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Exaggerated Neutrophil‐Mediated Reperfusion Injury after Ischemic Stroke in a Rodent Model of Type 2 Diabetes
Author(s) -
RITTER LESLIE,
DAVIDSON LISA,
HENRY MELISSA,
DAVISGORMAN GRACE,
MORRISON HELENA,
FRYE JENNIFER B.,
COHEN ZOE,
CHANDLER SIERRA,
McDONAGH PAUL,
FUNK JANET L.
Publication year - 2011
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2011.00115.x
Subject(s) - medicine , reperfusion injury , microcirculation , stroke (engine) , ischemia , infarction , inflammation , edema , diabetes mellitus , type 2 diabetes , integrin alpha m , middle cerebral artery , anesthesia , endocrinology , cardiology , receptor , myocardial infarction , mechanical engineering , engineering
Please cite this paper as: Ritter, Davidson, Henry, Davis‐Gorman, Morrison, Frye, Cohen, Chandler, McDonagh and Funk (2011). Exaggerated Neutrophil‐Mediated Reperfusion Injury after Ischemic Stroke in a Rodent Model of Type 2 Diabetes. Microcirculation 18 ( 7 ), 552–561. Abstract Objective: We tested the hypothesis that both chronic and acute inflammatory processes contribute to worse reperfusion injury and stroke outcome in an experimental model of T2DM. Materials and Methods: Twelve‐ to thirteen‐week‐old male Zucker Diabetic Fatty (ZDF) rats vs. Zucker Lean Controls (ZLC) rats were tested at baseline and after middle cerebral artery occlusion (ischemia) and reperfusion (I–R). Neutrophil adhesion to the cerebral microcirculation, neutrophil expression of CD11b, infarction size, edema, neurologic function, sICAM, and cerebral expression of neutrophil–endothelial inflammatory genes were measured. Results: At baseline, CD11b and sICAM were significantly increased in ZDF vs. ZLC animals ( p < 0.05). After I–R, significantly more neutrophil adhesion and cell aggregates were observed in ZDF vs. ZLC ( p < 0.05); infarction size, edema, and neurologic function were significantly worse in ZDF vs. ZLC ( p < 0.05). CD11b and sICAM‐1 remained significantly increased in ZDFs ( p < 0.05), and cerebral expression of IL‐1β, GRO/KC, E‐selectin, and sICAM were significantly induced in ZDF, but not ZLC groups ( p < 0.05) after 2.5 hours of reperfusion. Conclusion: Both sides of the neutrophil–endothelial interface appear to be primed prior to I–R, and remain significantly more activated during I–R in an experimental model of T2DM. Consequently, reperfusion injury appears to play a significant role in poor stroke outcome in T2DM.