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Obesity and the cerebral microvascular responses to ischemic stroke
Author(s) -
Terao Satoshi,
Yilmaz Gokhan,
Stokes Karen Y,
Granger D Neil
Publication year - 2007
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.21.6.a1275-b
Subject(s) - extravasation , medicine , evans blue , ischemia , stroke (engine) , endocrinology , blood–brain barrier , leptin , cardiology , anesthesia , pathology , obesity , central nervous system , mechanical engineering , engineering
Obesity is a well‐documented and modifiable risk factor for ischemic stroke. We tested the hypothesis that obesity exacerbates the microvascular dysfunction and brain damage induced by ischemia‐reperfusion (I/R). Middle cerebral artery occlusion (30 min) and reperfusion was induced in wild type (WT) and leptin‐deficient ob/ob mice. The adhesion of leukocytes (LA) and platelets (PA) in postischemic cerebral venules was monitored after 4 hrs of reperfusion by intravital microscopy. Infarct volume was estimated from brain slices (obtained 24 hrs after reperfusion) using the TTC staining method. Blood‐brain barrier dysfunction was quantified using the Evans blue (EB) method. Brain water (WC) content was determined as (wet weight–dry weight)/wet weight (%). I/R elicited significant increases in LA (116 ± 82 vs 308 ± 202 cells/mm 2 ) and PA in cerebral venules of both WT and ob/ob mice, however the responses were exaggerated in ob/ob mice. A similar pattern of I/R‐induced increases in infarct volume (16.4 ± 6.0 vs 27.6 ± 3.2 %), EB extravasation (0.013 ± 0.0082 vs 0.031 ± 0.012), and WC (79.8 ± 0.62 vs 81.3 ± 0.31%) was noted in WT and ob/ob mice, with the latter group exhibiting more profound changes. These findings indicate that the microvascular dysfunction and brain injury after I/R is exaggerated in ob/ob mice and that obesity leads to greater morbidity following ischemic stroke. (HL26441)