Journal of Neurophysiology, Vol 64, Issue 4 1125-1133, Copyright © 1990 by APS

ARTICLES

A rapid redistribution of hydrogen ions is associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion

T. P. Obrenovitch, D. Scheller, T. Matsumoto, F. Tegtmeier, M. Holler and L. Symon
Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, United Kingdom.

1. The aim of this study was to examine the rapid changes in extracellular hydrogen ion activity [( H+]o or pHo) which are associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion. Two parallel studies were performed with different rat models of ischemia: repetitive severe ischemia produced in anesthetized animals by occlusion of the vertebral and carotid arteries and temporary interruption of blood flow in isolated brain. [H+]o and direct current potential (DC potential) were recorded simultaneously in all experiments. Examination of these two parameters was supplemented by recording tissue concentration of carbon dioxide (PtCO2) in the four-vessel occlusion model and assaying major metabolites involved in energy production in experiments with isolated brains. 2. Measurements of [H+]o during ischemia consistently revealed a steady increase of [H+]o on which was superimposed an abrupt and transient fall in [H+]o closely related to the occurrence of the fast negative shift of DC potential characterizing brain-cell depolarization. Analysis of the relationship between the magnitude of the transient fall in H+ and the level of [H+]o at which this occurred showed that the amplitude of the transient fall in H+ increased with tissue acidosis. 3. We propose that this phenomenon is indirect evidence that rapid transfer of acid equivalents occurs across the plasmalemma, concomitantly to its depolarization. Both events probably result from a common cause, i.e., nonspecific increase of the cell-membrane permeability to ions subsequent to opening of membrane channels. 4. Early on during recirculation, an acidotic [H+]o shift associated with membrane repolarization was clearly visible whenever the ionic gradients recovered rapidly.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				G. Pignataro, R. P. Simon, and Z.-G. Xiong Prolonged activation of ASIC1a and the time window for neuroprotection in cerebral ischaemia Brain, January 1, 2007; 130(1): 151 - 158. [Abstract] [Full Text] [PDF]

				J. P. Dreier, J. Woitzik, M. Fabricius, R. Bhatia, S. Major, C. Drenckhahn, T.-N. Lehmann, A. Sarrafzadeh, L. Willumsen, J. A. Hartings, et al. Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations Brain, December 1, 2006; 129(12): 3224 - 3237. [Abstract] [Full Text] [PDF]

				O. Yermolaieva, A. S. Leonard, M. K. Schnizler, F. M. Abboud, and M. J. Welsh Extracellular acidosis increases neuronal cell calcium by activating acid-sensing ion channel 1a PNAS, April 27, 2004; 101(17): 6752 - 6757. [Abstract] [Full Text] [PDF]

				C. Sheldon and J. Church Intracellular pH Response to Anoxia in Acutely Dissociated Adult Rat Hippocampal CA1 Neurons J Neurophysiol, May 1, 2002; 87(5): 2209 - 2224. [Abstract] [Full Text] [PDF]

				S. Traynelis, M Hartley, and S. Heinemann Control of proton sensitivity of the NMDA receptor by RNA splicing and polyamines Science, May 12, 1995; 268(5212): 873 - 876. [Abstract] [PDF]