Repercussões clínicas e histopatológicas do dimetilsulfóxido em gerbils submetidos a isquemia cerebral experimental

• Autor(a) principal: Penasso, Poliana
• Data de Publicação: 2005
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório do Centro Universitário Braz Cubas
• Texto Completo: https://repositorio.cruzeirodosul.edu.br/handle/123456789/595
• topic: Dimetilsufóxido; Isquemia cerebral; Gerbil; CNPQ::CIENCIAS DA SAUDE::SAUDE COLETIVA::SAUDE PUBLICA

The aim of the present study was to investigate the neuroprotective actions of dimethyl sulfoxide in the clinical-behavioral and histopathological changes of the gerbil brain undergoing experimental cerebral ischemia through permanent occlusion of the left common carotid artery. The animals were divided into 5 groups with 6 animals each. Control animals were non-operated (group I), false operated (group II - sham) and untreated ischemia (group III). The animals receiving DMSO were from groups IV and V. Thirty minutes before the experimental surgery, 215mg / kg of 10% DMSO was administered intraperitoneally in the animals of group IV (DMSO I) and 645mg / kg of 10% DMSO in the animals. group V (DMSO II). Clinical signs of neurological injury were observed on the 1st day after ischemia. Exploratory motor behavior was evaluated through the frequency of crossings and surveys observed in the circular arena during the four days following ischemia. Euthanasia was performed on the 7th day after ischemia for later histological analysis of the brain. For statistical analysis, the ANOVA test was used (statistical significance p <0.05). The mortality rate after ischemia was 60% in the untreated ischemic group, 33.4% in the DMSO I group and 14.3% in the DMSO II group. The untreated animals showed clinical signs of injury, such as flexion of the forelimb (hemiparesis), spontaneous circle walking and eyelid ptosis. The treated animals (DMSO I and II) presented only eyelid pstosis. The treated animals (DMSO I and II) showed a higher frequency of crossings on the 2nd, 3rd and 4th days compared to the untreated ischemic group. The DMSO I group showed a higher frequency of surveys on the 2nd and 4th days and the DMSO II group on all evaluation days in relation to the untreated ischemic group. Histopathological results showed extensive areas of necrosis of nerve cells in the hippocampus and frontal, parietal and temporal cortex in the untreated ischemic group. In the treated animals, the ischemic areas were reduced. The DMSO II group had a lower percentage of ischemic hicocampal neurons (46.1 + or - 3.4) compared to the DMSO I group (54.6 + or - 11.7) and the untreated ischemic group (71.17 + or - 10). DMSO reduced post-ischemic mortality, allowed better exploratory motor behavior and reduced ischemic brain injuries, suggesting a neuroprotective effect for these animals.