Hyperglycemia increases brain injury caused by secondary ischemia after cortical impact injury in rats.

OBJECTIVE

To examine the effects of glucose infusion on the histologic brain damage caused by controlled cortical impact injury alone and by cortical impact injury complicated by secondary ischemia.

DESIGN

Prospective, randomized study.

SETTING

University laboratory.

SUBJECTS

Male Long-Evans rats.

INTERVENTIONS

Three experimental conditions were studied: a) 2.5-mm deformation impact (velocity 4 m/sec) injury followed by 40 mins of bilateral carotid occlusion; b) sham impact injury followed by 40 mins of bilateral carotid occlusion; and c) 2.5-mm deformation impact (velocity 4 m/sec) injury followed by sham carotid occlusion. For each experimental condition, animals were randomized to receive either glucose solution or saline solution before the induced injury and the sham impact injury. Contusion volume and neuron density in the CA1 and CA3 regions of the hippocampus were measured 2 wks after the injury.

MEASUREMENTS AND MAIN RESULTS

Parenteral administration of 2.2 g/kg glucose solution increased the blood glucose concentration from 6.7 +/- 3.3 to 17.9 +/- 10.6 mmol/L before the impact injury, and to 12.3 +/- 5.6 mmol/L before carotid occlusion. Hyperglycemia had the greatest effect on the consequences of the impact injury complicated by secondary ischemia, increasing contusion volume from 1 to 30.6 mm3 in the animals that received saline or glucose solution, respectively (p = .005), and reducing the density of normal appearing neurons in the CA1 area of the hippocampus from 201 to 144 cells/mm2 in the animals that received saline solution and glucose solution, respectively (p = .038). The impact injury alone and bilateral carotid occlusion alone caused minimal neuronal loss in the hippocampus and minimal contusion or infarction at the impact site. Individually, these mild injuries were not adversely affected by infusion of glucose solution.

CONCLUSION

Hyperglycemia increases brain damage when traumatic brain injury is complicated by secondary ischemia.