gms | German Medical Science

Objective: Metabolic changes and an accumulation of metabolic products such as lactate, pyruvate and glutamate are known following SAH. In the course of the disease, secondary brain injury appears which might be primarily responsible for the still very high mortality and morbidity following SAH. A possible cause for secondary brain injury could be a disability of oxygen utilization due to an enzymatic failure of aerobic glycolysis. Aim of this study was therefore the quantification of glucose metabolism using ¹⁸FDG-PET hoping to visualize a shift from aerobic to anaerobic metabolism.

Methods: In a prospective longitudinal study using the endovascular filament model in rats, glucose metabolism was visualized and quantified via ¹⁸FDG-PET. Eighteen Sprague-Dawley rats (weighing 250-300g) were randomly assigned into one of two groups: (1) SAH induced via endovascular filament model and (2) sham operated controls. Serial ¹⁸FDG-PETs were performed 3 hours following SAH, as well as on day 1, day 4 and day 7 and brain glucose metabolism was depicted.

Results: Animals with experimental SAH via endovascular filament model showed a clear increase of ¹⁸FDG uptake in contrast to sham operated animals. This effect was demonstrated to be significant (p < 0.05) three hours following SAH and could be shown through the course of the disease until day 7 following experimental SAH.

Conclusion: Through the use of the FDG-PET study, the visualization and quantification of glucose metabolism following experimental SAH in rats was successful. The clear increase of glucose uptake supports our theory, that there is a switch from aerobic to anaerobic glucose already in the early hours following SAH. Our data show that this metabolic malposition persists over the course of the disease and lasts at least until day 7 following SAH. Further studies should illuminate which clinical and neuronal correlates come with this metabolic disturbance and where clinical therapeutic insertions could be found to lower or even prevent secondary brain damage.