• Krista J Stewart, Bermans J Iskandar, Brenton M Meier, Elias B Rizk, Nithya Hariharan, Joyce Koueik, Adin-Christian Andrei, and Kirk J Hogan.
• From the Department of Ophthalmology, University of Minnesota, Minneapolis, Minnesota (K.J.S.) Department of Anesthesiology, ThedaCare Regional Medical Center, Appleton, Wisconsin (B.M.M.) Department of Neurosurgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin (B.J.I., N.H., J.K.) Department of Neurosurgery, Penn State Hershey Medical Center, Hershey, Pennsylvania (E.B.R.) Department of Preventive Medicine Biostatistics Faculty, Feinberg School of Medicine, Northwestern University, Chicago, Illinois (A.-C.A.) the Department of Anesthesiology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin (K.J.H.).
• Anesthesiology. 2019 Nov 1; 131 (5): 1063-1076.

BackgroundNitrous oxide can induce neurotoxicity. The authors hypothesized that exposure to nitrous oxide impairs axonal regeneration and functional recovery after central nervous system injury.MethodsThe consequences of single and serial in vivo nitrous oxide exposures on axon regeneration in four experimental male rat models of nervous system injury were measured: in vitro axon regeneration in cell culture after in vivo nitrous oxide administration, in vivo axon regeneration after sharp spinal cord injury, in vivo axon regeneration after sharp optic nerve injury, and in vivo functional recovery after blunt contusion spinal cord injury.ResultsIn vitro axon regeneration 48 h after a single in vivo 70% N2O exposure is less than half that in the absence of nitrous oxide (mean ± SD, 478 ± 275 um; n = 48) versus 210 ± 152 um (n = 48; P < 0.0001). A single exposure to 80% N2O inhibits the beneficial effects of folic acid on in vivo axonal regeneration after sharp spinal cord injury (13.4 ± 7.1% regenerating neurons [n = 12] vs. 0.6 ± 0.7% regenerating neurons [n = 4], P = 0.004). Serial 80% N2O administration reverses the benefit of folic acid on in vivo retinal ganglion cell axon regeneration after sharp optic nerve injury (1277 ± 180 regenerating retinal ganglion cells [n = 7] vs. 895 ± 164 regenerating retinal ganglion cells [n = 7], P = 0.005). Serial 80% N2O exposures reverses the benefit of folic acid on in vivo functional recovery after blunt spinal cord contusion (estimate for fixed effects ± standard error of the estimate: folic acid 5.60 ± 0.54 [n = 9] vs. folic acid + 80% N2O 5.19 ± 0.62 [n = 7], P < 0.0001).ConclusionsThese data indicate that nitrous oxide can impair the ability of central nervous system neurons to regenerate axons after sharp and blunt trauma.

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