Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Glutamic acid may protect the ischemic myocardium by increasing the flux through anaerobic pathways for ATP production. We tested this in isolated rabbit hearts that were treated with 0 or 2 mM glutamate. Hearts were stabilized for 30 min, subjected to ischemia for 30 min, and then reperfused for 30 min. Cardiac performance was defined by measuring peak left ventricular pressure (PLVDP) at the apex of a Starling curve and expressed as the %PLVDP attained during the preischemia period. Glutamate improved cardiac performance (%PLVDP, treated vs. untreated) after moderate ischemia (92 vs. 67), severe ischemia (79 vs. 65), and total ischemia (61 vs. 41). During severe ischemia, improved performance was associated with enhanced release (nmol X g wet wt -1 X min -1, treated vs. untreated) of alpha-ketoglutarate (2.3 vs. 1.3), succinate (21.7 vs. 12.3), and lactate (478 vs. 386). The ischemic myocardial content (nmol/mg myocardial protein, treated vs. untreated) of alpha-ketoglutarate (1.7 vs. 1.2) was increased by glutamate. The ischemic content of ATP (25.4 vs. 21.9) and succinate (15.7 vs. 12.1) showed a slight trend toward improvement under glutamate treatment. The study shows an association between improved postischemic cardiac performance and increased production of alpha-ketoglutarate and succinate during glutamate treatment.
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PMID:Protection of ischemic rabbit myocardium by glutamic acid. 613 48

Glutamic acid plays an important role as a main excitatory amino acid and also as one of the central metabolites in the central nervous system (CNS). This amino acid also acts as a toxic substance in the vertebrate CNS, including the retina, especially in ischemic conditions. This paper reviews recent advances in retinal research on glutamate metabolism and its relationship with pathogenesis of retinal diseases. Excessive administration of glutamate induces overstimulation of N-methyl-D-aspartate (NMDA) and non-NMDA receptors, and influx of Na+, Cl-, and water to postsynaptic elements, causing lysis and swelling. In hypoxic or ischemic conditions, accumulation of glutamate was observed in most parts of the retina. Morphological and functional changes induced by ischemia could be prevented by preadministration of an antagonist of NMDA receptors. These results suggest that the same pathological mechanism as in the CNS exists in the retina. They also suggest that a new pharmacological approach for treating retinal abnormalities caused by ischemia could be introduced in the ophthalmology clinic in the near future. Abnormality of glutamate dehydrogenase, an important enzyme in the glutamate metabolism, has been reported in patients with spinocerebellar degenerations. Retinal dystrophy was also reported in some of them. Partial deficiency of heat-labile activity of this enzyme has been reported to be profoundly related with those patients with retinal abnormalities. This suggests that not only glutamate itself, but also abnormalities in its metabolic path way might be deeply correlated with the pathogenesis of retinal degeneration.
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PMID:[Dual nature of excitatory amino acids in the vertebrate retina]. 819 8

We investigated the disruption of spatial cognition due to transient forebrain ischemia using an 8-arm radial arm maze task in rats. Five or 10 min of ischemia did not affect the task acquisition. When rats established spatial cognition by daily training of the task, 10 min of ischemia significantly decreased the number of correct choices and increased the errors in the task when performed 24 h after reperfusion. These changes, however, returned to the normal level after about 4 days of daily training. Glutamic acid (Glu) and acetylcholine (ACh) release from the dorsal hippocampus (DH) was observed to transiently increase during ischemia. However, neither the content of noradrenaline (NA) nor the release of NA in the DH changed during ischemia. The NA and ACh release from the DH, however, gradually decreased during reperfusion, and the decrease became significant at 24 h after reperfusion. The NA content of the frontal cortex (FC) and the DH increased 7 days after reperfusion. These results suggest that the disruption of spatial cognition induced by 10 min of ischemia may be attributed to a greater degree to the dysfunction of the hippocampal ACh and NA, and cortical NA systems, rather than to the development of neuronal cell death in these areas.
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PMID:The disruption of spatial cognition and changes in brain amino acid, monoamine and acetylcholine in rats with transient cerebral ischemia. 883 52

Glutamic acid, an excitatory amino acid, has been proposed to play a major deleterious influence in cerebral ischemia. However, the neuroprotective activity of various glutamate receptor antagonists is often low or absent, according to the animal model used. In the present study, we examined the effect of several antagonists acting on glutamate receptors of the N-methyl-D-aspartate (NMDA) type in rats submitted to a brief (5 minutes) global cerebral ischemia. The different compounds used were poorly active or inactive on behavioural and histologic alterations induced by ischemia. Our results suggest that, in this model, overactivation of NMDA receptor complex does not play a predominant role in the pathogenesis of ischemic brain damage.
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PMID:[Inefficacy of N-methyl-D-aspartate receptor complex antagonists on behavioral and histologic consequences of global cerebral ischemia in rats]. 1091 75

The efficacy of pre-, intra-, and postoperative prevention of hemodynamic disorders by creatinine phosphate, cytochrome C, and glutamic acid was evaluated in 61 coronary patients with decreased myocardial contractility. All these agents exerted a positive inotropic effect in coronary patients with ejection fraction below 0.4, increasing the stroke volume and left-ventricular ejection fraction without modifying heart rate. Glutamic acid is not recommended for preoperative treatment, because it increases oxygen consumption by the myocardium above the reserve potential of the coronary bed. Cytochrome C is the most effective drug for preoperative treatment. Intraoperative preischemic protection of the myocardium by cytochrome C in coronary patients during high risk operations prevents the development of unfavorable hemodynamic complications during induction and maintenance of anesthesia before artificial circulation, provides favorable recovery of cardiac activity, decreases the incidence of severe arrhythmias, promotes a rapid and full-value recovery of myocardial contractile function after ischemia, and decreases the incidence of acute heart failure.
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PMID:[Prevention of disorders of myocardial contractile function in patients with ischemic heart disease during aortocoronary shunting]. 1145 65