Recent evidence suggests that admission hypergly- cemia has deleterious effects on the survival and functional outcome of patients with intracerebral hemorrhage （ICH）. In this study, we first induced acute hyperglycemia in male adult Sprague-Dawley rats by intraperitoneal injection of 50% glucose （6 mL/kg）, and created the ICH model thereafter by delivering autologous whole blood or homologous normal- glucose blood into the right basal ganglia. Twenty- four hours later, we assessed the neurological injury, evaluated the hematoma and brain water content, and investigated autophagy. We found elevations of neurological deficit scores, brain water content, and microtubule-associated protein light chain-3 （LC3） and beclin-1 protein levels, and decreased SQSTM1/ p62 levels after ICH with normal-glucose blood （without hyperglycemia）. Acute hyperglycemia with ICH of high-glucose blood hematoma was associated with significantly increased forelimb-use asymmetry test scores, brain water content and SQSTM1/p62 protein levels, and evident decreases in the ratio of LC3-11/LC3-1 and beclin-1 protein levels. On the other hand, acute hyperglycemia and ICH with normal- glucose blood hematoma only slightly increased the neurological deficit scores and brain water content （P 〉0.05）. In conclusion, the autophagy pathway was activated after ICH, and acute hyperglycemia with hematoma of high-glucose blood exacerbates the neurological injury, and reduces autophagy around the hematoma.
