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The additional oxygen as a carrier gas during long-duration sevoflurane exposure ameliorate the neuronal apoptosis and improve the long-term cognitive function in neonatal rats.
Brain Res. 2018 Jan 01; 1678:220-230.BR

Abstract

The effects of the oxygen concentration as a carrier gas and long duration anesthesia exposure on neuroapoptosis and cognitive impairments in the developing brain are not fully understood. This study shows that long-duration sevoflurane anesthesia with or without additional oxygen induces neuroapoptosis and long-term cognitive dysfunction in neonatal rats. Seven-day-old rats were exposed to sevoflurane anesthesia for 2, 4, and 6 h with 21% or 30% oxygen. The control group received 21% oxygen alone for 6 h. Post-anesthesia blood gas analysis resulted in hypoxia and hypercapnia. Moreover, PO2 and base excess in the 30% oxygen group were significantly higher than the 21% oxygen group. The numbers of caspase-3-positive cells in both cortical layer 3 and the CA1 region in the hippocampus in the 6 h anesthesia exposure group with 21% oxygen were increased compared with the 6 h anesthesia exposure with 30% oxygen and control groups. Cognitive function was assessed in an additional group of rats, and the brains were stained for NeuN 6 weeks post-anesthesia. Although the Morris water maze task was acquired equally by all rats 3 weeks post-anesthesia, the escape latency was significantly longer in the 6 h sevoflurane with 21% oxygen group than the 6 h with 30% oxygen groups 6 weeks post-exposure. No difference was found with regard to freezing time among the groups in the fear conditioning test. The number of NeuN-positive cells in the CA1 region of the hippocampus in the control group was increased compared with the other groups. These findings indicate that long-duration sevoflurane exposure with 30% oxygen as a carrier gas would ameliorate neuronal apoptosis and improve long-term cognitive function in neonatal rats.

Authors+Show Affiliations

Department of Anesthesia and Intensive Care Medicine, Akita University Graduate School of Medicine, Akita, Japan. Electronic address: tgoyagi@doc.med.akita-u.ac.jp.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29061366

Citation

Goyagi, Toru. "The Additional Oxygen as a Carrier Gas During Long-duration Sevoflurane Exposure Ameliorate the Neuronal Apoptosis and Improve the Long-term Cognitive Function in Neonatal Rats." Brain Research, vol. 1678, 2018, pp. 220-230.
Goyagi T. The additional oxygen as a carrier gas during long-duration sevoflurane exposure ameliorate the neuronal apoptosis and improve the long-term cognitive function in neonatal rats. Brain Res. 2018;1678:220-230.
Goyagi, T. (2018). The additional oxygen as a carrier gas during long-duration sevoflurane exposure ameliorate the neuronal apoptosis and improve the long-term cognitive function in neonatal rats. Brain Research, 1678, 220-230. https://doi.org/10.1016/j.brainres.2017.10.014
Goyagi T. The Additional Oxygen as a Carrier Gas During Long-duration Sevoflurane Exposure Ameliorate the Neuronal Apoptosis and Improve the Long-term Cognitive Function in Neonatal Rats. Brain Res. 2018 Jan 1;1678:220-230. PubMed PMID: 29061366.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The additional oxygen as a carrier gas during long-duration sevoflurane exposure ameliorate the neuronal apoptosis and improve the long-term cognitive function in neonatal rats. A1 - Goyagi,Toru, Y1 - 2017/10/20/ PY - 2017/06/22/received PY - 2017/10/12/revised PY - 2017/10/14/accepted PY - 2017/10/25/pubmed PY - 2018/7/17/medline PY - 2017/10/25/entrez KW - Anesthesia KW - Apoptosis KW - Cognitive function KW - Neonate KW - Neural toxicity KW - Sevoflurane SP - 220 EP - 230 JF - Brain research JO - Brain Res. VL - 1678 N2 - The effects of the oxygen concentration as a carrier gas and long duration anesthesia exposure on neuroapoptosis and cognitive impairments in the developing brain are not fully understood. This study shows that long-duration sevoflurane anesthesia with or without additional oxygen induces neuroapoptosis and long-term cognitive dysfunction in neonatal rats. Seven-day-old rats were exposed to sevoflurane anesthesia for 2, 4, and 6 h with 21% or 30% oxygen. The control group received 21% oxygen alone for 6 h. Post-anesthesia blood gas analysis resulted in hypoxia and hypercapnia. Moreover, PO2 and base excess in the 30% oxygen group were significantly higher than the 21% oxygen group. The numbers of caspase-3-positive cells in both cortical layer 3 and the CA1 region in the hippocampus in the 6 h anesthesia exposure group with 21% oxygen were increased compared with the 6 h anesthesia exposure with 30% oxygen and control groups. Cognitive function was assessed in an additional group of rats, and the brains were stained for NeuN 6 weeks post-anesthesia. Although the Morris water maze task was acquired equally by all rats 3 weeks post-anesthesia, the escape latency was significantly longer in the 6 h sevoflurane with 21% oxygen group than the 6 h with 30% oxygen groups 6 weeks post-exposure. No difference was found with regard to freezing time among the groups in the fear conditioning test. The number of NeuN-positive cells in the CA1 region of the hippocampus in the control group was increased compared with the other groups. These findings indicate that long-duration sevoflurane exposure with 30% oxygen as a carrier gas would ameliorate neuronal apoptosis and improve long-term cognitive function in neonatal rats. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/29061366/The_additional_oxygen_as_a_carrier_gas_during_long_duration_sevoflurane_exposure_ameliorate_the_neuronal_apoptosis_and_improve_the_long_term_cognitive_function_in_neonatal_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(17)30472-9 DB - PRIME DP - Unbound Medicine ER -