Reperfusion after transient focal ischemia of 2 h duration is followed
by secondary bioenergetic failure after 4 h of reperfusion. The objec
tive 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 reperf
usion for 2, 4, 6 and 8 h. At predetermined reperfusion times, rats we
re injected with Evans blue and decapitated. Capillary patency was det
ermined using a fluorescent double-staining technique. No capillary pe
rfusion deficits were detected in the ischemic neocortical penumbra, n
eocortical focus or striatal focus. We concluded that the secondary de
terioration of bioenergetic state is not due to microcirculatory compr
omise. Since hyperglycemic animals show pan-necrotic lesions, a hyperg
lycemic group was added at 8 h of reperfusion to test if the adverse e
ffect of hyperglycemia on ischemic damage is related to capillary comp
romise. The results showed that, in hyperglycemic rats, capillary perf
usion in the striatal focus was compromised after 8 h of recirculation
following 2 h of MCA occlusion. It is concluded that when normoglycem
ic rats are subjected to 2 h of MCA occlusion, capillary patency is no
t affected during the first 4-6 h of reflow. At 8 h of reflow, though,
particularly in hyperglycemic rats, microcirculation is compromised i
n the caudoputamenal focus, probably reflecting infarction. (C) 1998 E
lsevier Science Ireland Ltd. All rights reserved.