RESUMO
Oxidative stress increases delayed neuronal death in the brain following ischemia. As a consequence, many attempts to reduce the damage resulting from cerebral ischemia under more highly oxidized conditions have focused on treatments aimed at maintaining the redox equilibrium of the local environment. This study demonstrates the synergistic effects of combining treatments with alpha-lipoic acid (LA) and vitamin E (VE) as an efficient measure to reduce the damage caused by cerebral ischemia. Two oral therapeutic protocols were examined: intensive treatment (100 mg/kg LA and 140 mg/kg VE for 7 days after ischemia) and prophylactic treatment (20 mg/kg LA and 50 mg/kg VE from 30 days before infarction up to the day of sacrifice). The prophylactic treatment reduced serum lipid peroxidation, and diminished brain infarct volume by approximately 50%. Furthermore, prophylactically treated rats showed a reduction in post-ischemia neurological scores. No significant differences were found in the intensively treated group. Our data indicate that pre-ischemia administration of the LA-VE antioxidant mixture reduced the volume of brain damaged and the functional consequences of embolic infarction. These findings suggest that prophylaxis with an LA-VE mixture may be valuable in reducing cerebral damage levels in patients with a high risk of stroke.
Assuntos
Infarto Cerebral/prevenção & controle , Embolia Intracraniana/prevenção & controle , Peroxidação de Lipídeos/efeitos dos fármacos , Ácido Tióctico/uso terapêutico , Vitamina E/uso terapêutico , Animais , Infarto Cerebral/patologia , Quimioterapia Combinada , Embolia Intracraniana/patologia , Peroxidação de Lipídeos/fisiologia , Masculino , Doenças do Sistema Nervoso/patologia , Doenças do Sistema Nervoso/prevenção & controle , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêutico , Ratos , Ratos Wistar , Ácido Tióctico/farmacologia , Vitamina E/farmacologiaRESUMO
An electrochemical brain fixation procedure (EBFP) to treat brains excised from human cadavers is described thoroughly. It is as precise as any other similar method currently available. However, it takes only as much as 36 h to completion instead of the much longer lapses required by immersion in formaldehyde. Actions were taken to secure that it is not a source of artifacts of any kind, neither neurons nor glia or blood vessels. It is, therefore, amenable to be used as a valuable research and teaching tool. Other advantages are that it does not pose any health hazard, is money- and time-saving, and cuts down on equipment and facilities
Assuntos
Encefalopatias/diagnóstico , Córtex Cerebral/citologia , Cérebro/patologia , Eletroquímica/métodos , Laboratórios/normas , Manejo de EspécimesRESUMO
This is the first attempt to harden all organs of a body together without excising them. This process was accomplished in bottom-belted, gastrointestinal (GI) or intravenously (IV) catheterized dog cadavers so as to influx en electrolytic solution containing formaldehyde (ESF). The IV influx of ESF was found to be the best perfusion pathway. After 48 h of immersion in ESF, 24 h current time of 17.5 A of current intensity, 24º to 56ºC, we ended up with thoroughly fixed dog cadavers that were wrapped with ethyl alcohol:glycerol gauzes and stored in plastic bags at room temperature. Optical microscopy of every sliced tissue showed normal blood vessels, neurons, glial and Purkinje cells and their nuclei of brain and cerebellum, respectively. Cardiac muscle fibers were of normal appearance. Kidney Bowman's capsule and space were found to be normal excepto for vacuolarly degenerated tubules. Small intestine showed normal epithelial cells andcrypts of Lieberkühn. In liver, sinusoids were normally arrayed but showed vacuolar cell degeneration. Herin a method to attain an electrochemical whole body fixation is described
Assuntos
Cães , Animais , Dissecação/métodos , Eletroquímica/métodos , Fixação de Tecidos/métodos , Fotomicrografia , Técnicas Histológicas/normasRESUMO
Los anticonvulsionantes pueden inducir efectos colaterales indeseables graves. Por lo tanto, se estudiaron los cambios morfológicos inducidos por el difenilhidantoinato de sodio (DFH-Na) en ratas. Se administró DFH-Na por vía bucal a ratas Sprague Dawley a dosis de 2.5, 5, 10, 15, 20, 50, 100 y 150mg/Kg durante 7, 14 y 30 días. Se realizó estudio histopatológico de cerebelo, cerebro, hígado, riñones e intestino delgado. El hígado menifestó esteatosis de gotas final y gruesas, tumefacción turbia y, ocasionalmente, hepatitis crónica focal inespecífica caracterizada por abundantes células plasmáticas en los espacios portales y células mononucleares que infiltraban el parénquima hepático. Los riñones manifestaron pielonefritis crónica inespecífica, tumefacción turbia y precipitados de hemosiderina, así como presencia de eritrocitos lisados dentro de los túbulos contorneados y colectores. Los tejidos restantes no mostraron alteraciones. Este estudio demuestra que el DFH-Na indujo cambios degenerativos e inflamatorios inespecíficos, tanto en tejido hepático como en tejido renal