PREISCHEMIC HYPERGLYCEMIA LEADS TO RAPIDLY DEVELOPING BRAIN-DAMAGE WITH NO CHANGE IN CAPILLARY PATENCY

The present experiments were undertaken to explore whether exaggeratio n of ischemic brain damage by preischemic hyperglycemia is due to lack of capillary patency in the postischemic period. Normo-and hyperglyce mic rats were exposed to 10 min of forebrain ischemia. Histopathologic al changes were evaluated after 6 and 16-18 h of recovery by light mic roscopy, and capillary patency was assessed at the same time points by a double-staining technique, depicting perfused and morphologically i dentifiable capillaries. The results demonstrate that some neuronal da mage was detectable after 6 h of recirculation which was aggravated af ter 16-18 h of recirculation in hyperglycemic rats. In contrast, the d egree of capillary patency was similar in normo- and hyperglycemic rat s. In both groups the perfusion marker, Evans blue, perfused about 95% of all capillaries when injected 10 s before decapitation. Since prei schemic hyperglycemia exaggerates brain damage without cessation of ca pillary perfusion the primary targets of hyperglycemic brain damage ma y not be capillaries but neurons or glial cells. (C) 1998 Elsevier Sci ence B.V.