This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kempski, O. Articles by Baethmann, A. Search for Related Content PubMed PubMed Citation Articles by Kempski, O. Articles by Baethmann, A.

Stroke, Vol 19, 385-392, Copyright © 1988 by American Heart Association

ARTICLES

Glial swelling during extracellular acidosis in vitro

O Kempski, F Staub, M Jansen, F Schodel and A Baethmann
Institute for Surgical Research, Klinikum Grosshadern, Ludwig- Maximilians-University, Munchen, Federal Republic of Germany.

Intracellular and extracellular acidosis may determine the ultimate outcome for brain tissue in cerebral ischemia. An extracellular acidosis that occurs in the penumbra zone was investigated in vitro as to its role in the formation of cytotoxic cell swelling. For that purpose, C6 glioma cells or primary cultured astrocytes were suspended in normal isotonic medium in normoxia during acidification to a final pH of 6.2. The cell volume response was determined by flow cytometry using hydrodynamic focusing, which allows one to recognize changes in cell size of less than 1%. A threshold pH of 6.8 was found that had to be crossed to induce cell swelling by acidosis. Once pH fell below this threshold, the increase in cell size appeared to be an all-or-nothing phenomenon. The cells rapidly assumed a final cell size of 115% of normal in the case of C6 glioma or of 118% in the case of primary cultured astrocytes independent of the actual level of acidosis or the duration of exposure. Acidosis-induced glial swelling could be significantly attenuated by 1) addition of amiloride, 2) administration of acetazolamide, or 3) replacement of bicarbonate buffer against N-2- hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES). Replacement of extracellular Na+ by choline chloride led to complete prevention of the acidosis-induced cell swelling. Taken together, the findings strongly indicate a central involvement of Na+/H+ and Cl-/HCO3- exchange mechanisms in the development of cell swelling under these conditions. Activation of the Na+/H+ antiporter can be considered an attempt to maintain a normal intracellular pH at the expense of an abnormal cell volume.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				K. L. Miller, D. P. Bulte, H. Devlin, M. D. Robson, R. G. Wise, M. W. Woolrich, P. Jezzard, and T. E. J. Behrens Evidence for a vascular contribution to diffusion FMRI at high b value PNAS, December 26, 2007; 104(52): 20967 - 20972. [Abstract] [Full Text] [PDF]

				Y. Matsumoto, S. Yamamoto, Y. Suzuki, T. Tsuboi, S. Terakawa, N. Ohashi, and K. Umemura Na+/H+ Exchanger Inhibitor, SM-20220, Is Protective Against Excitotoxicity in Cultured Cortical Neurons Stroke, January 1, 2004; 35(1): 185 - 190. [Abstract] [Full Text] [PDF]

				S. Behmanesh and O. Kempski Mechanisms of endothelial cell swelling from lactacidosis studied in vitro Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1512 - H1517. [Abstract] [Full Text] [PDF]

				F. LANG, G. L. BUSCH, M. RITTER, H. VOLKL, S. WALDEGGER, E. GULBINS, and D. HAUSSINGER Functional Significance of Cell Volume Regulatory Mechanisms Physiol Rev, January 1, 1998; 78(1): 247 - 306. [Abstract] [Full Text] [PDF]

				L. Regli, R. E. Anderson, and F. B. Meyer Effects of Intermittent Reperfusion on Brain pHi, rCBF, and NADH During Rabbit Focal Cerebral Ischemia Stroke, August 1, 1995; 26(8): 1444 - 1452. [Abstract] [Full Text]