The Effect of l-glutamic Acid on Cat Somatosensory Evoked Potentials in Infusion Brain Edema Model

ABSTRACT

The infusion edema model was applied to study the effect of l-glutamic acid on the central conduction time of the cat somatosensory pathway which was compromised in the deep white matter by infusion known amount of l-glutamic acid and physiologic saline in the left and right frontal respectively. According to the different acidity of the l-glutamic acid three groups A(pH=3.22), B(pH=5.13), and C(pH=7.39) were made, but the concentration of glutamic acid was 20m Mol/L in all groups. Infusion of normal saline(0.9%, pH=5.11) into the right frontal deep white matter was common in all groups. During 4 hours of slow infusion of the infusates (average 0.48ml in each side totally) central conduction times were measured every hour via contralateral median nerve stimulation, bilaterally. Finally the cat was sacrificed and specimens of the edematous white matter obtained bilaterally. Finally the cat was sacrificed and specimens of the edematous white matter obtained bilaterally at the corresponding points and percentage water content was measured. The results were as follows 1) Overall average percentage water content was 82.36% and there was no statistically significant differences between the glutamic acid and saline infusion sites in each group. 2) The I-N1 interpeak latency was labelled as central conduction time(CCT), and overal baseline CCT was 5.04msec, 5.09msec, left and right side respectively. 3) The differences of CCT between glutamic and saline infusion edema were statistically significant in group A and B at 2, 3, 4 hours infusion, but the differences of CCT from the baseline value in the same side were absent in group A and B. In contrast, group C showed no differences in CCT between glutamic acid and saline infusion edema, but CCT comparisons with baseline value among same infusate were significantly prolonged at 4 hours infusion on both sides. Intergroup unpaired t-test for checking intergroup differences among the three glutamic acid groups showed no intergroup differences in CCT. 4) In the combined group the CCT was significantly different between the glutamic and saline sides at 2 hours(P<0.005), 3 hours(P<0.005), 4 hours(P<0.025) infusion. The comparison of each hour CCT with the baseline value showed statistically significant prolongation of CCT only in glutamic side at 3,4 hours infusion. The results indicate the l-glutamic acid which is normally present in brain edema fluid can modulate local biochemical milieu of the brain as to increase the CCT.