Summary:The purpose of the present study was to de termine the consequences of postischemic neuronal dam age on CMRglc. Forebrain ischemia of \0 min duration was induced in male Wi star rats. The extent of neuronal damage and the numbers of immunocytochemically de tected astrocytes in the hippocampal CAl subfield as well as CMRglc were determined 2, 5, 7, and 14 days after ischemia. CBF was additionally measured 7 days post ischemia. CMRglc was decreased in cortical and thalamic structures up to 5 days postischemia, and was normalized again on day 7 after ischemia. In the hippocampal areas, CMRglc was decreased only on day 2 after ischemia, was normalized after 5 days, and increased in the stratum
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. Vinpocetine (14-ethoxycarbonyl-(3α,16α-ethyl)-14, l 5-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.
ABSTRACT-The effects of vinpocetine against hippocampal neuronal damage and on local cerebral blood flow (LCBF) were examined in a rat model of forebrain ischemia (10-min occlusion of the carotid arteries and hypotension). Histological evaluation of neuronal loss in the hippocampus was performed 7 days after ischemia . LCBF was measured before ischemia as well as after 2 min and 1 hr of recirculation . Vinpocetine (10 mg/kg) administered pre or post-ischemically reduced the hippocampal neuronal necrosis, while pre-ischemic administration of 2 or 20 mg/kg vinpocetine was ineffec tive. Since vinpocetine increased the LCBF after 1 hr of recirculation, it cannot be ex cluded that blood flow improvements contribute to its neuroprotective activity . On the other hand, there is no clear evidence that an elevation of post-ischemic hypoperfu sion could protect neurons against ischemic damage. It is, therefore, suggested that vinpocetine acts directly on brain cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.