Reperfusion after transient focal ischemia of 2 h duration is followed by secondary bioenergetic failure after 4 h of reperfusion. The objective of the present study was to explore whether or not this secondary deterioration is due to secondary microcirculatory compromise. Normal fasted rats were subjected to 2 h of MCA occlusion and allowed reperfusion for 2, 4, 6 and 8 h. At predetermined reperfusion times, rats were injected with Evans blue and decapitated. Capillary patency was determined using a fluorescent double-staining technique. No capillary perfusion deficits were detected in the ischemic neocortical penumbra, neocortical focus or striatal focus. We concluded that the secondary deterioration of bioenergetic state is not due to microcirculatory compromise. Since hyperglycemic animals show pan-necrotic lesions, a hyperglycemic group was added at 8 h of reperfusion to test if the adverse effect of hyperglycemia on ischemic damage is related to capillary compromise. The results showed that, in hyperglycemic rats, capillary perfusion in the striatal focus was compromised after 8 h of recirculation following 2 h of MCA occlusion. It is concluded that when normoglycemic rats are subjected to 2 h of MCA occlusion, capillary patency is not affected during the first 4-6 h of reflow. At 8 h of reflow, though, particularly in hyperglycemic rats, microcirculation is compromised in the caudoputamenal focus, probably reflecting infarction.