The addition of epinephrine to tetracaine injected intrathecally sustains an increase in glutamate concentrations in the cerebrospinal fluid and worsens neuronal injury
S. Oka et al., The addition of epinephrine to tetracaine injected intrathecally sustains an increase in glutamate concentrations in the cerebrospinal fluid and worsens neuronal injury, ANESTH ANAL, 93(4), 2001, pp. 1050-1057
Citations number
15
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
We have reported that lar-e concentrations of intrathecal tetracaine increa
se glutamate concentrations in the cerebrospinal fluid (CSF) and cause neur
onal injury in the spinal cord. In this study, we investigated whether the
addition of epinephrine to tetracaine modulates these events. New Zealand w
hite rabbits were assigned into five groups (six rabbits in each group) and
intrathecally received 0.3 mL of epinephrine 0.1 mg/mL in NaCl solution (c
ontrol), 1% tetracaine dissolved in saline (1%T), 1% tetracaine with epinep
hrine (1%TE), 2% tetracaine (2%T), or 2% tetracaine with epinephrine (2%TE)
. Glutamate concentrations in the lumbar CSF were monitored by microdialysi
s. Neurologic and histopathologic assessments were performed I wk after the
administration. Glutamate concentrations significantly increased in all fo
ur groups that received tetracaine, whereas no change was observed in the C
ontrol group. The addition of epinephrine to tetracaine sustained large con
centrations of glutamate. Sensory and motor dysfunction was observed in the
1%TE, 2%T, and 2%TE groups, and the dysfunction tended to be progressively
exacerbated in this order. Characteristic histologic changes in animals wi
th sensory and motor dysfunction were vacuolation in the dorsal funiculus a
nd chromatolytic damage of motor neurons. The vacuolation of the dorsal fun
iculus in the 1%TE group was significantly worse than in the 1%T group. The
se results suggest that the addition of epinephrine to tetracaine may incre
ase its neurotoxicity, which may possibly be related to a sustained increas
e of glutamate concentrations in the CSF.