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

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.
 ...
PMID:[Afferentation of the heart in pathological states of the myocardium]. 380 44

Brain ischemia was induced for 10 or 30 min by clamping the common carotid arteries in rabbits whose vertebral arteries had previously been electrocauterized. EEG and tissue content of high energy phosphates were used to verify the ischemic state and to evaluate the degree of postischemic recovery. Extracellular levels and total contents of amino acids were followed in the hippocampus during ischemia and 4 h of recirculation. At the end of a 30-min ischemic period, GABA had increased 250 times, glutamate 160 times, and aspartate and taurine 30 times in the extracellular phase. The levels returned to normal within 30 min of reflow. A delayed increase of extracellular phosphoethanolamine and ethanolamine peaked after 1-2 h of reflow. Ten minutes of ischemia elicited considerably smaller but similar effects. With respect to total amino acids in the hippocampus, glutamate and aspartate decreased to 30-50% of control while GABA appeared unaffected after 4 h of reflow. Alanine, valine, phenylalanine, leucine, and isoleucine increased severalfold. The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, are considered in relation to the pathophysiology of neuronal cell loss during cerebral ischemia.
 ...
PMID:Ischemia-induced shift of inhibitory and excitatory amino acids from intra- to extracellular compartments. 403 Sep 18

Ischemic stroke was induced in the Mongolian gerbil by left common carotid ligation. No change in uptake of [3H]dopamine, [3H]gamma-aminobutyric acid ([3H]GABA), or [14C]glutamate in synaptosomes obtained from the ischemic hemisphere was observed for up to 8 h. At 16 h after ligation, marked decrements in uptake were observed in animals showing hemiparesis: Uptake values expressed as a percent of the corresponding control hemisphere were 15.2% for dopamine, 28.9% for GABA, and 47.5% for glutamate. The differential sensitivity of dopamine terminals compared with glutamate terminals was highly significant. Separate experiments performed with synaptosomes isolated from the corpus striatum showed that the greater sensitivity to damage was intrinsic to the dopamine nerve terminal and not the result of regional variations in ischemic damage in brain. No bilateral effect of ischemia on dopamine uptake was evident. In animals exhibiting milder behavioral deficits (circling), a smaller and comparable decrement in uptake of dopamine, GABA, and glutamate was evident at 16 h, whereas animals not affected behaviorally showed no decrement at 16 h. Following uptake, the subsequent fractional release of neurotransmitter stimulated by 60 mM-potassium ions was not affected at any time point studied. Therefore, the loss in uptake at 16 h probably represents overt destruction of nerve terminals. Experiments with urethane used in place of pentobarbital for anesthesia during carotid occlusion showed that "protection" by pentobarbital was not a factor in the delayed response to ischemia. These results show that damage or destruction of nerve terminals is a delayed event following ischemia and that dopamine terminals are intrinsically more sensitive than glutamate terminals.
 ...
PMID:The differential effect of ischemia on the active uptake of dopamine, gamma-aminobutyric acid, and glutamate by brain synaptosomes. 612 Oct 6

The effect of anoxia and ischemia on the release of amino acid transmitters from cerebellar slices induced by veratridine or high [K+] was studied. Synaptic specificity was tested by examining the tetradotoxin (TTX)-sensitive and the Ca2+-dependent components of stimulated release. Evoked release of endogenous amino acids was investigated in addition to more detailed studies on the stimulated efflux of preloaded [14C]GABA and D-[3H]aspartate (a metabolically more stable anologue of acidic amino acids). [14C]GABA release evoked by either method of stimulation was unaffected by periods of up to 35 min of anoxia and declined moderately by 45 min. In contrast, induced release of D-[3H]Asp increased markedly during anoxia to a peak at about 25 min, followed by a decline when anoxia was prolonged to 45 min. Evidence was obtained that the increased evoked efflux of D'[3H]Asp from anoxic slices was not due to impaired reuptake of the released amino acid and that it was completely reversible by reoxygenation of the slices. Results of experiments examining the evoked release of endogenous amino acids in anoxia were consistent with those obtained with the exogenous amino acids. Only 4 of the 10 endogenous amino acids studied exhibited TTX-sensitive veratridine-induced release under aerobic conditions (glutamate, aspartate, GABA, and glycine). Anoxia for 25 min did not affect the stimulated efflux of these amino acids with the exception of glutamate, which showed a significant increase. Compared with anoxia, effects of ischemia on synaptic function appeared to be more severe. Veratridine-evoked release of [14C]GABA was already depressed by 10 min and that of D-[3H[Asp showed a modest elevation only a 5 min. Stimulated release of D-Asp and labelled GABA declined progressively after 5 min. These findings were compared with changes in tissue ATP concentrations and histology. The latter studies indicated that in anoxia the earliest alterations are detectable in glia and that nerve terminals were the structures by far the most resistant to anoxic damage. The results thus indicated that evoked release of amino acid transmitters in the cerebellum is compromised only by prolonged anoxia in vitro. In addition, it would appear that the stimulated release of glutamate is selectively accentuated during anoxia. This effect may have a bearing on some hypoxic behavioral changes and, perhaps, also on the well-known selective vulnerability of certain neurons during hypoxia.
 ...
PMID:Effects of anoxia on the stimulated release of amino acid neurotransmitters in the cerebellum in vitro. 612 87

The influence of forced motor activity (swimming) on quantitative shifts in neuroactive amino acids (GABA, glutamic and aspartic acids and glycine) was studied in brain tissues of rats and cerebrospinal fluid of cats in health and brain circulation disturbances. The data obtained point to the elevation of the content of amino acids in the brain and appearance of GABA in the cerebrospinal fluid during brain ischemia.
 ...
PMID:[Motor activity and the content of neuroactive amino acids in brain tissues]. 613 64

