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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well established that excitatory amino acid neurotransmitters are extensively liberated during ischemia and that they have neurotoxic properties contributing to neuronal injury. To study changes in the liberation of excitatory and other amino acids during cerebral ischemia, we measured their extracellular concentrations and related them to blood flow levels and electrophysiologic activity (electrocorticogram and auditory evoked potentials) before and for up to 2 hours after multiple cerebral vessel occlusion in 14 anesthetized cats. Blood flow levels between 0 and 43 ml/100 g/min were reached. Concentrations of the excitatory amino acid neurotransmitters increased most (aspartate 10-fold, glutamate 30-fold, and gamma-aminobutyric acid 300-fold compared with control values) below a blood flow threshold of 20 ml/100 g/min. The total power of the electrocorticogram and the amplitude of the auditory evoked potentials were affected below the same blood flow threshold. In contrast, concentrations of the nontransmitter amino acids taurine, alanine, asparagine, serine, and glutamine increased 1.5-5-fold as blood flow decreased, while concentrations of the essential amino acids phenylalanine, valine, leucine, and isoleucine did not change during cerebral ischemia. The great increases in concentrations of the excitatory amino acid neurotransmitters below a blood flow threshold close to that for functional disturbance is in accordance with the role of these amino acids in ischemic cell damage. Their release at blood flow levels compatible with cell survival and the increase in their concentrations with severity and duration of cerebral ischemia imply that excitotoxic antagonists may have potential as therapeutic agents.
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PMID:Differences in ischemia-induced accumulation of amino acids in the cat cortex. 197 18

Starting from the assumption that tumor cells constantly experience transient ischemia and anoxia, and that this results in metabolic stress which is reflected above all, on the concentration of ATP, ADP and AMP, in other words, the adenine nucleotide pool (AdN), the aim of our research was to study the degradation and resynthesis kinetics of that pool on two types of malignant cells. All experiments were conducted in vitro with cells of the transplantable tumors of Ehrlich's ascitic carcinoma and the AS 30D hepatoma, and metabolite analyses were carried out enzymatically or by way of the HPLC chromatography method. It was found that immediately after the setting on of anoxia, there comes not only to a fall in ATP, but also to a fall in the complete adenine nucleotide pool for about 50%. The further maintenance of anaerobiosis does not have a significant influence on the AdN pool. The adenine nucleotide pool resynthesis is very rapid in the examined cells, and in the presence of glutamine and inosine, there comes to an occurrence of its significant growth. Evidence is given that the resynthesis in Ehrlich's ascitic carcinoma cells is made possible through the purine nucleotide cycle, which probably brings about the intensive glutamine oxidation and aspartate production, while in the AS 30D hepatoma cells it develops by means of adenosine kinase. The AS 30D hepatoma cells maintain a high ATP level in the absence of oxygen for a long time, provided that iodine-acetate is not added, which points to the fact that they have some other kind of energetic reserve aside from ATP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Kinetics of degradation and resynthesis of the adenine-nucleotide pool in tumor cells]. 209 81

2D COSY 1H NMR with surface coil has been used to resolve and assign cerebral metabolites which had previously been detected but could not be resolved or assigned in situ in the living animal by conventional 1D 1H NMR. A wide range of cerebral metabolites, including alanine, N-acetyl aspartate, aspartate, choline derivatives, creatine/phosphocreatine pool, GABA, glucose, glutamate/glutamine pool, inositol, lactate and taurine were simultaneously resolved and assigned in situ in the whole animal using the 2D COSY correlation graphs. Global irreversible ischemia caused the appearance and the disappearance of cross-peaks in the 2D COSY 1H NMR map, corresponding to increases in alanine, GABA and lactate and glucose depletion.
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PMID:2D COSY 1H NMR: a new tool for studying in situ brain metabolism in the living animal. 235 67

