title: Leukocyte-endothelial cell interactions in diabetic retina after transient retinal ischemia.
abstract: 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.
authors.affiliation: Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. tujikawa@kuhp.kyoto-u.ac.jp
authors.forename: A
authors.initials: A
authors.lastname: Tsujikawa
authors.forename: J
authors.initials: J
authors.lastname: Kiryu
authors.forename: A
authors.initials: A
authors.lastname: Nonaka
authors.forename: K
authors.initials: K
authors.lastname: Yamashiro
authors.forename: H
authors.initials: H
authors.lastname: Nishiwaki
authors.forename: Y
authors.initials: Y
authors.lastname: Honda
authors.forename: Y
authors.initials: Y
authors.lastname: Ogura
mesh_terms: D000818:Animals; D001786:Blood Glucose; D002450:Cell Communication / Q000276:immunology*; D002465:Cell Movement / Q000276:immunology; D003921:Diabetes Mellitus, Experimental / Q000276:immunology / Q000473:pathology; D003930:Diabetic Retinopathy / Q000473:pathology*; D004730:Endothelium, Vascular / Q000166:cytology*; D005123:Eye / Q000098:blood supply; D002546:Ischemic Attack, Transient / Q000276:immunology / Q000473:pathology*; D007962:Leukocytes / Q000166:cytology*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D018715:Microscopy, Video; D051381:Rats; D020318:Rats, Long-Evans; D015427:Reperfusion Injury / Q000276:immunology / Q000473:pathology; D012161:Retinal Artery / Q000276:immunology / Q000473:pathology; D013314:Stress, Mechanical; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D001786:Blood Glucose