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

Transient arrest of the cerebral circulation leads to neuronal cell death in selectively vulnerable regions of the central nervous system. It has recently been shown at the light microscopical level that neuronal necrosis is accompanied by a rapid microglial reaction in ischemia (Gehrmann et al. (1992) J. Cereb. Blood Flow Metab. 12:257-269). In the present study we have examined the postischemic microglial reaction in the dorsal rat hippocampus at the ultrastructural level using immuno-electron microscopy. Global ischemia was produced by 30 min of four-vessel occlusion and the microglial reaction then studied after 8, 24 and 72 h. In sham-operated controls microglial cells were not phagocytic; they were randomly distributed throughout the neuropil and occasionally made contacts with other structures such as dendrites in CA1. Ultrastructural signs of activation were observed from 1 day postlesion onward. Reactive microglial cells were consistently seen to phagocytose degenerating neurons particularly in the CA1 stratum pyramidale and in the CA4 sector. They were sometimes interposed between two morphologically distinct types of CA1 neurons, i.e., "dark" (degenerating) and "pale" (surviving) types of neurons. Phagocytic microglial cells also became positive for major histocompatibility complex (MHC) class II antigens at these locations from 1 day after ischemia onward. Furthermore, activated microglial cells were frequent along degenerating dendrites in the stratum radiatum of CA1. After survival times of up to 72 h microglial cells, but not astrocytes, were occasionally observed to undergo mitosis. In addition to their random distribution across the neuropil, microglial cells were frequently observed in a perivascular position under normal conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The microglial reaction in the rat hippocampus following global ischemia: immuno-electron microscopy. 147 69

Electron microscope analysis of the CA1 Ammon's horn sector was performed in Mongolian gerbils three days after an incident of short-term ischemia of the forebrain. CA1 pyramidal neurons showed advanced disintegration. Some GABA-ergic interneurons revealed ultrastructural alteration of variable degree. The latter finding contradicts the generally helt view on the relative resistance of CA1 sector interneurons to the ischemic injury. Synapses localized in all cortical layers of the CA1 sector exhibited ultrastructural abnormalities involving both pre- and postsynaptic parts. They consisted in marked swelling and accumulation of unbound electron dense material, considered as calcium deposits. Presynaptic parts revealed additionally reduced number of synaptic vesicles and their abnormal distribution. Contrary to the early postischemic period, the most severe synaptic alterations appeared in stratum pyramidale, radiatum and oriens, involving both small dendritic branchings and their spines as well as large shafts of both basal and apical pyramidal dendrites. Synaptic alterations especially features of the postsynaptic damage correspond to those indicating excitotoxic neuronal lesions. Presynaptic alterations may indicate both cessation of neurotransmission function as well as direct ischemic damage. The presence of calcium deposition seems to favour the former possibility.
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PMID:Influence of short-term ischemia on the ultrastructure of hippocampal gyrus in Mongolian gerbil. III. Synapses in late stage of the pathological process. 148 6

Transient (5-min) global forebrain ischemia, induced by four- vessel occlusion, was assessed using a multiple fixed-ratio, fixed-interval schedule of food presentation in five rats. Under control conditions, the schedule produced distinctive response rates in each schedule component. Initially, ischemia disrupted responding under both schedule components, and to approximately the same degree. In general, total session responses returned to pre-occlusion levels during the course of 45 post-occlusion days, however, response rates under the fixed-interval component showed slightly less recovery than those under the fixed-ratio component. Histological assessment revealed considerable variability in hippocampal damage between rats. Severe damage in the CA1, CA2, and CA3 formations was observed in a single rat, and that rat also showed the greatest degree of response disruption. These results suggest that schedule-controlled responding may be a valuable method for assessing the effects of ischemic injury, and thus, putative neuroprotective compounds, on complex behavior.
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PMID:Evaluation of transient forebrain ischemia induced by four vessel occlusion using schedule-controlled behavior. 148 34

Alterations of beta/A4 amyloid protein precursor (APP) were investigated immunohistochemically in the gerbil brain after transient global ischemia and subsequent reperfusion. Marked accumulation of this protein peaking at 24 h occurred in the neurons of the CA3 and paramedian region of the hippocampus as well as layers III, V and VI of the cerebral cortex. On the contrary, the accumulation was not observed in the neurons of the CA1 region. These results indicate that distribution of APP is altered depending on tissue viabilities after cerebral ischemia.
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PMID:Regional accumulation of amyloid beta/A4 protein precursor in the gerbil brain following transient cerebral ischemia. 149 78

Experiments were performed with Mongolian gerbils to study the effect of the specific nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA) on ischemic brain damage induced by 5 min bilateral carotid occlusion. A single i.p. injection of L-NNA did not result in any neuronal loss in the central nervous system. In animals undergoing ischemia, a selective destruction of hippocampal CA1 cells was observed whereas pretreatment with 50 mg/kg L-NNA 4 h before administration of ischemia produced significantly more extensive cell damage in the hippocampus and other brain regions. These findings demonstrate that in this model inhibition of nitric oxide generation augments ischemia-induced neuronal cell injury in the brain.
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PMID:NG-nitro-L-arginine enhances neuronal death following transient forebrain ischemia in gerbils. 149 79

