Effect of barbiturate treatment on post-ischemic protein biosynthesis in gerbil brain

The effect of barbiturate treatment on post-ischemic cerebral protein biosynthesis was studied in gerbils subjected to 5 min transient occlusion of carotid arteries followed by 2 h or 48 h recirculation. Ischemia induced a remarkable decline of amino acid incorporation into brain proteins in most forebrain structures. The initial inhibition recovered to near normal after 2 days recirculation in all regions except the vulnerable CA1 sector. Barbiturate treatment, which previously has been shown to prevent delayed neuronal death in CA1 sector, did not ameliorate the initial inhibition of protein synthesis but it significantly improved subsequent recovery, especially in the vulnerable CA1 sector of hippocampus. These observations indicate that delayed neuronal death in CA1 sector of hippocampus results from selective failure of post-ischemic recovery and not from selective ischemic injury of the protein synthesizing machinery. This explains that delayed neuronal death can be prevented by therapeutic interventions which are initiated during the post-ischemic recirculation phase.