Diabetes is associated with increased neural damage after
transient cerebral ischemia. Recently, leukocytes, which are thought to play a central role in
ischemia-reperfusion injury, have been suggested to be involved in exacerbated damage after transient
ischemia in diabetic animals. The present study was designed to clarify whether the anticipated worse outcome after
transient cerebral ischemia in diabetic animals was due to augmented leukocyte-mediated neural injury. Using rats with
streptozotocin-induced diabetes of 4-wk duration, we investigated leukocyte-endothelial cell interactions during reperfusion after a transient 60-min period of
retinal ischemia. Unexpectedly, postischemic diabetic retina showed no active leukocyte-endothelial cell interactions during reperfusion. The maximal numbers of rolling and accumulating leukocytes in diabetic retina were reduced by 73.6 and 41.2%, respectively, compared with those in nondiabetic rats. In addition, neither preischemic
insulin treatment of diabetic rats nor preischemic
glucose infusion of nondiabetic rats significantly influenced leukocyte-endothelial cell interactions during reperfusion. The present study demonstrated that high
blood glucose concentration before induction of
ischemia did not exacerbate leukocyte involvement in the postischemic
retinal injury. Furthermore, diabetic retina showed suppressed leukocyte-endothelial cells interactions after transient
ischemia, perhaps due to an adaptive mechanism that developed during the period of induced diabetes.