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

The influence of prolonged postischemic hyperventilation was studied in the model of global brain ischemia produced by 15 min cardiac arrest in dogs with 8 h recirculation. Histopathological examination of neuronal damage using silver impregnation showed the presence of numerous heavy argyrophylic neurons in the striatum and CA2 hippocampal subfield after 8 h of normoxic reperfusion. In dogs with prolonged 8 h postischemic hyperventilation a reduction in the occurrence of argyrophylic neurons in the striatum and their significant decrease in the hippocampal area were found. Electron microscopic study was performed to characterize the effect of respiratory alkalosis on the ultrastructural changes in neurons and correlate them with the results of silver impregnation. Ultrastructural analysis after the cardiac arrest without recirculation did not reveal the presence of dark neurons within the striatal and hippocampal areas. Neuronal alterations included a decrease in endoplasmic reticulum, mitochondrial swelling and a mild chromatin clumping. After 8 h of normoxic reperfusion many dark, shrinked neurons containing perinuclear clusters of clear vesicles were found. In hyperventilated animals the occurrence of dark neurons with extensive perineuronal edema was substantially reduced in the CA2 subfield. The effect of hyperventilation on postischemic calcium overload is discussed.
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PMID:Effect of prolonged hyperventilation on ischemic injury of neurons after global brain ischemia in the dog. 756 Sep 2

The mechanisms underlying the response of the brain to ischemia are not fully understood. Biochemical and morphological changes following neocortical infarction can be investigated in rats using a model of focal cerebral ischemia induced by unilateral occlusion of the middle cerebral artery (MCA). Evaluation of ischemic damage often employs conventional histologic stains. Immunocytochemistry can be used as a valuable tool in this model to define changes in specific proteins of interest. In this study, an antiserum raised against insulin-like growth factor II (IGF-II) receptor was used to evaluate changes of IGF-II receptor immunoreactivity in the cerebral cortex of rats 4 and 7 days following permanent MCA occlusion. IGF-II receptor immunoreactivity was found to be associated with neocortical pyramidal neurons within the core of the ischemic infarct itself. The staining intensity was markedly elevated above that observed in nonischemic neurons. Immunopositive neurons exhibited a punctate staining pattern. These neurons appeared to correspond to argentophilic neurons, as defined by modified Bielschowsky silver staining. Evaluation of other neuronal markers revealed the absence of immunoreactivity for neuron-specific enolase and for tyrosine hydroxylase within the ischemic area. These observations show an increase in a specific growth factor receptor within neurons in the ischemic core of a focal infarct several days following permanent focal infarction, a time when neurons are presumed to be dead. The significance and the potential role of IGF-II receptor in lesion-induced plasticity are discussed.
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PMID:Increase in insulin-like growth factor II receptor within ischemic neurons following focal cerebral infarction. 759 34

Evidence suggests that ischemic neuronal necrosis may ultimately be the result of excessive intracellular calcium accumulation. In principle, abnormal calcium concentrations during ischemia are derived from three main sources: exaggerated influx via (a) voltage-operated channels, (b) receptor-controlled channels (f. ex. NMDA) and (c) the release of intracellular calcium ion stores. Previous studies using either calcium channel blockers or NMDA antagonists have demonstrated only limited protective effects of these agents in global transient cerebral ischemia, whereas little or no attention has been paid to the calcium sources listed under (c). Dantrolene has been shown to block the increase in free intracellular calcium ion stimulated by either NMDA or glutamate. Thus we postulated that dantrolene might improve neuronal survival in vulnerable regions to ischemia such as the CA1 hippocampus. Male Sprague-Dawley rats (300 approximately 400 g) were prepared for a four-vessel occlusion model of cerebral ischemia. Complete cerebral ischemia was induced by snaring the carotid arteries for 15 mins and maintaining mean arterial pressure at 80 mmHg. Strict attention was paid to keep normal blood gas values. Following ischemia halothane anesthesia was discontinued, and rats were extubated and when stable transferred to cages with free access to water and food. Rats survived for 7 days under close supervision, after which they were anesthetized with pentobarbital and perfused transcardially with 4% paraformaldehyde/sodium-phosphate buffer. The brain was removed and placed in fresh fixatives for another 7 days, after which 40 microns sections were cut and silver-stained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of dantrolene on histological and behavioral outcome in rat CA1 hippocampus after global transient cerebral ischemia]. 769 30

