COMPARATIVE, TOXICITY OF GLUCOSE AND LIDOCAINE ADMINISTERED INTRATHECALLY IN THE RAT

Citation
K. Hashimoto et al., COMPARATIVE, TOXICITY OF GLUCOSE AND LIDOCAINE ADMINISTERED INTRATHECALLY IN THE RAT, REGIONAL ANESTHESIA AND PAIN MEDICINE, 23(5), 1998, pp. 444-450
Citations number
30
Categorie Soggetti
Anesthesiology
ISSN journal
10987339
Volume
23
Issue
5
Year of publication
1998
Pages
444 - 450
Database
ISI
SICI code
1098-7339(1998)23:5<444:CTOGAL>2.0.ZU;2-I
Abstract
Background and Objectives. Glucose is a common component of anesthetic solutions used for spinal anesthesia. However, its possible contribut ion to recent injuries occurring with spinal anesthesia has not been a dequately addressed. Accordingly, the present studies compare the func tional and morphologic effects of intrathecally administered glucose w ith those of lidocaine. Methods. Twenty rats, implanted with intrathec al catheters, were divided into three groups to receive a 1-hour infus ion of 5% lidocaine (n = 6), 10% glucose (n = 7), or normal saline (n = 7). Four days after infusion, animals were evaluated for persistent sensory impairment using the tail-nick test. Three days later, the ani mals were sacrificed, and the spinal cord and nerve roots were examine d by a neuropathologist blinded to the solution received and the resul ts of sensory testing. Results. Lidocaine-treated animals exhibited pe rsistent sensory impairment, whereas glucose- and saline-treated anima ls did not. Neuropathologic evaluation revealed moderate to severe ner ve root injury in lidocaine-treated animals. Histologic changes in glu cose- and saline-treated animals were minimal, similar, and restricted to the area adjacent to the catheter. Morphologic damage associated w ith lidocaine preferentially affected the nerve roots, with relative s paring of the spinal cord and dorsal root ganglia. Conclusions. These results suggest that, at clinically relevant concentrations, glucose d oes not induce neurologic injury, providing indirect evidence that rec ent clinical injuries occurring after spinal anesthesia resulted from a neurotoxic effect of the local anesthetic. Additionally, the present studies suggest that deficits resulting from neurotoxicity of intrath ecally administered anesthetic result from injury to the axon.