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Article: Swelling, Intracellular Acidosis, and Damage of Glial Cells

TitleSwelling, Intracellular Acidosis, and Damage of Glial Cells
Authors
Issue Date1996
Citation
Acta Neurochirurgica, Supplement, 1996, v. 1996 n. 66, p. 56-62 How to Cite?
AbstractCerebral ischemia and severe head injury among others are associated with a limited availability of oxygen, leading to cell catabolism as well as anaerobic glycolysis. Resulting metabolites, such as arachidonic- and lactic acid, can be expected to leak into perifocal brain areas, contributing there to cytotoxic swelling and damage of neurons and glia. Since elucidation of mechanisms underlying cell swelling and damage in the brain is difficult in vivo, respective investigations were carried out in vitro using suspended glial cells. Thereby, effects of arachidonic acid (AA) and of lactacidosis on glial cell volume, intraccHular pH (pH1), and cell damage were analyzed utilizing flow cytometry. AA led to an immediate, dose dependent swelling and intracellular acidosis of glial cells. A concentration of 0.1 mM increased cell volume to 110 % of control and decreased pH1 to 7.05. Whereas glial swelling was permanent, pH1 recovered to baseline after 90 min. Cell viability of 90 % remained unchanged after addition of AA up to 0.1 mM, while at 0.5 mM it was significantly decreasing. Glial swelling from AA was nearly completely inhibited by the aminosteroid U-74389F or by using a Na+-free suspension medium for the experiment. Acidification of the medium to pH 6.8 or A.2 led to a cell volume of 110 % or 120 % of control without affecting cell viability. The cells were not capable to defend their normal pH1 during lactacidosis of the suspension medium but became acidotic as well. Addition of amiloride or utilization of Na+-free medium inhibited cell swelling from lactacidosis, while intracellular acidosis was even more pronounced. The results indicate that AA as well as acidosis are potent mediators of glial swelling and damage at levels found under pathophysiological conditions in the brain in vivo. Whereas intracellular aciditication caused by AA was reversible, glial cells were unable to regulate their pH1 during maintenance of extracellular acidosis. Concerning the mechanisms of glial swelling by AA, the production of oxygen- and lipid radicals might play a major role in the swelling process. The results indicate a role of the Na+/H+-antiporter in acidosis-induced glial swelling, whereas the exchanger has a limited significance for maintenance of pH1. As seen, the final pathway of glial swelling from both, AA and lactacidosis, requires a net influx of Na+-ions, probably together with Cl -ions, and osmotically obliged water.
Persistent Identifierhttp://hdl.handle.net/10722/149555
ISSN
2015 SCImago Journal Rankings: 0.379
References

 

DC FieldValueLanguage
dc.contributor.authorStaub, Fen_US
dc.contributor.authorWinkler, Aen_US
dc.contributor.authorHaberstok, Jen_US
dc.contributor.authorPlesnila, Nen_US
dc.contributor.authorPeters, Jen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorKempski, Oen_US
dc.contributor.authorBaethmann, Aen_US
dc.date.accessioned2012-06-26T05:55:14Z-
dc.date.available2012-06-26T05:55:14Z-
dc.date.issued1996en_US
dc.identifier.citationActa Neurochirurgica, Supplement, 1996, v. 1996 n. 66, p. 56-62en_US
dc.identifier.issn0065-1419en_US
dc.identifier.urihttp://hdl.handle.net/10722/149555-
dc.description.abstractCerebral ischemia and severe head injury among others are associated with a limited availability of oxygen, leading to cell catabolism as well as anaerobic glycolysis. Resulting metabolites, such as arachidonic- and lactic acid, can be expected to leak into perifocal brain areas, contributing there to cytotoxic swelling and damage of neurons and glia. Since elucidation of mechanisms underlying cell swelling and damage in the brain is difficult in vivo, respective investigations were carried out in vitro using suspended glial cells. Thereby, effects of arachidonic acid (AA) and of lactacidosis on glial cell volume, intraccHular pH (pH1), and cell damage were analyzed utilizing flow cytometry. AA led to an immediate, dose dependent swelling and intracellular acidosis of glial cells. A concentration of 0.1 mM increased cell volume to 110 % of control and decreased pH1 to 7.05. Whereas glial swelling was permanent, pH1 recovered to baseline after 90 min. Cell viability of 90 % remained unchanged after addition of AA up to 0.1 mM, while at 0.5 mM it was significantly decreasing. Glial swelling from AA was nearly completely inhibited by the aminosteroid U-74389F or by using a Na+-free suspension medium for the experiment. Acidification of the medium to pH 6.8 or A.2 led to a cell volume of 110 % or 120 % of control without affecting cell viability. The cells were not capable to defend their normal pH1 during lactacidosis of the suspension medium but became acidotic as well. Addition of amiloride or utilization of Na+-free medium inhibited cell swelling from lactacidosis, while intracellular acidosis was even more pronounced. The results indicate that AA as well as acidosis are potent mediators of glial swelling and damage at levels found under pathophysiological conditions in the brain in vivo. Whereas intracellular aciditication caused by AA was reversible, glial cells were unable to regulate their pH1 during maintenance of extracellular acidosis. Concerning the mechanisms of glial swelling by AA, the production of oxygen- and lipid radicals might play a major role in the swelling process. The results indicate a role of the Na+/H+-antiporter in acidosis-induced glial swelling, whereas the exchanger has a limited significance for maintenance of pH1. As seen, the final pathway of glial swelling from both, AA and lactacidosis, requires a net influx of Na+-ions, probably together with Cl -ions, and osmotically obliged water.en_US
dc.languageengen_US
dc.relation.ispartofActa Neurochirurgica, Supplementen_US
dc.subject.meshAcid-Base Equilibrium - Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArachidonic Acid - Physiologyen_US
dc.subject.meshBrain Damage, Chronic - Physiopathologyen_US
dc.subject.meshBrain Edema - Physiopathologyen_US
dc.subject.meshBrain Ischemia - Physiopathologyen_US
dc.subject.meshBrain Neoplasmsen_US
dc.subject.meshCell Survival - Physiologyen_US
dc.subject.meshGliomaen_US
dc.subject.meshIntracellular Fluid - Physiologyen_US
dc.subject.meshLactic Acid - Metabolismen_US
dc.subject.meshNeuroglia - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleSwelling, Intracellular Acidosis, and Damage of Glial Cellsen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8780798en_US
dc.identifier.scopuseid_2-s2.0-0029692624en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029692624&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1996en_US
dc.identifier.issue66en_US
dc.identifier.spage56en_US
dc.identifier.epage62en_US
dc.publisher.placeAustriaen_US
dc.identifier.scopusauthoridStaub, F=7006611117en_US
dc.identifier.scopusauthoridWinkler, A=7102499893en_US
dc.identifier.scopusauthoridHaberstok, J=6602914696en_US
dc.identifier.scopusauthoridPlesnila, N=7003609441en_US
dc.identifier.scopusauthoridPeters, J=7404191248en_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridKempski, O=7006127304en_US
dc.identifier.scopusauthoridBaethmann, A=7004994793en_US

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