Comparison of microdialysate arginine and glutamate levels in severely head-injured patient.

L-arginine concentrations in the brain are of interest following TBI because L-arginine is the immediate precursor of nitric oxide (NO). In addition, in vitro studies suggest that glutamate, which is a mediator of secondary injury after TBI, may stimulate release of arginine from glial cells. This study examines arginine concentrations in brain tissue using the microdialysis technique after human TBI. From 78 TBI patients, a total of 1739 microdialysate samples were collected using a CMA-70 probe perfused with normal saline at 2 microliters/min and concentrations of amino acids in microdialysate were determined. Amino acid concentrations for each patient were averaged for 8-hour periods during the first 3 days after injury, and daily for postinjury days 4 and 5. Following an initial rapid decrease in arginine, the dialysate arginine concentrations were low on days 1-3 and then increased over the days 4-5 after injury. In contrast, the microdialysate glutamate levels decreased slowly over the first 48 hours after TBI and thereafter remained low. Thirty-five episodes of jugular venous desaturation (SjvO2 < 50%) occurred during monitoring. Arginine and glutamate levels simultaneously doubled during desaturation and decreased as the clinical episode resolved. The low concentrations of arginine during the first 3 days after TBI may indicate that substrate unavailability could contribute to the decreased NO concentrations that have been observed after TBI. The simultaneous increase in glutamate and arginine during ischemic events is consistent with experimental data which has observed that glutamate induces release of arginine.