Abstract
The objective of the study was to explore if pre-ischemic hyperglycemia exaggerates or accelerates neuronal damage in the hippocampus of rats by inducing delayed mitochondrial dysfunction, and if signs of such dysfunction precede the development of morphologically detectable neuronal necrosis. Mitochondrial function in homogenates from dorsal CA1 and CA3 and from ventral parts of hippocampus was examined in normo- (˜5 mM) and hyperglycemic (˜20 mM) rats subjected to 10 min of forebrain ischemia followed by 0, 6, and 16-18 h of reperfusion. Histopathological changes were evaluated after 6 and 16-18 h of recovery by light microscopy. Since animals recirculated for 16-18 h are normoglycemic, respiratory variables in recirculated animals were compared to normoglycemic controls. The analyses failed to show dysfunction of mitochondria. Delayed neuronal damage in the CA1 sector of hippocampus was observed in 5/8 hyperglycemic rats after 16-18 h of recirculation, whereas no detectable morphological alterations were observed in hippocampus in normoglycemic rats. Since brain mitochondrial function was normal when neuronal damage appeared, unaltered mitochondrial injury cannot be made responsible for delayed neuronal death. However, it cannot be excluded that mitochondria suffer functional injury, e.g. by the assembly of a mitochondria permeability transition pore.
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