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首页> 外文期刊>Life sciences >Desflurane but not sevoflurane augments laryngeal C-fiber inputs to nucleus tractus solitarii neurons by activating transient receptor potential-A1
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Desflurane but not sevoflurane augments laryngeal C-fiber inputs to nucleus tractus solitarii neurons by activating transient receptor potential-A1

机译：地氟醚而不是七氟醚通过激活瞬时受体电位-A1增强咽喉孤核神经元的喉C纤维输入。

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Aims: Volatile anesthetics have distinct odors and some are irritating to the upper airway and may cause cough and laryngospasm, which may result, in part, from stimulation of C-fiber reflex. Local exposure of such anesthetics increases the sensitivity of capsaicin-sensitive laryngeal C-fiber endings compatible with airway irritability presumably by activation of transient receptor potential (TRP) ion channels, but the physiological relevance of this sensitization transmitted to the higher-order neurons in the central reflex pathway and output is unknown. Main methods In anesthetized young guinea pigs, baseline and left atrial capsaicin evoked changes in the extracellular unit activity of laryngeal C-fiber-activated neurons in the nucleus tractus solitarii (NTS) and phrenic nerve activity were compared between irritant (desflurane) and non-irritant (sevoflurane) anesthetic gas exposure to the isolated larynx. Key findings Desflurane significantly augmented the peak and duration (p < 0.01) of the NTS neuronal responses and the prolongation of expiratory time (p = 0.017). The effect was enhanced by iontophoretic application of the TRPA1 agonist allyl-isothiocyanate (p < 0.05), inhibited by TRPA1 antagonist HC-030031 (p < 0.01), but not by TRPV1 antagonist BCTC. Sevoflurane did not affect the central pathway. Significance Thus, the sensitization of the laryngeal C-fiber endings by irritant volatile anesthetics is transmitted to the NTS via activation of the TRPA1 and is associated with a prolonged reflexively evoked expiratory apnea. The findings may help to explain local deleterious effects of irritant volatile general anesthetics on the airways during inhaled induction or bronchodilator therapy for status asthmatics.
机译：目的：挥发性麻醉剂具有独特的气味，有些会刺激上呼吸道，并可能引起咳嗽和喉痉挛，这可能部分是由于刺激C纤维反射引起的。此类麻醉剂的局部暴露可能通过激活瞬时受体电势（TRP）离子通道来增加与气道易怒性相容的辣椒素敏感性喉C纤维末端的敏感性，但这种敏感性的生理相关性传递给了大鼠的高阶神经元。中枢反射途径和输出未知。主要方法在麻醉的豚鼠中，比较基线刺激性和左心房辣椒素引起的孤束核（NTS）中喉C纤维激活神经元的胞外单位活性变化，并比较刺激性（去氟醚）和非刺激性phr神经活动。刺激性（七氟醚）麻醉气体暴露于孤立的喉部。主要发现地氟醚显着增加了NTS神经元反应的峰值和持续时间（p <0.01）和呼气时间的延长（p = 0.017）。离子电渗疗法应用TRPA1激动剂烯丙基异硫氰酸酯（p <0.05）增强了这种效果，TRPA1拮抗剂HC-030031（p <0.01）抑制了TRPA1拮抗剂，但BCTC却没有抑制这种作用。七氟醚不影响中枢途径。重要性因此，刺激性挥发性麻醉药对喉C纤维末端的敏化作用是通过激活TRPA1传递到NTS的，并与反射性呼气性呼吸暂停延长有关。该发现可能有助于解释在状态哮喘患者的吸入诱导或支气管扩张剂治疗期间，挥发性挥发性全身麻醉剂对呼吸道的局部有害作用。

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