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

The levels of the neurotransmitter amino acids glutamate, aspartate, and GABA were determined in different brain regions during ischemia and post-ischemic recirculation periods using the unilateral carotid artery occlusion model of stroke in gerbils. The levels of glutamate, aspartate and GABA in ischemic hemisphere were increased significantly by 10 min of ischemia and later declined with time. Reperfusion for 30 min following 10 min. of ischemia further enhanced the levels of glutamate and aspartate. Increase in GABA levels were found during early periods of reperfusion. Regional variations in the changes of amino acids' levels were noticed following ischemia. Hippocampus showed the highest increase in glutamate levels followed by striatum and cerebral cortex. Aspartate levels in striatum and hippocampus increased during 10 min ischemia (46% and 30%) and recirculation (70% and 79%), whereas in cerebral cortex the levels were doubled only during recirculation. Ischemia induced elevations of GABA levels were observed in cerebral cortex (68%) and in hippocampus (30%), and the levels were normalized during recirculation. No changes in GABA levels were found in striatum. It is suggested that the large increase in the levels of excitatory neurotransmitter amino acids in brain regions specially in hippocampus during ischemia and recirculation may be one of the causal factors for ischemic brain damage.
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PMID:Changes in regional levels of putative neurotransmitter amino acids in brain under unilateral forebrain ischemia. 257 Oct 93

N-methyl-D-aspartate (NMDA) receptors are thought to mediate much of the central neuronal loss produced by certain neurologic insults, including hypoxia-ischemia, hypoglycemia, and trauma. Therefore, the specific vulnerability of GABAergic inhibitory neurons to NMDA receptor-mediated toxicity might be an important determinant of the potential for epileptogenesis following these insults. We have examined the fate of GABAergic cortical neurons in mouse cell cultured neuronal population) were identified either by immunoreactivity with antisera to GABA or by autoradiography following high-affinity uptake of 3H-GABA. Cultures exposed for 5 min to 20 to 750 microM NMDA showed NMDA concentration-dependent, widespread neuronal loss. However, GABAergic neurons were relatively spared, and thus represented an enhanced fraction of neuronal survivors. These observations suggest that GABAergic cortical neurons may possess some intrinsic resistance to NMDA receptor-mediated neurotoxicity, a property which might convey an anticonvulsant "inhibitory safety factor" to neocortex against certain forms of injury.
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PMID:GABAergic neocortical neurons are resistant to NMDA receptor-mediated injury. 265 68

Based on changes in glucose and related brain metabolism in aging, it is discussed whether or not age is a risk factor for dementia. Normal brain function is tightly coupled with the availability of sufficient amounts of ATP which is normally formed from the oxidation of glucose only. The glycolytic and oxidative cerebral glucose metabolism is controlled by various mechanisms. Glucose breakdown also contributes to the formation of the neurotransmitters acetylcholine, glutamate, aspartate, and GABA. ATP yields the basis for the maintenance of neuronal homeostasis via ion homeostasis, integrity of cellular components, and intracellular transportation processes. It is also necessary for the formation of several neurotransmitters and neurohormones. Normal cerebral aging is associated with an incipient perturbation in cerebral glucose and related metabolism causing an energy deficit and thus an imbalance of cell homeostasis beyond the seventh or eighth decade of life, pointing to a threshold phenomenon. Such processes may begin insidiously, but may be assumed to progress exponentially in a self-propagating manner. These events markedly reduce the biological plasticity of the brain which may become abnormal after cerebral stress situations such as ischemia, etc. Thus, the increasing damage of neuronal homeostasis may give rise to the assumption that age, or several age-related metabolic abnormalities at the cellular level, may be regarded as risk factors for dementia.
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PMID:[Age as a risk factor for the development of dementias? Consideration of changes in cerebral glucose metabolism with increasing age]. 267 95

