BACKGROUND AND PURPOSE: Hyperglycemia has a deleterious effect on brain ischemia. However, the effect of hyperglycemia in intracerebral hemorrhage (ICH) is not well known. We investigated the effect of hyperglycemia on the development of brain edema and perihematomal cell death in ICH. METHODS: Hyperglycemia was induced by intraperitoneal injection of streptozotocin (60 mg/kg) in adult Sprague-Dawley male rats. ICH was induced by stereotaxic infusion of 0.23 U of collagenase into the left striatum. Seventy-two hours after ICH, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining was performed for perihematomal cell death. We also measured brain water content to evaluate edema formation. RESULTS: The serum glucose level of the hyperglycemic group was 394.0+/-180.3 mg/dL (n=31), and that of the normoglycemic group was 97.5+/-27.4 mg/dL (n=31). The size of hemorrhage was similar between groups, without any significant difference (n=8 in each group). The brain water content of hyperglycemic rats (n=17) increased in both lesioned (81.0+/-0.5%) and nonlesioned hemispheres (78.7+/-0.6%) compared with the normoglycemic group (n=17; lesioned: 78.9+/-0.8%; nonlesioned: 77.3+/-1.1%). In the hyperglycemic group, more TUNEL-positive cells were found in the perihematomal regions (n=6). CONCLUSIONS: Hyperglycemia caused more profound brain edema and perihematomal cell death in experimental ICH.
BACKGROUND AND PURPOSE:Hyperglycemia has a deleterious effect on brain ischemia. However, the effect of hyperglycemia in intracerebral hemorrhage (ICH) is not well known. We investigated the effect of hyperglycemia on the development of brain edema and perihematomal cell death in ICH. METHODS:Hyperglycemia was induced by intraperitoneal injection of streptozotocin (60 mg/kg) in adult Sprague-Dawley male rats. ICH was induced by stereotaxic infusion of 0.23 U of collagenase into the left striatum. Seventy-two hours after ICH, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining was performed for perihematomal cell death. We also measured brain water content to evaluate edema formation. RESULTS: The serum glucose level of the hyperglycemic group was 394.0+/-180.3 mg/dL (n=31), and that of the normoglycemic group was 97.5+/-27.4 mg/dL (n=31). The size of hemorrhage was similar between groups, without any significant difference (n=8 in each group). The brain water content of hyperglycemic rats (n=17) increased in both lesioned (81.0+/-0.5%) and nonlesioned hemispheres (78.7+/-0.6%) compared with the normoglycemic group (n=17; lesioned: 78.9+/-0.8%; nonlesioned: 77.3+/-1.1%). In the hyperglycemic group, more TUNEL-positive cells were found in the perihematomal regions (n=6). CONCLUSIONS:Hyperglycemia caused more profound brain edema and perihematomal cell death in experimental ICH.
Authors: Daniel T Laskowitz; Beilei Lei; Hana N Dawson; Haichen Wang; Steven T Bellows; Dale J Christensen; Michael P Vitek; Michael L James Journal: Neurocrit Care Date: 2012-04 Impact factor: 3.210
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Authors: Jizong Zhao; Liangfu Zhou; Dingbiao Zhou; Renzhi Wang; Mei Wang; Dejiang Wang; Shuo Wang; Ge Yuan; Shuai Kang; Nan Ji; Yuanli Zhao; Xun Ye Journal: Front Med China Date: 2007-02-01
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