protein kinase C inhibitor, and was not observed when the cells were cultured in the presence of the inactive phorbol ester 4 alpha-phorbol 12,13-didecanoate.

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Nicorandil is a compound with hybrid properties of nitrates and adenosine triphosphate (ATP)-sensitive potassium channel (KATP) opening. The effects of nicorandil and isosorbide dinitrate (ISDN) were investigated in a model of 60-min coronary occlusion/180-min reperfusion in open chest pigs. Three groups of 10 pigs were randomly assessed to receive saline or equihypotensive doses of nicorandil or ISDN.

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We report a patient who intentionally ingested a large amount of delayed release fenfluramine and was successfully treated with whole bowel irrigation. To our knowledge this is the first case of this kind to be reported in the literature. This therapeutic method, commonly used for acute poisonings with enteric coated and other modified release pharmaceuticals appears effective and risk-free in the treatment of delayed release fenfluramine overdose.

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The expression of the prodynorphin gene was investigated in adult cultured rat ventricular cardiac myocytes by using a sensitive solution hybridization RNase protection assay for the quantitative analysis of prodynorphin mRNA. Myocyte culture in high KCl resulted, after 4 h, in a marked increase in cellular prodynorphin mRNA, while a KCl treatment for 6, 12, or 24 h progressively down-regulated the levels of prodynorphin mRNA below the control value. Immunoreactive dynorphin B, a biologically active end product of the precursor, was found to be present in the culture medium in significantly higher amounts than in the cardiac myocytes.

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The prevention of oxidant-induced damage following reperfusion was experimentally evaluated. Two pharmacological regimens containing different combinations of antioxidant factors and membrane-stabilizing compounds, such as alpha-tocopherol (vitamin E), methionine, dexamethasone, mannitol and cysteine, were administered. The reduced/oxidized glutathione (GSH/GSSG) ratio in muscle was used to evaluate oxidative stress.

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The GSH level in myocardial tissue represents an important defense mechanism against oxygen toxicity. Since the ischemia-induced depletion of GSH might favour the cytotoxicity of oxygen-derived free radicals produced during reperfusion, we assessed the effects of the GSH donor, glutathione monoethylester, in anaesthetized pigs subjected to 90 minutes of coronary occlusion followed by 30 minutes reperfusion. The drug was infused intracoronarily at a dose of 1 mg/ml (0.

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Prodynorphin mRNA was synthesized both in rat atrial and ventricular tissue, as well as in adult cultured rat ventricular cardiac myocytes. In the cultured cells, the content of prodynorphin mRNA did not differ from that detected in the original ventricle, indicating that the myocardial cell is an important source for prodynorphin mRNA in the rat ventricular tissue. This study demonstrated the presence of immunoreactive dynorphin B-like material in the cultured cardiomyocytes.

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In the myocardial cell, stimulation of the K opioid receptor is involved in the modulation of cytosolic calcium and pH homeostasis, as well as in the regulation of myofilament responsiveness to calcium. In the present study, we found that prodynorphin mRNA, which encodes for the synthesis of a common precursor of opioid peptides interacting with K sites, is synthesized both in atrial and ventricular tissue of the rat heart. In adult cultured rat ventricular cardiomyocytes, the level of prodynorphin mRNA did not differ from that detected in the original ventricular tissue.

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The in situ and in vitro rate of lipid peroxidation of hearts were determined in two groups of pigs which had been fed diets which differed only in fatty acid composition for 8 weeks. During the dietary period venous plasma levels of malondialdehyde and lipofuscin were not higher in pigs receiving the highly unsaturated fatty acid-containing mackerel oil than those receiving lard fat. Malondialdehyde was produced in the coronary system of the mackerel oil fed animals.

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The addition of external GSSG at concentrations in the range 50-500 microM produces in isolated adult rat heart myocytes an increase of GSH level and only a slight increase of GSSG level. On the contrary, external GSH at the above same indicated concentrations did not change the cell glutathione pool. The pretreatment of the cells with diethylamaleate depleted the myocytes of glutathione and enhanced the GSSG-induced replenishment effect on GSH level.

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1. The perfusion for 15 min of isolated rat hearts with 100 microM t-butylhydroperoxide leads to a 75% diminuition of the tissue GSH/GSSG ratio. 2.

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The intraperitoneal administration of 3, 10 and 80 mg/Kg isoproterenol produced in the cardiac muscle a dose dependent increase of GSH content and a slight elevation of GSSG content. In addition, the treatment with the catecholamine at the doses of 3 and 10 mg/Kg produced a slight decrease of the mixed glutathione disulfides level, whilst at the dose of 80 mg/Kg, this effect was more pronounced. These changes were not accompanied by modifications of the activities of the enzymes glutathione peroxidase, glutathione reductase and glutathione S-transferase.

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