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      Pro-Con Debate: Nitrous Oxide for Labor Analgesia

      review-article
      Author(s): 1 , , 2
      Publication date (Electronic):
      Journal: BioMed Research International
      Publisher: Hindawi

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          Abstract

          This Pro-Con debate will provide the practitioner with an evidence-based knowledge approach to assist the clinician in determining whether to employ (Pro) or not to employ (Con) this technique in the obstetrical suite for labor analgesia. Nitrous oxide has been used safely in dentistry and medicine for many centuries. However, accumulating preclinical and clinical evidence increasingly suggests previously unrecognized adverse maternal and fetal effects of nitrous oxide, which warrants reconsideration of its use in pregnant women and a more detailed informed consent. Nitrous oxide is associated with metabolic, oxidative, genotoxic, and transgenerational epigenetic effects in animals and humans that may warrant limiting its usefulness in labor. This debate will discuss and review the clinical uses, advantages, and disadvantages of nitrous oxide on occupational effects of nitrous oxide exposure, neuroapoptosis, FDA warning on inhalational anesthetics and the developing brain, research limitations, occupational exposure safety limits, effects on global warming, and potential for diversion.

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          Early exposure to anesthesia and learning disabilities in a population-based birth cohort.

          Robert Wilder, Randall P. Flick, Juraj Sprung … (2009)
          Anesthetic drugs administered to immature animals may cause neurohistopathologic changes and alterations in behavior. The authors studied association between anesthetic exposure before age 4 yr and the development of reading, written language, and math learning disabilities (LD). This was a population-based, retrospective birth cohort study. The educational and medical records of all children born to mothers residing in five townships of Olmsted County, Minnesota, from 1976 to 1982 and who remained in the community at 5 yr of age were reviewed to identify children with LD. Cox proportional hazards regression was used to calculate hazard ratios for anesthetic exposure as a predictor of LD, adjusting for gestational age at birth, sex, and birth weight. Of the 5,357 children in this cohort, 593 received general anesthesia before age 4 yr. Compared with those not receiving anesthesia (n = 4,764), a single exposure to anesthesia (n = 449) was not associated with an increased risk of LD (hazard ratio = 1.0; 95% confidence interval, 0.79-1.27). However, children receiving two anesthetics (n = 100) or three or more anesthetics (n = 44) were at increased risk for LD (hazard ratio = 1.59; 95% confidence interval, 1.06-2.37, and hazard ratio = 2.60; 95% confidence interval, 1.60-4.24, respectively). The risk for LD increased with longer cumulative duration of anesthesia exposure (expressed as a continuous variable) (P = 0.016). Exposure to anesthesia was a significant risk factor for the later development of LD in children receiving multiple, but not single anesthetics. These data cannot reveal whether anesthesia itself may contribute to LD or whether the need for anesthesia is a marker for other unidentified factors that contribute to LD.
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            Early Exposure to Common Anesthetic Agents Causes Widespread Neurodegeneration in the Developing Rat Brain and Persistent Learning Deficits

            Vesna Jevtovic-Todorovic, Richard Hartman, Yukitoshi Izumi … (2003)
            Recently it was demonstrated that exposure of the developing brain during the period of synaptogenesis to drugs that block NMDA glutamate receptors or drugs that potentiate GABA A receptors can trigger widespread apoptotic neurodegeneration. All currently used general anesthetic agents have either NMDA receptor-blocking or GABA A receptor-enhancing properties. To induce or maintain a surgical plane of anesthesia, it is common practice in pediatric or obstetrical medicine to use agents from these two classes in combination. Therefore, the question arises whether this practice entails significant risk of inducing apoptotic neurodegeneration in the developing human brain. To begin to address this problem, we have administered to 7-d-old infant rats a combination of drugs commonly used in pediatric anesthesia (midazolam, nitrous oxide, and isoflurane) in doses sufficient to maintain a surgical plane of anesthesia for 6 hr, and have observed that this causes widespread apoptotic neurodegeneration in the developing brain, deficits in hippocampal synaptic function, and persistent memory/learning impairments.
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              Oxidative DNA damage is epigenetic by regulating gene transcription via base excision repair.

              Aaron M Fleming, Yun Ding, Cynthia Burrows (2017)
              Reactive oxygen species (ROS) have emerged as important cellular-signaling agents for cellular survival. Herein, we demonstrate that ROS-mediated oxidation of DNA to yield 8-oxo-7,8-dihydroguanine (OG) in gene promoters is a signaling agent for gene activation. Enhanced gene expression occurs when OG is formed in guanine-rich, potential G-quadruplex-forming sequences (PQS) in promoter-coding strands, initiating base excision repair (BER) by 8-oxoguanine DNA glycosylase (OGG1), yielding an abasic site (AP). The AP enables melting of the duplex to unmask the PQS, adopting a G-quadruplex fold in which apurinic/apyrimidinic endonuclease 1 (APE1) binds, but inefficiently cleaves, the AP for activation of vascular endothelial growth factor (VEGF) or endonuclease III-like protein 1 (NTHL1) genes. These details were mapped via synthesis of OG and AP analogs at single-nucleotide precision within the promoter of a luciferase reporter system. The reporters were analyzed in human and mouse cells while selectively knocking out or down critical BER proteins to identify the impact on luciferase expression. Identification of the oxidatively modified DNA base OG to guide BER activity in a gene promoter and impact cellular phenotype ascribes an epigenetic role to OG.
              Article 0 comments Cited 134 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Manuel C. Vallejo:
                ORCID: https://orcid.org/0000-0002-1240-3670
                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date Collection: 2019
                Publication date (Electronic): 20 August 2019
                Volume: 2019
                Electronic Location Identifier: 4618798
                Affiliations
                1West Virginia University, Morgantown, WV 26506, USA
                2Cedar-Sinai Medical Center, Los Angeles, CA 90048, USA
                Author notes

                Academic Editor: Davor Zeljezic

                Author information
                https://orcid.org/0000-0002-1240-3670
                Article
                DOI: 10.1155/2019/4618798
                PMC ID: 6720045
                PubMed ID: 31531352
                SO-VID: 3bf86751-bf97-4cf8-b390-4ea7183d7adb
                Copyright © Copyright © 2019 Manuel C. Vallejo and Mark I. Zakowski.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 6 February 2019
                Date revision received : 19 May 2019
                Date accepted : 19 July 2019
                Categories
                Subject: Review Article

                Data availability:

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