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Medicinas Complementares
Métodos Terapêuticos e Terapias MTCI
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1.
Endoscopy ; 38(12): 1230-4, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-17163324

RESUMO

BACKGROUND AND STUDY AIMS: Creation of a submucosal cushion before endoscopic mucosal resection (EMR) significantly reduces perforation risk. We evaluated six solutions as cushioning agents in live pigs. MATERIAL AND METHODS: 5 ml of normal saline, normal saline plus epinephrine, albumin 12.5 %, albumin 25 %, hydroxypropyl methylcellulose, and the pig's own whole blood were endoscopically injected into the porcine esophageal submucosa. Blood was obtained from a peripheral vein immediately before injection. Injections were made every 4 cm from the gastroesophageal junction. The time from completion of the injection to disappearance of the cushion was recorded. Endoscopy was repeated at 48 hours post injection. Two EMRs were performed after blood injection. Statistical analysis employed one-way analysis of variance followed by pairwise T test comparisons using the Bonferroni correction. RESULTS: Five animal experiments were completed. The mean time to dissipation of the submucosal cushion was shortest for saline plus epinephrine sites (2.87 minutes, SD 2.21) followed by the saline (4.8 minutes, SD 1.56), albumin 12.5 % (5.68 minutes, SD 3.48), albumin 25 % (7.83 minutes, SD 2.02), hydroxypropyl methylcellulose (9.77 minutes, SD 1.55), and blood sites (38.6 minutes, SD 6.07). Injection of blood resulted in significantly longer mucosal elevation than any other solution ( P < 0.0007). Blood from the cushion did not hamper visualization and facilitated EMR. CONCLUSION: Blood produces the most durable cushion compared with standard agents, also having the advantages of being readily available and without cost. Albumin 25 % provides as durable a cushion as hydroxypropyl methylcellulose.


Assuntos
Transfusão de Sangue Autóloga/métodos , Mucosa , Albuminas/administração & dosagem , Animais , Esôfago , Derivados da Hipromelose , Injeções , Metilcelulose/administração & dosagem , Metilcelulose/análogos & derivados , Modelos Animais , Suínos , Fatores de Tempo
2.
Neurochem Int ; 45(1): 157-70, 2004 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-15082233

RESUMO

We evaluated whether combined treatment with selegiline, a selective MAO-B inhibitor, and EGb 761, a standard extract of Ginkgo biloba, has synergistic effects against ischemic reperfusion injury (IRI) in gerbils. Interestingly, we observed that pretreatment with EGb 761 significantly attenuated selegiline-induced hyperactivity. This finding paralleled striatal fos-related antigen immunoreactivity (FRA-IR) in mice. Four minutes of bilateral carotid artery occlusion caused substantial cell loss in the CA1 of the hippocampus 5 days post-ischemic insult. Pretreatment with EGb 761, with or without selegiline, significantly attenuated this neuronal loss. Combined treatment with EGb 761 plus selegiline was more efficacious in preventing this loss. Synaptosomal formations of protein carbonyl, lipid peroxidation (malondialdehyde (MDA) + 4-hydroxyalkenal (4-HDA)), and reactive oxygen species (ROS) in the hippocampus remained elevated 5 days post-ischemic insult. The antioxidant effects appeared to be most significant in the group treated with EGb 761 plus selegiline. This combined treatment produced more significant attenuation of IRI-induced alterations in intramitochondrial calcium accumulation, the mitochondrial transmembrane potential, and mitochondrial Mn-superoxide dismutase-like immunoreactivity (Mn-SOD-IR) than either treatment alone. Our results suggest that co-administration of EGb 761 and selegiline produces significant neuroprotective effects via suppression of oxidative stress and mitochondrial dysfunction without affecting neurological function.


Assuntos
Isquemia Encefálica/tratamento farmacológico , Extratos Vegetais/uso terapêutico , Selegilina/uso terapêutico , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/patologia , Isquemia Encefálica/metabolismo , Isquemia Encefálica/patologia , Sinergismo Farmacológico , Gerbillinae , Ginkgo biloba , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Atividade Motora/efeitos dos fármacos , Atividade Motora/fisiologia , Extratos Vegetais/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Selegilina/farmacologia
3.
Brain Res ; 851(1-2): 76-86, 1999 Dec 18.
Artigo em Inglês | MEDLINE | ID: mdl-10642830

RESUMO

Multiple dose administration of methamphetamine (MA) results in long-lasting toxic effects in the nigrostriatal dopaminergic system. These effects are considered to be primarily due to oxidative damage mediated by increased production of hydrogen peroxide or other reactive oxygen species in the dopaminergic system. The present study was designed to determine the protective effects of dietary antioxidant selenium on MA-induced neurotoxicity in the nigrostriatal dopaminergic system. Male C57BL/6J mice were fed either selenium-deficient (< 0.01 ppm Se) or selenium-replete (0.2 ppm Se) diets for 90 days. MA treatment decreased the dopamine (DA) levels in the striatum and substantia nigra (SN) of both Se-replete and Se-deficient animals. However, in Se-replete animals, this DA depletion was significantly attenuated in both the striatum and SN. A novel observation is that MA administration resulted in increased activity of Cu,Zn-SOD in the brains of both Se-deficient and Se-replete animals. However, MA administration to Se-deficient animals exhibited a higher Cu,Zn-SOD activity in the nigrostriatal system than the control animals. Elevated malondialdehyde (MDA) levels in the striatum and SN were also observed in Se-deficient MA-treated animals. Se repletion significantly increased the glutathione peroxidase (GPx) activity and the ratio of reduced glutathione (GSH)/oxidized glutathione (GSSG) in the MA-treated animals. In conclusion, we have shown that dietary Se attenuated methamphetamine neurotoxicity and that this protection involves GPx-mediated antioxidant mechanisms. Even though Cu,Zn-SOD activity was significantly elevated by MA treatment, the role of this enzyme in MA-mediated neurotoxicity is not yet clear.


Assuntos
Corpo Estriado/efeitos dos fármacos , Glutationa Peroxidase/metabolismo , Glutationa/metabolismo , Selênio/farmacologia , Substância Negra/efeitos dos fármacos , Superóxido Dismutase/metabolismo , Animais , Peso Corporal/efeitos dos fármacos , Corpo Estriado/metabolismo , Dopamina/metabolismo , Dopaminérgicos/toxicidade , Glutationa/efeitos dos fármacos , Glutationa Peroxidase/efeitos dos fármacos , Masculino , Metanfetamina/antagonistas & inibidores , Metanfetamina/toxicidade , Camundongos , Camundongos Endogâmicos C57BL , Doença de Parkinson/metabolismo , Substância Negra/metabolismo , Superóxido Dismutase/efeitos dos fármacos
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