The effects of in vitro anoxia and membrane depolarization by veratridine on the uptake and release of amino acids were investigated in suspensions of synaptosomes isolated from the forebrains of rats. It was observed that GABA, aspartate and glutamate were released from synaptosomes in anaerobic conditions and upon addition of veratridine in a time-dependent manner. The release of the two latter amino acids was faster and more pronounced than that of GABA. The other amino acids were not affected in any systematic way by either condition. Re-introduction of oxygen or addition of tetrodotoxin to veratridine-treated synaptosomes resulted in the re-uptake of GABA, aspartate and glutamate, which was much faster and more complete for GABA than for the acidic amino acids, especially at acid pH values. The amounts of aspartate and glutamate in the incubation mixture remained constant during all the manipulations whereas that of GABA increased by about 30% during anaerobiosis, in agreement with the results obtained during in vivo ischemia. It is postulated that synaptosomes which utilize glutamate and aspartate as neurotransmitters are more damaged by anoxia and depolarization with veratridine than the population which utilizes GABA. These observations may explain reports that those neurons which are thought to receive major glutamatergic input are particularly sensitive to the lack of oxygen.
 ...
PMID:Neurotransmitter amino acids in the CNS. II. Some changes in amino acid levels in rat brain synaptosomes during and after in vitro anoxia and simulated ischemia. 614 82

The levels of amino acids in 6 regions of the brain (cortex, hippocampus, striatum, diencephalon, stem and cerebellum) were determined during an ischemic insult of 30 min and after recovery periods of up to 10 h. The results were analyzed in two groups: putative neurotransmitters (GABA, aspartate, glutamate, taurine, glycine and alanine) and non-neurotransmitters. In the neurotransmitter group, it was found that at the end of 30 min ischemia the levels of aspartate and glutamate slightly decreased whereas those of GABA and alanine rose substantially. The amounts of glycine and taurine remained unchanged. In 30 min after the ischemic insult, there were much larger decreases in aspartate and glutamate and increases in GABA and alanine with no change in glycine and taurine. At 2 h recovery the levels of the neurotransmitter amino acids had almost returned to control values and were fully recovered by 10 h after ischemia. It is postulated that glutamate and aspartate are released during ischemia into the extracellular space and subsequently 'washed-out' into the blood during the reperfusion. Release of GABA, if it occurs, is however, compensated by increase in its synthesis and decrease in its degradation under anaerobic conditions, both of which contribute to the rise in its steady-state level. In the non-transmitter category, increases were seen in amino acids present normally in very small concentrations; tyrosine, lysine, leucine and 3 hydrophobic amino acids: valine, methionine and phenylalanine, which were most pronounced at 2 h after ischemia. It is suggested that the rise in the levels of these molecules is the consequence of stimulation of protein breakdown caused by activation of intracellular proteases by calcium and H+ during the ischemic episode. Regional variations in the patterns of changes were small although in the ischemic models used the brainstem seemed to be least affected.
 ...
PMID:Neurotransmitter amino acids in the CNS. I. Regional changes in amino acid levels in rat brain during ischemia and reperfusion. 614 83

Activity of protein-O-methyltransferase in synaptosomal fractions was obtained. Km values calculated for S-adenosylmethionine as substrate were 1 microM and Vmax = 4.3 pmoles/mg p/min. In the presence of gelatin (exogenous protein acceptor), activity was about 3 times higher. Without gelatin, activity of endogenous protein-O-methyltransferase decreased by about 20% under hypoxic conditions and by about 15% in ischemia. Exogenous activity under both hypoxic and ischemic conditions did not change. These results can possibly be explained by the changes in methyl acceptor proteins. In normal conditions, after inhibition methylcarboxylation by S-adenosyl-L-homocysteine, the decrease of GABA uptake and increase in the uptake of dopamine were observed. Uptake of serotonine and noradrenaline were unchanged.
 ...
PMID:Protein-O-methyltransferase in brain synaptosomal fraction under normal, ischemic and hypoxic conditions. Possible role in neuronal function. 614 61

Sodium-independent binding of [3H]gamma-aminobutyric acid ([3H]GABA) to membranes prepared from ischemic-damaged rat striatum was studied by kinetic and time-course analysis. Three days after 40 min of ischemia, [3H]GABA binding increased fourfold over control values. Scatchard analysis of the binding showed that ischemia significantly increased the affinity (KD) and the total number of binding sites (Bmax) for the high-affinity GABA receptor. These results support the conclusion that transient forebrain ischemia damages striatal GABAergic neurons.
 ...
PMID:Increased binding of [3H]GABA to striatal membranes following ischemia. 630 Mar 37

Electron microscopy of the sensomotor cortex in 27 rats was performed at varying times (1, 3, 7 days) after arteria carotis communis occlusion. Three groups of rats (5 rats in every group) were treated by nootropil (500 mg/kg daily) in accordance with three time intervals. Control rats were undrugged. More preserved were neurons in the brain of rats treated by nootropil. Neuronal organelles had rare signs of irreversible damages. Membranes were more often preserved, organelles fragmentation and vacuolization were less pronounced. The experimental rats showed neurons containing numerous ribosomes and small new-formed mitochondria. The difference in neuronal structure in treated and untreated rats became more distinct 3-7 days after occlusion. The results obtained are suggested to be connected with the drug ability to normalize ATP metabolism, to stimulate phospholipid synthesis and ribosome function and to increase glucose utilization. The problem of using GABA derivatives in conditions of the most acute brain ischemia is discussed.
 ...
PMID:[Ultrastructural aspects of acute cerebral ischemia during nootropil administration (experimental study)]. 662 31


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>