Effects of vinpocetine on local cerebral blood flow and glucose utilization seven days after forebrain ischemia in the rat.

A marked neuronal cell loss has been determined in the hippocampal CA1-subfield of the rat 7 days after 10 min of ischemia. The purpose of the present study was to evaluate the consequences of ischemia-induced hippocampal neuronal damage on local cerebral glucose utilization (LCGU) and blood flow (LCBF). Forebrain ischemia of 10 min duration was induced in male Wistar rats. Seven days after ischemia LCGU was measured with the [14C]-2-deoxy-D-glucose method, and LCBF was determined with the [14C]-iodoantipyrine technique in sham-operated and in ischemic rats. Furthermore, postischemic LCGU and LCBF were determined in vinpocetine-treated ischemic rats. Vinpocetin (14-ethoxycarbonyl-(3 alpha, 16 alpha-ethyl)-14,15-eburnamine) has already proved to protect hippocampal neurons against ischemic damage. In comparison with sham-operated rats, LCGU increased and LCBF decreased significantly in the CA1-subfield 7 days after ischemia. Both effects were abolished by preischemic vinpocetine treatment supporting the presumption that this drug is protective against ischemic damage.