Plasma corticosterone, epinephrine, and norepinephrine levels increase during administration of nitrous oxide in rats.
Plasma corticosterone, epinephrine, and norepinephrine levels increase during administration of nitrous oxide in rats.
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DOI：
10.1080/10253890.2017.1402175
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发表时间：
2018-05
期刊：
影响因子：
--
通讯作者：
Ramsay DS
中科院分区：
文献类型：
--
作者：
Al-Noori S;Cimpan A;Maltzer Z;Kaiyala KJ;Ramsay DS
一氧化二氮 (N2O) 是一种具有滥用潜力的气态药物。尽管 N2O 临床用途广泛，但人们对 N2O 给药是否会激活 HPA 轴和/或交感肾上腺髓质系统知之甚少。本研究的目的是确定 60% N2O 是否会改变雄性 Long-Evans 大鼠体内皮质酮 (CORT)、肾上腺素 (EPI) 和去甲肾上腺素 (NE) 的血浆浓度。气体管理室盖上的气密旋转组件允许在四个时间点从留置颈静脉导管远程采集血样：基线以及在 60% N2O 两小时管理期间的 30、60 和 120 分钟。相对于基线，吸入 N2O 期间的所有三个时间点血浆 CORT (n=9) 均显着升高（混合模型分析，p=0.001），并且在 30 分钟评估时血浆 EPI 和 NE 水平均显着升高（n=8，p≤0.001）。随后 EPI 下降，并且在 60 分钟和 120 分钟评估时与基线没有差异 (p>0.05)，而 NE 仍然升高 (120 分钟，p=0.001)。施用 60% N2O 会增加循环 CORT、EPI 和 NE，支持 N2O 作为生理应激源。 N2O 诱导的 CORT 增加与成瘾药物通常激活 HPA 轴导致血浆糖皮质激素水平增加的观察结果一致。药物成瘾的稳态模型通常涉及应激系统，并且讨论了应激激素在 N2O 诱导的稳态失调中的可能作用。尽管一氧化二氮在临床上很常见，也有滥用的可能性，但人们对一氧化二氮对循环应激激素的影响知之甚少。这项研究发现，吸入 60% 一氧化二氮会增加大鼠体内应激激素的循环水平。这项工作将有助于进一步研究一氧化二氮作为生理应激源的作用及其临床用途和成瘾潜力。
Nitrous oxide (N2O) is a gaseous drug with abuse potential. Despite its common clinical use, little is known about whether N2O administration activates the HPA axis and/or the sympathetic adrenomedullary system. The goal of this study was to determine whether 60% N2O alters plasma concentrations of corticosterone (CORT), epinephrine (EPI), and norepinephrine (NE) in male Long-Evans rats. A gas-tight swivel assembly in the lid of a gas administration chamber allowed the remote collection of blood samples from an indwelling jugular vein catheter at four time-points: baseline and at 30, 60, and 120 min during a two-hour administration of 60% N2O. Relative to baseline, plasma CORT (n=9) was significantly elevated at all three time-points during N2O inhalation (mixed model analysis, p=0.001), and plasma EPI and NE levels were each significantly elevated (n=8, p≤0.001) at the 30-min assessment. EPI then declined and did not differ from baseline at the 60-min and 120-min assessments (p>0.05) whereas NE remained elevated (120-min, p=0.001). Administration of 60% N2O increases circulating CORT, EPI, and NE, supporting N2O as a physiological stressor. An N2O-induced increase in CORT is consistent with the observation that addictive drugs typically activate the HPA axis causing increased plasma levels of glucocorticoids. Allostatic models of drug addiction typically involve stress systems and the possible role of stress hormones in N2O-induced allostatic dysregulation is discussed. Despite its common clinical use and abuse potential, little is known about nitrous oxide’s effect on circulating stress hormones. This study found that inhalation of 60% nitrous oxide increases circulating levels of stress hormones in rats. This work will facilitate further research on the actions of nitrous oxide as a physiological stressor with relevance to its clinical use and addictive potential.
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