Brain glucose transporter alterations following experimental cortical impact

Document Type

Journal Article

Publication Date



Critical Care Medicine








Introduction: Microdiatysis studies in head injured patients snow elevated lactate and reduced glucose in the extracellular space of the cerebral cortex correlate with poor outcome. These alterations usually occur in the context of ischemia or hypoxia. Facilitated glucose diffusion through the blood brain bamer is mediated by glucose transporter 1 (GLUT1) while neuronal glucose entry is mediated by glucose transporter 3 (GLUTS). We studied GLUT1 and GLUTS expression in impacted cerebral cortex to test the hypothesis that alterations of glucose transporters take place following head injury Methods: While under anesthesia, adult fasted rats underwent direct cortical impact injury delivered by a pneumatically driven piston. Animals were sacrificed at 5 min, 1 hr, 4 hr and 24 hr after injury, and the brains were examined using antibodies against GLUT1 and GLUTS. The intensity of staining was measured using absorption microspectroscopic image analysis. Results: GLUT1 expression was unchanged throughout, but GLUTS expression was higher in neurons in the impacted zone and underlying hippocampus compared to their non-injured counterparts in the opposite hemisphere. No elevation of GLUT 3 was seen at 5 min, but was increased at 1,4, and 24 hours. The maximal elevation was present at 1 and 4 hours. Conclusions: Increased GLUTS permits increased movement of glucose into neurons, while unchanged endothelial GLUT1 does not permit increased replenishment of the extracellular glucose resulting in low olucose levels measured by microdialvsis. Neuronal anaerobic metabolism also leads to elevated extracellular lactate.

This document is currently not available here.