The aim of this study was to measure changes in the extracellular fluid (ECF) concentration of lactate, pyruvate, purines, amino acids, dopamine, and dopamine metabolites in the striatum of rats subjected to focal cerebral ischemia, using intracerebral microdialysis as the sampling technique. Microdialysis probes were inserted into the lateral part of the caudate-putamen bilaterally 2 h before the experiment. Ischemia was induced by permanent middle cerebral artery occlusion (MCAO) on the left side. Microdialysis samples were analyzed by high performance liquid chromatography. Following MCAO, the concentration of lactate, adenosine, inosine, and hypoxanthine rose markedly in the ECF on the occluded side, while there was no significant change in pyruvate. These changes were accompanied by dramatically elevated levels of aspartate, glutamate, taurine, gamma-aminobutyric acid, and dopamine. There was also a marked increase in alanine/tyrosine, while minor or no changes occurred with other amino acids. Concomitantly, the ECF level of the dopamine metabolites 3,4-dihydroxyphenylacetate and homovanillic acid decreased. There was no significant increase in any of the metabolites measured on the right, nonoccluded side. In relation to the concept of excitotoxicity in brain ischemia, it is concluded that during the acute stage of focal cerebral ischemia, the ECF is flooded with both potentially harmful (e.g., aspartate, glutamate, and DA) and protective (e.g., taurine, GABA, and adenosine) agents. The relative importance of these events for the development of cell death in the ischemic penumbra needs to be elucidated. In addition, lactate, inosine, and hypoxanthine, measured in the ECF by intracerebral microdialysis, may prove to have diagnostic and/or prognostic value in neurometabolic monitoring of the ischemic brain.
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PMID:Dynamics of extracellular metabolites in the striatum after middle cerebral artery occlusion in the rat monitored by intracerebral microdialysis. 277 32

Focal brain lesion is known to induce changes of blood flow and glucose metabolism in the areas other than the lesioned part itself. A well known example of this remote effect is so called diaschisis. To clarify the role of neurotransmitters in this phenomenon, amino acid neurotransmitters were measured in rat basal ganglia after middle cerebral artery occlusion. In the same ischemia model, blood flow and glucose metabolism have been reported to increase in the ipsilateral substantia nigra and globus pallidus in the postischemia period. Our results showed that GABA and aspartate were reduced in ipsilateral substantia nigra and globus pallidus from the 3rd day on, with glutamate level showing no significant change. In the contralateral substantia nigra, GABA increased significantly from the 1st day through the 28th day, whereas glutamate or aspartate showed no significant change. The same, although less pronounced, tendency was observed in the contralateral globus pallidus. In contralateral striatum, GABA increased only during the 1st week. These results may be interpreted as follows. GABA and aspartate were reduced in ipsilateral substantia nigra and globus pallidus due to the afferent pathway interruption caused by focal ischemia. The reduction of inhibitory GABA probably set neurons in these nuclei in a relatively activated state, resulting in the elevation of glucose metabolism and blood flow. Increment of GABA in contralateral substantia nigra and globus pallidus can be attributed to a compensation for the reduction inn ipsilateral nuclei, because the increment was observed even in a chronic phase. This hitherto unknown phenomenon will raise an interesting problem as to the plasticity of the damaged brain.
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PMID:[Regional and time-sequential changes in amino acid neurotransmitters after focal cerebral ischemia in the rat]. 288 Jun 1

Anticonvulsant sodium valproate, an inhibitor of GABA transaminase, which induces GABA accumulation in the brain, has been shown to possess a potent antiarrhythmic effect. In acute ischemia and reperfusion in conscious rats with closed chest, it decreased fourfold total duration of arrhythmias, while in nonanesthetized animals with open chest, it substantially limited the heart electrical fibrillation threshold and reduced fourfold total duration of arrhythmias. In both experimental models, sodium valproate decreased threefold the rate of ischemia-induced heart fibrillations. Clinicophysiological evaluation of the effect of sodium valproate on arrhythmias in coronary patients appears warranted.
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PMID:[Prevention of arrhythmias and cardiac fibrillation in acute ischemia and reperfusion by using a factor causing GABA accumulation in the brain]. 311 16

