The
barbiturate anesthetic thiopental enhances recovery of the evoked population spike recorded from rat hippocampal slices after short periods of
anoxia.
Thiopental reduces changes in
sodium,
potassium and
calcium but enhances the fall in
ATP levels during
anoxia. The postsynaptic population spike recorded from the CA1 pyramidal cell region of the slices treated with
thiopental (600 microM) recovered to 67% of the preanoxic amplitude after 3.5 min of
anoxia. There was less recovery (24%) when a lower concentration of
thiopental (250 microM) was used. Untreated slices recovered to only 10% of their preanoxic amplitude after 3.5 min of
anoxia. Other studies have demonstrated that maintaining
ATP levels during
anoxia may be an important mechanism of protection. In contrast to those studies,
thiopental was protective although it enhanced the fall of
ATP levels after 3.5 min of
anoxia in the CA1 region and after 3.5 and 5 min in the dentate region. Thus enhanced recovery of the population spike with
thiopental is not due to its preservation of
ATP levels. This result allows a clear separation of improved
ATP levels during
anoxia from other mechanisms of protection. We therefore looked for other mechanisms of protection.
Sodium and
potassium levels were measured after 10 min of
anoxia. In untreated tissue,
sodium levels in the slice rose and
potassium levels fell significantly. In
thiopental-treated tissue, changes in
sodium and
potassium caused by
anoxia and by
veratridine under normoxic conditions were significantly reduced. During
anoxia calcium-45 uptake increases;
thiopental significantly reduces this uptake.(ABSTRACT TRUNCATED AT 250 WORDS)