A morphometric analysis of constituents of the rat hippocampus was performed in the different hippocampal regions that are known to be vulnerable in various degrees to experimental global ischemia. In the hippocampus formation of the normal Fisher rat the number and areas of neuronal nuclei and of their constituents, nucleoli and AgNOR particles, were counted and measured. Nuclear and nucleolar size were different in the various parts of the Ammon's formation. AgNORs, i.e. silver stainable proteins that represent actively rRNA transcribing genes, equally varied in number and extension in the different hippocampal subfields. In granule cells of the dentate gyrus and in pyramidal cells of CA 1, CA 3 and CA 4, AgNORs usually occupy half of the nucleolar area. Using the determined values an estimate of the length and volume of the neuronal layers within the different parts of the rats Ammon's horn was performed. After the development of delayed ischemia all measured structures were significantly smaller despite the fact that only nuclei with well preserved outlines could be analysed. They represent only 5-10% of controls. Nuclear sizes were reduced between 20 and 55%. The strongest reduction was observed in the transition zone between CA 1 and CA 3, the least in CA 3. Nucleoli and AgNORs equally were considerably smaller than in normal cells. For AgNORs a skewed distribution to the left resulted, whereas the nuclear size had normally distributed shape with peak at lower values. We conclude that an architecture of both nucleoli and AgNORs exists in the hippocampal subfields in addition to the known cytological architecture. Under ischemic conditions, even the healthy looking cells remain damaged to a variable extent in the different subfields corresponding to their selective vulnerability. There are some indications that damage to nucleoli and AgNORs is earlier and stronger than to nuclei. A time course of AgNOR damage can be constructed.
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PMID:Morphometric investigation on nuclear and nucleolar arrangement and AgNOR content in the rat hippocampus under normal and ischemic conditions. 770 82

We have examined the effects of transient cerebral ischemia on performance of a one-trial passive avoidance task by chicks. Transient forebrain ischemia was induced by bilateral carotid artery occlusion for a period of 10 min. In one experimental group, ischemia was produced prior to training on the avoidance task whereas in the other group ischemic intervention was not made until 3 h after initial training. Sham-operated groups were matched to each of the experimental groups. All four groups were tested for retention of the avoidance response 24 h post-surgery. The sham-operated birds and those receiving post-training ischemia showed good retention of the avoidance response, whereas in birds which received ischemia prior to training there was significant amnesia. Neuronal damage, determined qualitatively using a silver impregnation method, was observed in several forebrain regions including the hippocampus, hyperstriatal regions, paleostriatum primitivum, ventral archistriatum, and lateral corticoid area. Damage was also observed in the Purkinje cells of the cerebellum. The behavioural and anatomical effects of transient forebrain ischemia have not been previously investigated in an avian species and the finding of significant amnesia for a learning task following ischemia is in good agreement with several behavioural studies in mammals.
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PMID:Transient cerebral ischemia disrupts performance on a one-trial passive avoidance task in the domestic chick and is associated with neuronal degeneration in the central nervous system. 783 91

The therapeutic efficacy of intrathecally administered MK-801 (dizocilpine maleate), a noncompetitive receptor antagonist of N-methyl-D-aspartate receptor complex, was investigated in a rabbit spinal cord ischemia model. Normal saline, 0.3 ml (control, n = 4) or MK-801, 150 micrograms in 0.3 ml of saline, was administered intrathecally at the level of the lumbar enlargement, 30 min before (pretreatment, n = 7) or in the first min after (post-treatment, n = 4) 30 min of aortic occlusion followed by 2-h reperfusion. Nauta silver method was used for histopathological evaluation of lumbosacral segments. The degree of gray matter damage (argyrophilic neurons) was evaluated in three areas: A1, Rexed's laminae I-VI; A2, laminae VII and X; and A3, laminae VIII-IX. Pre- and post-treatment with MK-801 decreased the number of argyrophilic neurons (P < 0.05) in all areas examined. The number of argyrophilic neurons in A1, A2, and A3 was reduced by 59, 28, and 29%, respectively, by MK-801 pretreatment and by 87, 66, and 46%, respectively, by MK-801 post-treatment. Our results show that with single bolus intrathecal administration the efficacy of MK-801 was greater with post- compared to pretreatment and most dramatic in Rexed's laminae I-VI compared to laminae VII-X. Intrathecal administration of MK-801 prior to or at the beginning of the recirculation diminishes the extent of postischemic neuronal spinal cord damage at early postreperfusion period.
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PMID:Intrathecal administration of dizocilpine maleate (MK-801) attenuates ischemic damage in the rabbit spinal cord. 786 63