After portacaval shunt in the rat, the transport of tryptophan and other neutral amino acids across the blood-brain barrier is enhanced. To determine the role of NH3 in the intracerebral transfer of tryptophan and serotonin metabolism, solutions containing either saline or NH3 or tryptophan or NH3 + tryptophan together were infused, respectively, into the internal carotid artery of rats in order to achieve blood levels similar to those observed after liver ischemia. After tryptophan infusion, a significant increase in the hypothalamic levels of tryptophan and 5-hydroxyindoleacetic acid was observed. A similar increment was found after NH3 infusion. NH3 + tryptophan infusion induced a significant increment in hypothalamic tryptophan and 5-hydroxyindoleacetic acid levels which were 2-fold greater than after tryptophan infusion. There was no significant change in 5-hydroxytryptamine levels in any of these experiments. Glutamine levels increased significantly after NH3 infusion. When tryptophan and NH3 were infused simultaneously, a significant reduction in glutamine levels occurred. These results cannot be explained by any modification of cerebral blood flow nor of the cerebral intercellular pH. Our data suggest that NH3 enhances the transfer of tryptophan across the blood-brain barrier and thus stimulates serotonin metabolism. The mechanism by which tryptophan transfer across the blood-brain barrier is facilitated is unknown. The reduction in glutamine levels in the hypothalamus when NH3 and tryptophan are infused together may be explained either by an inhibition of synthesis or by an intercellular influx of neutral amino acids and an efflux of glutamine as suggested by James et al.
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PMID:Evidence for the role of ammonia in the intracerebral transfer and metabolism of tryptophan. 242 70

Rats with a portacaval anastomosis and ligation of the hepatic artery 2 days later were infused for 6 hr with a 10% glucose solution (group I) or the same solution combined with 0.24 M/liter branched-chain amino acids (BCAA, group II). Control animals with portacaval anastomosis and sham-operation (group III) or two sham-operations (group IV) were infused with a 10% glucose solution. The rats were killed by decapitation and indoleamines and amino acids were determined in the brain. Rats with liver ischemia were stuporous at the end of the experiment irrespective of treatment. The concentrations in the cortex of lysine, methionine, phenylalanine, threonine, alanine, glutamine, glycine, histidine, and tyrosine were significantly increased in group I compared to group IV. Infusion of BCAA to rats with liver-ischemia (group II) resulted in significantly lower concentrations of lysine, methionine, phenylalanine, threonine, histidine and tyrosine and increased concentrations of isoleucine, leucine, valine, and arginine compared to group I. The content of serotonin in the cortex and brain stem was significantly increased in group I compared with the BCAA-treated animals (group II) and the control groups III and IV. The concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in the cortex and brain stem were higher in group I than in group IV. Infusion of BCAA to rats with liver ischemia normalized the concentrations of 5-HIAA in the cortex and brain stem.
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PMID:Amino acids and indoleamines in the brain after infusion of branched-chain amino acids to rats with liver ischemia. 242 87

Glucose metabolism is altered in various pathologic conditions in the brain, i. e. ischemia, epilepsy and hypoglycemia. Therefore, analysis of glucose metabolism in pathologic conditions needs careful investigation of that in steady state. 13C-NMR method allows continuous sequential monitoring of changes in metabolism of glucose in vivo. The natural abundance of 13C is quite low (1.1%) and by administering 13C labelled in various skeleton in glucose, it is possible to monitor the metabolites in vivo. In this study, 13C glucose labelled in 1-position of carbon was employed to investigate the metabolic pathways in the control and transient ischemic gerbil brain with reperfusion. Male mongolian gerbils weighing 60-80 g were employed in this study. The gerbils were anesthetized by intraperitoneal administration of pentobarbital. The right skull was exposed and a surface coli was placed directly above the skull bone. After the operation, the animals were fastened to the NMR probe vertically. 500 mg/kg of [1-13C] glucose was injected via femoral catheter. 13C-NMR spectra were serially obtained before and after injection with GX-270 NMR spectrometer (JEOL, Tokyo, Japan, 6.34 T). In other series of experiments, 30 minutes of cerebral ischemia were induced after 15 minutes of glucose injection by the bilateral common carotid artery occlusion. In the normal gerbil brain, after administration of [1-13C] glucose (500 mg/kg), alpha and beta-anomers of [1-13C] glucose peak appeared abruptly and reached its peak level at 7.5-15 min acquisition period. The C2 peak representing glutamate and/or glutamine appeared later. The C3 and C4 peak started to appear even later at 30-40 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The metabolism of glucose monitored by 13C-NMR in the gerbil brain in vivo-natural course and application to the ischemic model]. 273 47