Hippocampal brain slices show CA1 injury similar to that seen after global ischemia in vivo. Cooling rats to 31 degrees C prior to sacrifice or cooling slices to 21 degrees C for 45 min increased the percentage of normal CA1 pyramidal cells after 5 h in vitro from 30% to over 80%. Brain slices also show a unique, consistent injury in dentate which is lessened by transient cooling to 21 degrees C but not by cooling the animal.
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PMID:Preservation of hippocampal brain slices with in vivo or in vitro hypothermia. 150 77

The present experiments were designed to assess whether brain hypothermia can reduce the behavioral and histopathological deficits associated with global forebrain ischemia. Animals were subjected to 12.5 min of four vessel occlusion (4VO) with moderate hypotension, and brain temperature maintained at either 37 degrees C (4VO-37) or 30 degrees C (4VO-30). Behavioral tests designed to assess forelimb reflexes and sensorimotor function were given on post-operative weeks 2 and 4. Beginning in week 5, the rats were trained on a variety of navigation problems in the Morris water maze. Histopathological examination of the tissue 2 months following reperfusion revealed that 4VO-37 animals sustained substantial cell death in hippocampal region CA1 and moderate damage to the dorsolateral neostriatum. 4VO-30 animals showed minimal cell death in CA1 and neostriatum. There were no group differences for any of the sensorimotor measures, or for acquisition performance on either the simple place task or visible platform version of the water maze. In contrast, during acquisition of the learning set task, the performance of 4VO-37 animals was impaired relative to either of the other groups, whereas the performance of 4VO-30 animals was not significantly different from the sham controls. These data suggest that moderate intra-ischemic brain hypothermia provides long-lasting protection from behavioral deficits as well as neuronal injury following transient global ischemia.
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PMID:Protective effects of brain hypothermia on behavior and histopathology following global cerebral ischemia in rats. 150

Distributions of heat shock protein (HSP)-70 mRNAs and heat shock cognate protein (HSC)-70 mRNAs after 10 min of transient global ischemia were investigated in gerbil forebrain by in situ hybridization using cloned cDNA probes selective for the mRNAs. Expression of HSP70 immunoreactivity was also examined in the same brains. In hippocampal CA1 neuronal cells, in which only a minimal induction of immunoreactive HSP70 protein was found, the strong hybridization for HSP70 mRNA disappeared at around 2 days before the death of CA1 cells became evident. Furthermore, in hippocampal CA3 cells, a striking induction of HSP70 mRNA was sustained even at 2 days along with a prominent accumulation of HSP70 immunoreactivity. In contrast to the case of HSP70 mRNA, HSC70 mRNA was present in most neuronal cells, especially dense in CA3 cells, of the sham brain. A co-induction of HSP70 and HSC70 mRNAs was observed in several cell populations after the reperfusion with a peak at 8 h, although the magnitude of HSC70 mRNA induction was lower than that of HSP70 mRNA, particularly in CA1 cells. The expression of HSC70 mRNA in CA1 cells also disappeared at around 2 days. All the induced signals of HSP70 and HSC70 mRNAs in other cell populations were diminished and returned to the sham level, respectively, by 7 days. These results are the first to show the time courses of distribution of HSP70 and HSC70 mRNAs and the immunoreactive HSP70 protein in the same gerbil brain after ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distributions of heat shock protein-70 mRNAs and heat shock cognate protein-70 mRNAs after transient global ischemia in gerbil brain. 150 43

Excessive neuronal activity combined with an increased release of neurotransmitters is supposed to contribute to the delayed neuronal degeneration in animal models of transient cerebral ischemia. Since evidence is accumulating that serotonin (5-HT) exerts an excitatory effect on neurons via 5-HT2 receptors we tested the hypothesis that 5-HT2 receptor antagonists could protect neurons in the gerbil after transient bilateral carotid occlusion. In a first series of experiments, the 5-HT2 receptor antagonist ketanserin was injected intraperitoneally 15 min prior to 5 min of forebrain ischemia and given twice daily on the following 3 days. At a dose of 10 mg/kg i.p., the number of intact hippocampal CA1 neurons was significantly higher than in the saline-treated group and reached 74% of the sham-operated controls. In addition, the degree of neuronal damage correlated with an increased intracellular Ca2+ content in CA1 pyramidal neurons as revealed by arsenazo(III) staining with a procedure modified for paraffin sections. In a second series of experiments, ketanserin (10 mg/kg) was injected at various times after onset of ischemia. Up to a period of 90 min after ischemia, the number of intact CA1 pyramidal cells in ketanserin-treated animals was still significantly higher than in the saline-treated group. These results indicate that 5-HT2 receptor antagonists may protect neurons against ischemic damage even when the treatment is started after onset of ischemia. It remains to be investigated whether the neuroprotective effect of ketanserin is due to a neuronal action or to an inhibition of cerebrovascular vasospasm.
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PMID:Ketanserin reduces neuronal calcium accumulation and cell death in the hippocampus of the Mongolian gerbil after transient forebrain ischemia. 151 Dec 66

Amphetamine with appropriate motor experience has been found to facilitate the recovery of motor function after several different types of brain injuries. We investigated whether amphetamine would hasten the recovery of spatial mapping ability in gerbils previously subjected to a 3-min episode of forebrain ischemia. Amphetamine did not promote behavioral recovery, nor did it attenuate ischemic cell damage of hippocampal CA1 neurons. The beneficial effects of amphetamine after brain injury may be limited to restoration of sensorimotor ability and not to cognitive functions such as memory.
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PMID:Effects of d-amphetamine on the recovery of function following cerebral ischemic injury. 151 51


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