Abstract
Intracellular acidosis is thought to be one of the major factors that contribute to cerebral injury during ischemia. Upon reperfusion, intracellular pH (pHi) eventually recovers, but normalization is not immediate (Smith et al. 1986). The speed of recovery of pHi is probably slower than the speed at which pHi drops during the onset of ischemia because regeneration of intracellular buffers requires a finite time. We postulated that the rate of recovery of pHi may be a marker of cerebral injury because it may reflect the brain’s ability to restore ionic gradients necessary for conductive function. In addition, persistent acidosis during reperfusion may further augment injury.
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Reference
Smith M-L, von Hanwehr R, Siesjö BK (1986) Changes in extra- and intracellular pH in the brain during and following ischemia in hyperglycemic and in moderately hypoglycemic rats. J Cereb Blood Flow Metab 6: 574–583
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© 1989 Springer-Verlag Berlin Heidelberg
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Nishijima, M.K. et al. (1989). Recovery Rates of Evoked Potentials, Intracellular pH and Bicarbonate Ion After ICP-Induced Ischemia. In: Hoff, J.T., Betz, A.L. (eds) Intracranial Pressure VII. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73987-3_245
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DOI: https://doi.org/10.1007/978-3-642-73987-3_245
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-73989-7
Online ISBN: 978-3-642-73987-3
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