Gamma-aminobutyric acid and dl-baclofen decrease the resistance against ischemia appraised by the number of ischemic episodes tolerated before electrocorticographic silence or cardiac arrest. D-enantiomer of baclofen does not exhibit this deleterious result in high doses either; it even counteracts the effect of its racemate and that of GABA. These data suggest that, in the brain, GABA and baclofen act at the same GABA-B receptor. This is in contrast to the existence of two distinct receptors demonstrated for the antinociceptive effects on the spinal cord.
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PMID:Stereoselectivity of the inhibiting effects of baclofen on the electrogenesis of the rat cortex under ischemia. 360 13

Marked systemic resistance to damaging effects of stress develops as a result of repeated short-term stress exposures. This kind of adaptation is ensured by the activation of stress-limiting systems, namely, the opioidergic, GABA-ergic, serotoninergic, as well as antioxidant and prostaglandin ones. Proceeding from the stress-limiting system concept, adaptation to repeated stress exposure, as well as metabolites, synthetic analogues and activators of stress-limiting systems were successfully used to prevent and eliminate cardiac arrhythmias and fibrillations associated with acute ischemia, myocardial infarction and postinfarction cardiosclerosis. Prospects of further studies of stress-limiting systems' metabolites and activators as antiarrhythmic agents are considered.
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PMID:[Stress-limiting systems and the problem of the prevention of arrhythmia]. 365 20

Changes in cerebral free amino acids, catecholamines and uric acid levels were explored for up to 7 days after cerebral ischemia in the rat. Fifty male Sprague-Dawley rats were subjected to occlusion of the middle cerebral artery on the olfactory tract, under halothane anesthesia. The animals were decapitated at 2, 4, 6, 12, 24 hours and 2, 3, 5, 7 days after the surgery, respectively. The brains were rapidly removed. The cerebral hemispheres were divided into right and left halves, and homogenized in sulfosalicylic acid solution. Free amino acids were analyzed by colormetric method. Cathecholamines and uric acid were analyzed by high-performance liquid chromatography. Each parameters were measured both on the ischemic and contralateral hemispheres. The time course of changes in each parameters were observed by means of the ratio, which is the value of ischemic side divided by that of contralateral side. Free amino acids Dicarboxylic group; Decreases in glutamate and increases in glutamine suggest one aspect of detoxication of ammonia within the ischemia tissue. Monocarboxylic group; GABA, glycine, alanine were increased in early ischemic state, and gradually lowered to the normal values. These suggest the impairment of tricarboxylic acid (TCA) cycle in the ischemic tissues, since these amino acids are closely related to TCA cycle. Essential amino acids, except for tryptophan, were increased until the end of study. These increases suggest the utilization of essential amino acids for protein synthesis might be disturbed in the ischemic tissues. Catecholamines and precursors; Norepinephrine and dopamine were lowered gradually. On the other hand, phenylalanine and tyrosine were increased during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Biochemical studies of the cerebral ischemia in the rat--changes in cerebral free amino acids, catecholamines and uric acid]. 370 75

The state of afferent connections between sinoatrial node zone (SNZ) in the normal and affected myocardium (reversible ischemia, necrosis) and rostral parts of the brain cortex (RPC) was studied with the help of evoked potentials in acute experiments on cats. Interruption of afferent connections (SNZ-RPC) during reversible ischemia and experimental myocardial necrosis of the right ventricle was revealed. Ultramicroscopic data of SNZ studies as well as electrophysiologic changes registered in RCP during irritation of the peripheral part of the right vagus nerve and local application of GABA on SNZ suggest possible interruption of cardiac afferentation at the level of SNZ due to the mechanism of presynaptic inhibition.
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PMID:[Afferentation of the heart in pathological states of the myocardium]. 380 44


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