Preischemic hyperglycemia leads to rapidly developing brain damage with no change in capillary patency.

The present experiments were undertaken to explore whether exaggeration of ischemic brain damage by preischemic hyperglycemia is due to lack of capillary patency in the postischemic period. Normo- and hyperglycemic rats were exposed to 10 min of forebrain ischemia. Histopathological changes were evaluated after 6 and 16-18 h of recovery by light microscopy, and capillary patency was assessed at the same time points by a double-staining technique, depicting perfused and morphologically identifiable capillaries. The results demonstrate that some neuronal damage was detectable after 6 h of recirculation which was aggravated after 16-18 h of recirculation in hyperglycemic rats. In contrast, the degree of capillary patency was similar in normo- and hyperglycemic rats. In both groups the perfusion marker, Evans blue, perfused about 95% of all capillaries when injected 10 s before decapitation. Since preischemic hyperglycemia exaggerates brain damage without cessation of capillary perfusion the primary targets of hyperglycemic brain damage may not be capillaries but neurons or glial cells.