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dimethylxanthine/hypoxia
Veza se sprema u međuspremnik
9 rezultati
Systemic hypoxia and the depression of synaptic transmission in rat hippocampus after carotid artery occlusion.
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The relationship between step reductions in inspired oxygen and the amplitude of evoked field excitatory postsynaptic potentials (fEPSPs) recorded from hippocampal CA1 neurons was examined in anaesthetized rats with a unilateral common carotid artery occlusion. The amplitudes of fEPSPs recorded from
Adenosine A1 receptor activation mediates NMDA receptor activity in a pertussis toxin-sensitive manner during normoxia but not anoxia in turtle cortical neurons.
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Adenosine is a defensive metabolite that is critical to anoxic neuronal survival in the freshwater turtle. Channel arrest of the N-methyl-d-aspartate receptor (NMDAR) is a hallmark of the turtle's remarkable anoxia tolerance and adenosine A1 receptor (A1R)-mediated depression of normoxic NMDAR
Adenosine A1-receptor mechanisms antagonize beta-adrenergic pulmonary vasodilation in hypoxia.
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Hypoxic pulmonary vasoconstriction is refractory to beta-adrenergic receptor (beta-AR)-mediated pulmonary vasodilation. We hypothesized that hypoxic pulmonary arteries release adenosine (Ado) that antagonizes beta-AR-mediated pulmonary vasodilation. Using isolated rat pulmonary artery rings, we
Synthesis, brain antihypoxic activity and cell neuroprotection of 1-substituted-3,7-dimethylxanthines.
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Five newly synthesised original compounds were investigated for acute toxicity, influence on hexobarbital sleeping time, effect on the locomotor activity, and brain antihypoxic activity. Two of the compounds were tested in a model of glutamate induced neurotoxicity in the brain cell culture using a
Endogenous adenosine does not activate ATP-sensitive potassium channels in the hypoxic guinea pig ventricle in vivo.
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BACKGROUND
The activation of ATP-sensitive K+ (K+ ATP) channels by K+ ATP openers, eg, pinacidil, hypoxia, and ischemia, is known to shorten the ventricular action potential. Since adenosine is released in increased amounts during cardiac hypoxia and ischemia, the hypothesis that endogenous
Endogenous adenosine delays the onset of hypoxic depolarization in the rat hippocampus in vitro via an action at A1 receptors.
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The effect of endogenous adenosine on the delay to hypoxic depolarization (HD) was examined utilizing in vitro slices of gerbil hippocampus. Adenosine receptor antagonists were used to block the actions of adenosine during hypoxia, and the delay to HD was measured in the CA1 region. Both a broad
Mechanism of adenosine accumulation in the hippocampal slice during energy deprivation.
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The mechanism by which adenosine accumulates in the hippocampal slice during energy deprivation was investigated by examining the adenosine A1 receptor mediated depression of synaptically evoked field potentials in the CA1 area. Blocking of the mitochondrial electron transport chain with 200 microM
The effects of post-treatment with lisofylline, a phosphatidic acid generation inhibitor, on sepsis-induced acute lung injury in pigs.
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The effects of lisofylline [(R)-1-(5-hydroxyhexyl)-3,7-dimethylxanthine] (LSF), an inhibitor of de novo phosphatidic acid (PA) generation, on sepsis-induced acute lung injury was studied using Hanford minipigs weighing 18 to 25 kg. Sepsis was induced by an intravenous infusion of Pseudomonas
Hypothesis: adenosine mediates hemodynamic changes in renal failure.
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The decreased filtration fraction and glomerular filtration rate characteristic of renal failure could be produced, at least in part, by increased concentration of an endogenous substance which constricts afferent and dilates efferent arterioles. Adenosine satisfies several criteria: (a) exogenous
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