Abstract W P217: The Impaired Leptomeningeal Collateral Flow Recruitment in the Type II Diabetic Mice is Independent of Hyperglycemia
Introduction: Previously we found that type II diabetic mice db/db strain exhibited impaired collateral flow recruitment between the middle cerebral artery (MCA) and anterior cerebral artery (ACA) vascular networks during MCA occlusion (MCAO)contributed to the worse stroke outcome when compared to their normoglycemic strain. However, it is unclear whether the underlying etiology in the diabetic stroke mice is attributed to hyperglycemia or other vascular pathology.
Methods: Adult male db/+ received intraperitoneal injection of dextrose (HG) or normal saline (NG) (n=5-6/group), respectively, 60 minutes prior to distal MCAO. Doppler optical coherence tomography (DOCT) was used to quantify the MCA flow direction and velocity at baseline and 30 min after MCAO. The chosen regions of interest of MCA network were classified according to branching order as segment 1 (seg1), seg2 and seg3, with seg1 most proximal to ACA while most distal to MCA. 5-10 points corresponding to the same location of each segment were selected for quantification.
Results: Blood glucose level was maintained at approximately 382± 83.8 mg/dl in the HG group during blood flow imaging, compared to 166± 60.1 mg/ml in the NG group. It fell to 141± 36.3 mg/dl and 142± 46.3 mg/dl at 24h after stroke in both groups. Hyperglycemia didn't change baseline flow velocity (NG: 6.8±0.8/9.2±0.7/12.5±0.5mm in seg1/seg2/seg3; HG: 5.7±0.7/8.2±0.5/12.6±0.9 mm/s, NS in all segments). At 30 min after MCAO, collateral flow was induced in both groups and there was no significant difference in flow velocity between groups (NG: -3.8±0.3/-2.7±0.1/-2.7±0.3mm/s; HG: -4.1±0.2/-3.1±0.3/2.2±0.4mm/s, NS in all segments). There was also no significant difference in vessel diameter between the groups both at baseline (NG: 48.9±3.5/55.1±1.6/61.5±2.7μm; HG: 45.6±1.7/48.8±2.7/59.2±2.7μm, NS in all segments) and 30 min after MCAO (NG: 48.4±2.0/50.8±2.6/55.5±2.6μm, HG: 42.6±2.3/49.9±2.0/52.5±2.6 μm in HG, NS in all segments).
Conclusions: Temporary induction of hyperglycemia doesn't affect collateral flow in normoglycemic mice during acute stroke, suggesting that the observed impairment of collateral flow recruitment in the type II diabetic mice is likely attributed to chronic vascular pathology.
Author Disclosures: Y. Akamatsu: None. C. Lee: None. J. Liu: None.
This research has received full or partial funding support from the American Heart Association, Western States - Alaska, Arizona, California, Hawaii, Idaho, Montana, Nevada, Oregon, Utah, Washington.
- © 2014 by American Heart Association, Inc.