Department of Systems Neuroscience, University Medical Centre Hamburg-Eppendorf, Martinistr, 52, Hamburg, D-20246, Germany.
J Headache Pain. 2013 Apr 10;14(1):33. doi: 10.1186/1129-2377-14-33.
Nasal insufflation of CO2 has been shown to exert antinociceptive respectively antihyperalgesic effects in animal pain models using topical capsaicin with activation of TRPV1-receptor positive nociceptive neurons. Clinical benefit from CO2 inhalation in patients with craniofacial pain caused by a putative activation of TRPV1 receptor positive trigeminal neurons has also been reported. These effects are probably mediated via an activation of TRPV1 receptor - positive neurons in the nasal mucosa with subsequent central inhibitory effects (such as conditioned pain modulation). In this study, we aimed to examine the effects of intranasal CO2 on a human model of craniofacial pain elicited by nasal application of capsaicin.
In a first experiment, 48 healthy volunteers without previous craniofacial pain received intranasal capsaicin to provoke trigeminal pain elicited by activation of TRVP1 positive nociceptive neurons. Then, CO2 or air was insufflated alternatingly into the nasal cavity at a flow rate of 1 l/min for 60 sec each. In the subsequent experiment, all participants were randomized into 2 groups of 24 each and received either continuous nasal insufflation of CO2 or placebo for 18:40 min after nociceptive stimulation with intranasal capsaicin. In both experiments, pain was rated on a numerical rating scale every 60 sec.
Contrary to previous animal studies, the effects of CO2 on experimental trigeminal pain were only marginal. In the first experiment, CO2 reduced pain ratings only minimally by 5.3% compared to air if given alternatingly with significant results for the main factor GROUP (F1,47=4.438; p=0.041) and the interaction term TIME*GROUP (F2.6,121.2=3.3; p=0.029) in the repeated-measures ANOVA. However, these effects were abrogated after continuous insufflation of CO2 or placebo with no significant changes for the main factors or the interaction term.
Although mild modulatory effects of low-flow intranasal CO2 could be seen in this human model of TRPV-1 mediated activation of nociceptive trigeminal neurons, utility is limited as observed changes in pain ratings are clinically non-significant.
在使用辣椒素激活 TRPV1 受体阳性伤害性神经元的动物疼痛模型中，已经证明鼻内吸入 CO2 具有抗伤害性和抗痛觉过敏作用。在由推测的 TRPV1 受体阳性三叉神经神经元激活引起的颅面疼痛患者中，CO2 吸入也有临床获益。这些作用可能是通过鼻黏膜中 TRPV1 受体阳性神经元的激活介导的，随后产生中枢抑制作用（如条件性疼痛调制）。在这项研究中，我们旨在检查鼻内 CO2 对鼻内应用辣椒素引起的颅面疼痛的人体模型的影响。
在第一个实验中，48 名无先前颅面疼痛的健康志愿者接受鼻内辣椒素以诱发 TRPV1 阳性伤害性神经元激活引起的三叉神经痛。然后，以 1 l/min 的流速交替将 CO2 或空气鼻内吹入鼻腔 60 秒。在随后的实验中，所有参与者随机分为两组，每组 24 人，在鼻内给予辣椒素引起伤害性刺激后，分别连续 18:40 分钟接受 CO2 或安慰剂的鼻内吹入。在这两个实验中，疼痛评分每隔 60 秒用数字评分量表进行评估。
与以前的动物研究相反，CO2 对实验性三叉神经痛的影响仅略有差异。在第一个实验中，与空气交替给予 CO2 仅使疼痛评分轻微降低 5.3%，但主要因素组（F1,47=4.438;p=0.041）和重复测量方差分析中的时间*组交互项（F2.6,121.2=3.3;p=0.029）的结果具有显著意义。然而，在连续给予 CO2 或安慰剂后，这些作用被消除，主要因素或交互项没有明显变化。
尽管在 TRPV-1 介导的伤害性三叉神经神经元激活的人体模型中可以看到低流量鼻内 CO2 的轻度调节作用，但由于观察到的疼痛评分变化在临床上无意义，因此其用途有限。
Zotero 插件
