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Diabetes Increases Cerebrovascular Permeability: Relevance to Ischemia/Reperfusion Injury
Author(s) -
Li Weiguo,
Elgebaly Mostafa M,
ElRemessy Azza,
Kozak Anna,
Schreihofer Derek A,
Dorrance Anne M,
Fagan Susan C,
Ergul Adviye
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1151.17
Subject(s) - medicine , diabetes mellitus , ischemia , vascular permeability , evans blue , occlusion , reperfusion injury , stroke (engine) , cerebral blood flow , hemodynamics , cardiology , anesthesia , endocrinology , mechanical engineering , engineering
Diabetes not only increases the risk of stroke but also is associated with a worse stroke outcome. We have shown that the Goto‐Kakizaki (GK) rat model of Type 2 diabetes exhibited smaller infarct size but increased hemorrhagic transformation (HT) following 3 h middle cerebral artery occlusion (MCAO) and 21 h reperfusion. Pial vessels were also more tortuous in this model. Taken together, we hypothesized that there is potential neovascularization and increased permeability in the cerebrovasculature of diabetic rats. The baseline cerebral blood flow (CBF) was assessed by a scanning laser Doppler. The cerebrovascular density and permeability was assessed by fluorescein isothiocyanate labeled dextran and BSA, respectively, in diabetic and control rats without MCAO. Blood glucose was higher (168 ± 5 vs. 108 ± 3 mg/dl, p<0.05) and baseline CBF was lower in the GK rats (2.74 ± 0.20 vs. 3.93 ± 0.16 pixel/mm 2 , p<0.05). Permeability of cerebral vessels was increased in the GK group (84 ± 9 vs. 47 ± 6 OD, p=0.018). A slightly higher vascular density in GKs (n=3, p=0.18) may be a potential mechanism contributing to smaller infarcts. These findings suggest that diabetes promotes cerebral vascular permeability and accordingly augments ischemia/reperfusion injury induced HT.