Efeitos do nitrosil rutênio na lesão cerebral induzida por isquemia e reperfusão em ratos wistar

• Ano de defesa: 2009
• Autor(a) principal: Campelo, Marcio Wilker Soares
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Estresse Oxidativo; Óxido Nítrico
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/7596

Background and purpose - Nitric oxide (NO) donors are known to reduce neuronal damage during brain ischemia and reperfusion by increasing the blood flow. Rut-bpy is a novel nitrosyl-ruthenium complex releasing NO directly into the vascular smooth musculature. The objective of the study was to evaluate the effect of Rut-bpy on a rat model of brain ischemia and reperfusion. Methods - Ninety-six male Wistar rats weighing approximately 290g were randomly assigned to 16 groups. Four groups and their respective sham groups were submitted to ischemia (Stage 1), while four groups and their respective sham groups were submitted to ischemia + reperfusion (Stage 2). At each stage of the experiment the groups were treated pairwise with saline solution (SS), Rut-bpy, L-NAME and L-NAME+Rut-bpy, respectively. The study was based on an incomplete global brain ischemia model with occlusion of the common bilateral carotid arteries and intraperitoneal administration of the study drugs. Following the experiment the animals were decapitated and the brain was sectioned for histochemical evaluation of the area of damage. The mean arterial blood pressure (MABP) was monitored throughout the experiment. Results - In the groups receiving Rut-bpy the damaged area/total area ratio decreased significantly during both ischemia (SS: 0.526 ± 0.012 vs. Rut-bpy: 0.216 ± 0.07; p<0.05) and reperfusion (SS: 0.4201 ± 0.04 vs. Rut-bpy: 0.114 ± 0.03; p<0.05). MABP oscillated significantly less during the transition from ischemia to reperfusion in the groups treated with Rut-bpy (SS: 20.89 mmHg ± 11.77 vs. Rut-bpy: 6.49 mmHg ± 4.65; p<0.05). Conclusion - Rut-bpy was shown to protect rat brain cells during ischemia and reperfusion and helped maintain the blood pressure relatively stable during the transition from ischemia to reperfusion.