Acta Cirúrgica Brasileira (Oct 2004)
Avaliação metabólica das lesões de isquemia e reperfusão cerebrais após oclusão bilateral das artérias carótidas comuns: estudo experimental em ratos Metabolic evaluation of ischemic and reperfusion brain injury following bilateral occlusion of common carotid arteries: an experimental study in rats
Abstract
OBJETIVO: Caracterizar as alterações no metabolismo energético após isquemia/reperfusão cerebral através de um modelo experimental de isquemia global reversível por simples oclusão das artérias carótidas comuns (ACCs) em ratos da linhagem Wistar. MÉTODOS: Quarenta e oito ratos Wistar machos foram distribuídos aleatoriamente em dois grupos (C - Controle; T - Teste) e cada um deles redistribuídos em quatro tempos de estudos. Após oclusão bilateral das ACCs por 30min, permitiu-se reperfusão aos animais do grupo T nos tempos 0, 5, 10 e 15min. Foram coletadas amostras de tecido cerebral e sangue arterial sistêmico e quantificados os metabólitos D-glicose (GLI), piruvato (PRV), lactato (LCT) e adenosina trifosfato (ATP). RESULTADOS: Observou-se aumento nos níveis sangüíneos de GLI e PRV de, respectivamente, 85,00% (pPURPOSE: To describe alterations on the energy metabolism after cerebral ischemia/reperfusion, through an experimental model of reversible global ischemia, by simple occlusion of common carotid arteries (CCAs) in rats of Wistar lineage. METHODS: Forty-eight male Wistar rats were randomly distributed on two groups (C - Control; T - Test) and further redistributed into four times sets of study. After bilateral occlusion of CCAs for 30min, the animals of group T were allowed reperfusion for 0, 5, 10 and 15min. Samples of cerebral tissue and systemic arterial blood were collected and the metabolites D-glucose (GLI), pyruvate (PRV), lactate (LCT) and adenosine triphosphate (ATP) quantified. RESULTS: Increases of GLI and PRV blood values of, respectively, 85,00% (p<0,05) and 51,72% (p<0,01) were observed at 5min of reperfusion, which reflect a systemic response to the cerebral ischemia. The brain's LCT remained stable despite a reduction of 52,66% (p<0,05) in its blood concentration at 15min of reperfusion. The cerebral concentrations of ATP decreased 85,40% (p<0,05) after ischemia, followed by an augmentation of 3.033,40% (p<0,05) at 5min of reperfusion, becoming evident the recovery of cell respiration by fosforilation pathway. CONCLUSIONS: The proposed experimental model produced partial transitory global ischemia, with systemic repercussions. The greatest metabolic alterations were verified in the initial minutes of reperfusion, typifying reperfusion injury. Such observations prove its value as an important instrument in the study of physiopathology and therapeutic sources of ischemic cerebrovascular disease.
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