The effect of intravenous glutamic acid infusion (3 mg/kg/min) was studied during myocardial ischemia and reperfusion in anesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Glutamic acid reduced the ischemic contractile depression 2 min after a 60%-reduction of the coronary blood flow. The left ventricular systolic pressure was decreased by 9% versus 22%, dP/dt by 16% versus 29%, left ventricular systolic pressure heart rate product by 16% versus 31%. Reperfusion with glutamic acid improved the recovery of cardiac performance without any increase in myocardial oxygen consumption. Glutamic acid infusion resulted in a 2-fold augmentation of glutamate uptake by the ischemic myocardium. It led to cessation of ammonia release by the heart due to activation of glutamine synthesis, enhancement of alanine formation coupled with pyruvate utilization and did not change lactate production. The mechanisms of the protective action of glutamic acid are discussed.
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PMID:[Correction of contractile function and metabolism in canine ischemic myocardium due to exogenous glutamic acid]. 286 92

The effect of intravenous infusion of glutamic acid on cardiac contractile function during short-term ischemia and subsequent reperfusion was studied in anaesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Infusion of glutamic acid at 3 mg/kg/min resulted in less depression of cardiac function when given after a 2 min period of 60% coronary blood flow reduction: left ventricular systolic pressure decreased by 9% vs. 22%, dP/dt decreased by 16% vs. 29%, the double product (left ventricular systolic pressure by heart rate) was reduced by 16% vs. 31%. When reperfusion was carried out during glutamic acid infusion there was a significantly enhanced recovery in cardiac function. The augmentation of cardiac performance in ischemia and reperfusion caused by glutamic acid was not accompanied by changes in myocardial oxygen consumption. Glutamic acid uptake by the ischemic myocardium increased 2-fold during infusion. This led to cessation of ammonia release from the heart due to stimulation of glutamine synthesis, and an enhancement of alanine formation coupled with pyruvate uptake but it did not effect lactate production. However, glutamic acid infusion did not influence cardiac performance and metabolism under conditions of normal coronary flow. The results suggest that elevation of glutamate arterial concentration exerts a beneficial effect on ischemic heart. The mechanisms of the protective action are discussed.
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PMID:Function and metabolism of dog heart in ischemia and in subsequent reperfusion: effect of exogenous glutamic acid. 286 19

Seventeen patients undergoing radical correction of Fallot's tetrad or defects of interventricular septum were investigated. Needle biopsies from the left ventricular apex region were obtained at the 1st min after cross-clamping of the aorta and at the end of cardiac arrest to determine adenosine triphosphate (ATP), glutamate, aspartate, alanine and ammonia. The losses of ATP during clamping period were related to decrease in glutamate. The fall in ATP by more than 20% of the initial level was accompanied by a significant decrease in aspartate, an accumulation of alanine and ammonia in cardiac tissue but did not affect glutamine content. The data obtained prove the participation of specific nitrogenous compounds of human heart, and especially glutamate, in response to energy depletion during ischemia.
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PMID:Ischemic heart arrest: nitrogenous metabolism in energy-depleted human myocardium. 288 54

The effects of balloon inflation on myocardial perfusion and metabolism were studied during aortic valvuloplasty in 17 patients with aortic stenosis, including 6 with associated coronary artery disease. Coronary sinus flow and blood samples were obtained before and during the first inflation, and 5 to 10 minutes after the last inflation. During inflation, coronary blood flow decreased (272 +/- 111 standard deviation to 166 +/- 92 ml/min; p less than 0.05), myocardial oxygen uptake fell and transcardiac lactate handling shifted from extraction to production (35 +/- 54 to -41 +/- 48 mumol/min; p less than 0.01). At the end of the procedure, aortic valve area had increased from 0.51 +/- 0.22 to 0.81 +/- 0.48 cm2 (p less than 0.002). Coronary sinus flow increased slightly above control values (+6%; difference not significant) and myocardial oxygen and lactate uptakes were back to control values. However, myocardial alanine production had increased from -3.6 to -6.6 mumol/min (p less than 0.05) and glutamine production was reduced or replaced by extraction (-3.3 +/- 2.1 to 3.5 +/- 3.8 mumol/min; p less than 0.05). Recovery of coronary flow, oxygen and lactate uptakes was not significantly different in patients with or without coronary artery disease, although the former patients tended to have less glutamine extraction and less improvement in their ejection fraction at the end of the procedure. Thus, aortic balloon valvuloplasty produces brief episodes of low-flow ischemia. Recovery of oxidative metabolism is almost immediate after deflation and no detrimental effect seems to persist at the end of the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in coronary blood flow and myocardial metabolism during aortic balloon valvuloplasty. 296 50


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