Histological study of neuronal damage following 18 minutes of global brain ischemia in dogs

The neuronal damage of small to medium sized striatal neurons, hippocampal CA1 pyramidal cells and cerebellar Purkinje cells was histologically studied after reperfusion following 18 minutes of global brain ischemia in dogs. Neuronal damage of small to medium sized striatal neurons progressed up to 6 hours after reperfusion, but further damage was not observed from 6 hours to 7 days after reperfusion. Little damage of either the hippocampal CA1 pyramidal cells or cerebellar Purkinje cells was observed 6 hours after reperfusion, but severe delayed damage of those cells was observed from 24 to 48 hours after reperfusion. These results suggest that the delayed onset of neuronal damage of both hippocampal CA1 pyramidal cells and cerebellar Purkinje cells is due to secondary injury factor (s) after reperfusion subsequent to ischemia. The delayed neuronal damage in this model may be prevented or reduced by treatment of secondary injury factor (s).