Changes at the focus of experimental ischemic stroke treated with neuroprotective agents |
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Authors: | L. S. Onishchenko O. N. Gaikova S. N. Yanishevskii |
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Affiliation: | (1) Department of Nervous Diseases (Director: Corresponding Member of the Russian Academy of Medical Sciences Doctor of Medical Sciences M. M. Odinak), S. M. Kirov Military Medical Academy, St. Petersburg |
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Abstract: | The aim of the present work was to compare the morphological changes occurring at the focus of experimental ischemic stroke treated with agents of the neurotrophic group (alpha-GPC, cerebrolysin), an agent with nootropic properties (piracetam), and a mixed-action agent (vinpocetin). Experiments were performed on 18 rats. Transient cerebral circulatory lesions (acute ischemia) were produced in the right hemisphere by clipping the stem of the innominate artery for 40 min. Light microscopic and electron microscopic studies were performed on fragments of cerebral cortex, brainstem, and cerebellum. Use of alpha-GPC and cerebrolysin increased the tolerance of neurons to ischemic damage and slowed the execution of the cell death program. Intracellular changes were seen and were interpreted as adaptive and reparative: these included folding of the nuclear membrane, abundance of polyribosomes, and endoplasmic reticulum and Golgi complex hypertrophy. These agents preserved the structures of the nuclear membranes and major cellular organelles. When piracetam and vinpocetin were used, all morphological measures indicated inadequate energy provision for repair processes in the acute stage of ischemic stroke. Morphological signs of functional tension of cerebral cortex neurons were seen, with gliocytes in different stages of apoptosis, along with the phenomenon of incomplete separation of gliocytes during proliferation, pathological changes to myelin and non-myelinated fibers, and abnormalities in synapse structure. __________ Translated from Morfologiya, Vol. 130, No. 6, pp. 40–46, November–December, 2006. |
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Keywords: | cerebral cortex ischemic stroke neurons glia |
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