• Y Morimoto, T Yamamura, and O Kemmotsu.
• Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, N15 W7, Kita-ku, 060, Sapporo, Japan.
• J Anesth. 1994 Sep 1;8(3):334-8.

AbstractThe present study was designed to determine whether acidosis modifies the effect of simulated ischemia on neuronal function. Hippocampal evoked potentials were recorded in vitro from the CA1 region after stimulation of the Schaffer collaterals and the change in the evoked potentials was analyzed in response to glucose-oxygen deprivation under variable acid-base conditions ranging from pH 7.4 to pH 4.5. Population spike (PS) activity was almost abolished with glucose-oxygen deprivation except for pH 6.5, indicating that mild acidosis minimizes the depressant effect of glucose-oxygen deprivation on neuronal transmission. The recovery of PS amplitude during recovery from glucose-oxygen deprivation was not significantly inhibited by moderate acidosis of pH 6 and 5.5 but was significantly inhibited when the pH was 5 or lower. The results suggest that severe acidosis may depress PS amplitude and prevent their recovery after reversal of glucose-oxygen deprivation, and that moderate acidosis may have no significant effect on PS amplitudes on their recovery.

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