In a model that combines hypoxia with ischemia, the relationship between histological outcome, evoked rise in blood glucose, and striatal glutamate release was investigated in the 24-h food-deprived and normally fed rat. Food deprivation protected the dorsolateral striatum very effectively, as was shown with a silver stain. An online monitoring technique based on microdialysis showed that, in the protected condition, more glutamate was released into the striatal extracellular space than in the compromised condition. The possibility that the microdialysis results were influenced by a difference in shrinking of the extracellular space following food deprivation was excluded by the measurements of whole-tissue impedance. During the hypoxic-ischemic challenge, blood glucose rose in normally fed rats, but was suppressed almost completely after food deprivation. These results led us to conclude that, in our model of hypoxia-ischemia, the amount of glutamate released is not related directly to the extent of brain damage, but the increase in blood glucose may determine at least part of the brain damage.
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PMID:Food deprivation protects the rat striatum against hypoxia-ischemia despite high extracellular glutamate. 790 46

The mechanisms by which brain cells die after brief episodes of cerebral ischemia are not fully understood. In certain brain regions this damage may not be apparent for days. Hypothyroidism is known to decrease cerebral metabolism. We postulated that this slowing in cerebral metabolism may be neuroprotective after transient cerebral ischemia. To test this hypothesis, a total of 10 gerbils had thyroidectomies performed 2 weeks prior to ischemia. Six gerbils served as euthyroid controls. All animals were exposed to 5 min of transient ischemia and sacrificed 7 days after the insult. Silver degeneration staining was used for histological evaluation. Hippocampal damage [subiculum (P < 0.001), CA1 (P = 0. < .001), CA3 (P < 0.05), and CA4 (P < 0.001)] was significantly less in the hypothyroid animals. There was also significantly less damage in the cerebral cortex (P < 0.05) and thalamus (P < 0.05) in the hypothyroid animals. The exact mechanism of this protection is not fully understood but could be secondary to a decrease in the metabolic activity, or a reduced generation of free radicals (as is seen with protection from ischemia in kidney and liver under hypothyroid conditions). Further studies are required in order to gain a better understanding of the protective effects of hypothyroidism on cerebral ischemia.
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PMID:Hypothyroidism protects the brain during transient forebrain ischemia in gerbils. 791 Oct 86

Repeated ischemic insults at one hour intervals result in more severe neuronal damage than a single similar duration insult. The mechanism for the more severe damage with repetitive ischemia is not fully understood. We hypothesized that the prolonged reperfusion periods between the relatively short ischemic insults may result in a pronounced generation of oxygen free radicals (OFRs). In this study, we tested the protective effects of superoxide dismutase (SOD) and catalase (alone or in combination), and U78517F in a gerbil model of repetitive ischemia. Three episodes (two min each) of bilateral carotid occlusion were used at one hour intervals to produce repetitive ischemia. Superoxide dismutase and catalase were infused via osmotic pumps into the lateral ventricles. Two doses of U78517F were given three times per animal, one half hour prior to each occlusion. Neuronal damage was assessed 7 days later in several brain regions using the silver staining technique. The Mann-Whitney U test was used for statistical comparison. Superoxide dismutase showed significant protection in the hippocampus (CA4), striatum, thalamus and the medial geniculate nucleus (MGN). Catalase showed significant protection in the striatum, hippocampus, thalamus, and MGN and the substantia nigra reticulata. Combination of the two resulted in additional protection in the cerebral cortex. Compared to the controls, there was little protection in a dose of 3 mg/kg of U78517F. There was significant protection with a dose of 10 mg/kg in the hippocampus (CA4), striatum, thalamus, medial geniculate nucleus and the substantia nigra reticulata.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Superoxide dismutase, catalase, and U78517F attenuate neuronal damage in gerbils with repeated brief ischemic insults. 806 23

The method of photochemically induced thrombosis was used to produce severe ischemia in the rat retina. Flat mounts of the retina were prepared at 3 h, and 1, 2, 3, 4, 6, 7, and 22 days after lesioning and Nissl-stained, which facilitated the study of the topography of the ischemic lesions. The regional variability of ischemic damage and the cytological features of ischemic cell death in the ganglion cell layer were evaluated. Neuropathological analysis showed ischemic cell damage of ganglion cells at 3 h, an infarction-type lesion at 1 to 7 days, and scar formation at 3 weeks. As an additional parameter of ischemic ganglion cell death, the degeneration of retinal axons was visualized in the contralateral dorsal lateral geniculate nucleus by Fink-Heimer silver impregnation and by immunohistochemical staining for glial fibrillary acidic protein (GFAP) in reactive astrocytes.
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PMID:Ischemic damage visualized in flat mounts of rat retina after photochemically induced thrombosis. 808 41


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