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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiological chain of events occurring during cerebral ischemia is still poorly understood on a molecular level. Therefore, an in vitro model to study glial swelling mechanisms, using C6 glial cells under controlled extracellular conditions, has been established. Flow cytometry serves to determine even small cell volume changes. In this report, the effects of anoxia and acidosis on glial swelling are summarized. Anoxia alone, or in combination with iodoacetate to inhibit anaerobic glycolysis, did not cause an increase of glial volume for up to 2 h. Acidification of the incubation medium below pH 6.8, on the other hand, was immediately followed by cell swelling to 115% of normal. Amiloride or the absence of bicarbonate and Na+ in the medium significantly reduced glial swelling. The data support the contention that swelling results from an activation of the Na+/H+-antiporter to control intracellular pH. It is suggested that swelling in an ischemic penumbra is promoted by this mechanism. Therapeutic approaches to control cerebral pH might be useful to protect brain tissue in cerebral ischemia.
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PMID:Molecular mechanisms of glial swelling in vitro. 324 66

Cerebral ischemia induces major neuronal morphological alterations. It is not clear, however, whether this is directly caused by O2 deprivation. To determine the effect of hypoxia on cytoskeletal structures and neuronal morphology, we performed experiments and examined anoxia-induced changes in microtubule-associated protein 2 (MAP2) and cell morphology in hippocampal slices in vitro. Anoxia (measured PO2 = 0 Torr) induced a marked loss in dendritic MAP2 immunoreactivity and cell swelling of hippocampal neurons by 2 h after O2 reinstitution. These changes were severe in CA1 and CA3 neurons and comparatively mild in dentate gyrus neurons. Quantitative analysis showed that 10 min of anoxia induced a 30% loss of MAP2-positive dendrites but this increased to 70% after 30 min of anoxia. A concurrent major increase in somata area of about 100% and 200% was observed in CA1 and CA3 neurons respectively. Somata area in the lower dentate gyrus, however, increased either insignificantly or by only 30% for the respective periods of anoxia. These results suggest that deprivation of O2 can by itself induce a major loss in dendritic MAP2 immunoreactivity and changes in cell morphology in hippocampal neurons. These alterations occur rapidly after hypoxia, and the severity of these changes is directly related to the duration of anoxia and brain region in the hippocampus.
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PMID:Acute anoxia-induced alterations in MAP2 immunoreactivity and neuronal morphology in rat hippocampus. 836 56

To improve the understanding of neuronal cell swelling in cerebral ischemia, cell volume regulation, viability, intracellular electrolytes, and lactate production of Neuro-2A neuroblastoma cells were studied using an in vitro model. The volume regulatory capacity of Neuro-2A cells was assessed after incubation in hypo- and hypertonic media. Anoxia was studied alone and together with inhibition of glycolysis by iodoacetate. Reducing the tonicity of the incubation medium to 250, 200, or 150 mosm/l caused immediate swelling followed by a regulatory volume decrease within 20 min, which, however, was not complete. The final cell volume after regulation depended on the tonicity of the medium and remained above control. There was no regulatory volume increase after cell shrinking in hypertonic media. Despite the severe anisotonic incubation, viability decreased only slightly without reaching statistical significance. In contrast to in vivo conditions, anoxia for 90 min with or without iodoacetate for additional inhibition of anaerobic energy metabolism neither caused neuronal cell swelling nor a decrease of viability. Reoxygenation after the anoxic period also did not induce volume and viability changes. Intracellular K+ of Neuro-2A cells was markedly decreased, while Na+ increased in a 1:1 ratio during complete energy failure by anoxia plus iodoacetate. A similar effect, occurring however somewhat delayed, was seen when the Neuro-2A suspension was exposed to iodoacetate alone. Anoxia without inhibition of glycolysis had no effect on intracellular ion concentrations, but lactate production was nearly six times higher than normal. In vitro, with a large extracellular volume and sufficient glucose supply, the energetic demands of Neuro-2A cells to maintain stable transmembraneous ion gradients during anoxia are obviously met by anaerobic glycolysis. The current results confirm that neuronal cells are able to adequately regulate cell volume in response to hyposmotic stress. On the other hand, maintenance of a normal cell size during complete energy deprivation suggests strongly that energy failure per se does not suffice to induce neuronal swelling. Cell swelling in cerebral ischemia in vivo thus appears a secondary phenomenon due to mediator mechanisms such as tissue acidosis or elevated extracellular glutamate levels.
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PMID:Anoxia in vitro does not induce neuronal swelling or death. 883 70

Increased extracellular glutamate ([GLU]e), under the condition of cerebral ischemia, anoxia or hypoxia, has been recognized as being associated with neuronal cell damage and death. We performed real-time monitoring of [GLU]e dynamics in vivo in the rat striatum during systemic acute anoxia or hypoxia, as well as monitoring the direct current potential (DC) and cerebral blood flow (CBF). Adult Wistar rats were orotracheally intubated and artificially ventilated with room air. A microdialysis electrode, temperature sensor probe, DC microelectrode and laser Doppler probe were then implanted. The inspired gas was changed to 100% N(2) (anoxia), or to 3, 5 or 8% O(2) (remainder N(2)) (hypoxia). With 100% N(2), distinct biphasic [GLU]e elevations were observed. With 3% O(2), a transient [GLU]e increase was seen before anoxic depolarization (AD). With 5% O(2), however, the start of the transient [GLU]e increase was significantly delayed. Anoxia-induced depolarization started at about 100 s. The 3% O(2)-induced transient depolarization and AD began at nearly the same time as the transient and AD-induced increase in [GLU]e. Similarly, the responses to 5% O(2) showed significant delays in the transient depolarization and AD-induced increase in [GLU]e. CBF during 3 or 5% O(2) hypoxic insult was consistently maintained above the control level, i.e., prior to cardiac arrest. Our new dialysis electrode method employing both GOX and ferrocene-conjugated bovine serum albumin allowed evaluation of transient [GLU]e dynamics in the early phase of severe hypoxia in vivo.
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PMID:Transient in vivo membrane depolarization and glutamate release before anoxic depolarization in rat striatum. 1041 6