GADOBENATE DIMEGLUMINE AND CEREBRAL GLUCOSE METABOLISM

Purpose: Brain contrast-enhanced MR imaging reflects the leakage of contrast material into the brain tissue due to blood-brain barrier (BBB) disruption. The contact between brain tissue and contrast material requires a high level of neurotolerability of the contrast agent (CA). In the present study, we investigated the neurotolerability of the paramagnetic CA gadobenate dimeglumine, locally applied into the corpus striatum of freely moving rats, by evaluating its potential effects on cerebral glucose metabolism based on lactate levels.

Material and Methods: Lactate levels were monitored using a microdialysis technique coupled with an enzyme reaction. A microdialysis probe for extracellular fluid sampling, together with a stainless steel cannula for CA administration, were inserted into the right corpus striatum of rats. Lactate levels were monitored for 2 h after gadobenate dimeglumine administration at 120 nmol/rat, at fixed volume of 1.2 μl. The same volume of artificial cerebrospinal fluid (aCSF) was administered to control rats.

Results: Gadobenate dimeglumine did not induce any significant changes in the lactate striatal levels over the 30-min period after administration. Small, but significant, reductions in lactate concentration were found from the 45-min control point after gadobenate dimeglumine administration. Lactate response showed the same pattern in rats given aCSF.

Conclusion: Gadobenate dimeglumine, intracerebrally administered, did not affect cerebral glucose metabolism in rats as it showed the same behaviour as aCSF on cerebral glucose utilization. The gradual attenuation in the endogenous lactate release observed 45 min after test compound administration is possibly due to a slight reduction in the probe recovery. The present findings confirm the neurotolerability of gadobenate dimeglumine previously shown in behavioural and electrophysiological studies.