Aim: Diabetes mellitus is a chronic metabolic disease that is associated with peripheral microvascular complications and an increased risk of neurological events. Following closed head injury, diabetic rats suffer greater neurological dysfunction, associated with further lipid peroxidation than normal rats. The mechanistic factors in diabetes which cause neurological dysfunction are not clear, but disruption of the blood-brain barrier (BBB) may be one reason. We experimentally investigated alterations in the BBB after traumatic brain injury in streptozotocin-induced diabetic rats.

Methods: Thirty-two adult male Sprague-Dawley rats were divided randomly and evenly into four groups as trauma only, diabetes only, diabetes plus trauma, and sham-operated control. Diabetes was induced by a single injection of streptozotocin. Diabetic rats were exposed to trauma 4 weeks after streptozotocin injection to allow development of chronic diabetes. Permeability to Evans blue dye (EBD) was evaluated to assess the BBB integrity following trauma. Brains perfused with EBD were divided into six anatomically distinct brain regions (cortex, hippocampus, corpus striatum, midbrain, thalamus, and cerebellum), and EBD extravasation was quantified using spectrophotometric methods 60 min after injury.

Results: Spectrophotometric measurements of EBD revealed that BBB permeability was increased significantly in the cerebellum and corpus striatum in the diabetes plus trauma group compared with the trauma only and control groups.

Conclusion: The disruption of the BBB caused by traumatic brain injury is more severe in diabetics than normal subjects, and also region specific with cerebellum and corpus striatum appearing to be most susceptible to trauma-induced microvascular damage in diabetics.

Keywords: Blood brain barrier, brain edema, diabetic rats, streptozotocin, traumatic brain injury