Morphological changes of microvessels of cerebral cortex were evaluated in a model of cerebral infarction initiated by a photochemical reaction. Rats were treated with intravenous injection of rose Bengal and irradiated from a halogen lamp source through an intact cranium to precipitate microvascular damage. Investigations in transmission and scanning electron microscopy revealed platelet aggregation on endothelial cells preceded by its early ultrastructural damage. Other typical microscopic features of brain ischaemic injury were present suggesting that the present method may be used as a model for investigating ischaemic brain damage. Since the photochemical activation of the rose Bengal dye results in formation of reactive oxygen species this model may be particularly useful to elucidate the role of free radical-mediated endothelial damage in the formation of microthrombi and blood-brain-barrier integrity.
Spatial and temporal relations between metalloproteinase (MMP-2 and MMP-9) activation and laminin degradation in gerbil hippocampus after transient cerebral ischemia has been studied. Activity of MMPs was determined by gelatin zymography in homogenates from dorsal (DP, an equivalent of CA1 sector) and abdominal (AbP, containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of both investigated metalloproteinases was found at 72 h of recovery. Whereas MMP-2 up-regulation did not show any spatial preferences, the increase of MMP-9 activity was observed exclusively in DP. Activation of MMP-9 at this time point correlated spatially with degradation of laminin - protein of extracellular matrix. These results show that MMP pathway may function as a component of delayed neuronal death cascade in the apoptogenic CA1 sector after transient global ischemia.t