carnitine/hypoxia

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Effect of acetyl-L-carnitine on hyperactivity and spatial memory deficits of rats exposed to neonatal anoxia.

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The effect of acetyl-L-carnitine (ALC) on behavioral deficits following neonatal anoxia (N2 100% for 25 min at 30 h after birth) was studied in the rat. Transient hyperactivity at P20-P45 postnatal days and permanent spatial memory deficits were shown by anoxic rats. A chronic ALC treatment (50

Effects of l-carnitine on membrane potential derangements induced by palmitoylcarnitine and anoxia in isolated superfused guinea-pig papillary muscle.

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We examined in isolated superfused guinea-pig papillary muscle whether palmitoylcarnitine caused electrophysiological derangements similar to those caused by anoxia, and whether l-carnitine was similarly effective in improving membrane potential characteristics in both cases. Superfusion with

Cardioprotective profile of MET-88, an inhibitor of carnitine synthesis, and insulin during hypoxia in isolated perfused rat hearts.

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3-(2,2,2-trimethylhydrazinium) propionate (MET-88) is an inhibitor of carnitine synthesis. This study was carried out to investigate whether or not reduction of carnitine content could attenuate hypoxic damage in isolated perfused rat hearts. Rats were divided into four groups: 1) vehicle control;

[The neurotropic effect of aplegin (carnitine) in cerebral hypoxia].

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Intravenously injected aplegin (carnitine) competitively displacing glucose, includes metabolic shunt of fatty acids, the activity for which was determined by the presence of free carnitine and was not limited by oxygen unlike the aerobic glycolysis. This effect may have paramount importance in

Hypoxia-induced coronary flow changes in the perfused rat heart: effects of high L-carnitine concentrations.

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1. Hemodynamic effects of physiological (0.04 and 0.07 mM) and high (8, 15 and 25 mM) L-carnitine (LC) concentrations were tested on the normally oxygenated and hypoxic perfused rat heart. 2. No effect was detected on aerobic hearts, whereas a dose-dependent rise in coronary flow (CF) during both

Carnitine deprivation adversely affects cardiac performance in the lipopolysaccharide- and hypoxia/reoxygenation-stressed piglet heart.

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Sepsis and hypoxia are important stressors for the neonate. Newborn infants receiving total parenteral nutrition are routinely deprived of carnitine and develop low carnitine plasma and tissue levels. Because of its high metabolic rate and dependence on fatty acids for energy, the newborn heart may

Role of intrapartum hypoxia in carnitine nutritional status during the early neonatal period.

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We analyze markers of carnitine insufficiency and deficiency, lysine (LYS) and methionine (MET), in 39 neonates with intrapartum hypoxia (selection criteria: umbilical artery pH <7.20, lactate >1.8 mmol/l and PaO2 <25 mm Hg), and in 35 healthy newborn infants (control group) in the early neonatal

Hypoxia-induced lipid peroxidation in rat brain and protective effect of carnitine and phosphocreatine.

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The exposure to hypobaric hypoxia increased lipid peroxidation as indicated by thiobarbituric acid-reactive substances [TBARS] in rat brain. Plasma lactate/pyruvate ratio was used as a marker of hypoxia. We compared the protective effect of alpha-tocopherol with the effect of L-carnitine or

Effects of L-arginine and L-carnitine in hypoxia/reoxygenation-induced intestinal injury.

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BACKGROUND This study was designed to show the role of oxidative stress, nitric oxide and glutathione-related antioxidant enzymes in hypoxia/reoxygenation (H/R)-induced intestinal injury model in mice and to evaluate the potential benefits of arginine and carnitine supplementation. METHODS A total

Effects of L-carnitine administration on VO2max and the aerobic-anaerobic threshold in normoxia and acute hypoxia.

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Seven healthy young male adults were subjected to a total of 56 tests to ascertain the effects of L-carnitine (L-C) and a placebo (P) on ventilation, O2 intake (VO2), CO2 output, heart rate, blood pressure and serum lactic acid, non-esterified fatty acid, glycerol and glucose during strenuous and

[L-carnitine decreases oxidative stress induced by experimental hypobaric hypoxia].

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BACKGROUND It is known that exposure to severe hypobaric hypoxia induces changes of reactive oxygen species (ROS) and antioxidant systems. L-carnitine, a natural compound, has an antioxidant effect and decreases lipid peroxidation. The aim of this study was to investigate the protective effects of

Hypoxia-induced deactivation of NGF-mediated ERK1/2 signaling in hippocampal cells: neuroprotection by acetyl-L-carnitine.

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Cellular and molecular pathways underlying hypoxic neurotoxicity and cell death are multifaceted and complex. Although many potentially neuroprotective agents have been investigated, the protection conferred is often inadequate, resulting in their insufficient clinical utility. In light of the

Metabolic aspects of acute tissue hypoxia during extracorporeal circulation and their modification induced by L-carnitine treatment.

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In this study the authors examine the effects of acute hypoxia due to extracorporeal circulation (ECC) and the role played by L-carnitine treatment on some plasmatic metabolites linked to glycolytic cellular metabolism. To obtain biochemical data, 120 patients in extracorporeal circulation during

Effect of propionyl carnitine on energy charge and adenine nucleotide content of cardiac endothelial cells during hypoxia.

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Adenine mucleotide metabolism is very active in endothelial cells. These cells are very rich in xanthine oxidase which may produce oxygen reactive species during ischaemia and reperfusion when a high amount of adenine nucleotides may be catabolized to hypoxanthine. We investigated the effect of

Influence of acetyl-carnitine on some mitochondrial enzymic activities in the human cerebral tissue in conditions of acute hypoxia.

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Following previous research on human tissue in conditions of acute and massive hypoxia, in the present work the authors compared the cellular enzymic response to oxidative stress in normoxic (perifocal) and hypoxic (focal) areas in human brain affected by regional acute vasculopathies. Two

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