Mild acidosis inhibits the rise in intracellular Ca2+ concentration in response to oxygen-glucose deprivation in rat hippocampal slices.

Changes in the intracellular Ca2+ concentration ([Ca2+]i) induced by ischemia in vitro (oxygen-glucose deprivation) were continuously recorded using fura-2-loaded hippocampal slices under normal (pH 7.4), acidotic (pH 6.8) and alkalotic (pH 7.8) conditions. Oxygen-glucose deprivation induced an initial slow and a subsequent characteristic rapid increase in [Ca2+]i in most of the normal and alkalotic preparations regardless of whether or not Ca2+ was present in the bathing solutions. This characteristic rapid increase in [Ca2+]i was observed in a minority of the acidotic preparations and its latency was significantly longer in acidotic preparations than in normal and alkalotic preparations. The rise in [Ca2+]i at 10 min of oxygen-glucose deprivation was significantly smaller in the acidotic preparations than in the normal and alkalotic preparations, regardless of whether or not Ca2+ was present. At 15 min, the differences in the increase in [Ca2+]i between normal and acidotic preparations in Ca(2+)-containing solutions (2.5 mM) were insignificant. However, significant differences were still observed between the acidotic preparations and either the normal or alkalotic preparations under Ca(2+)-free conditions. These results suggest that acidosis inhibits the ischemia-induced rise in [Ca2+]i by attenuating both Ca2+ influx from the extracellular space and Ca2+ release from intracellular sites.