Kuribayashi Junya, Sakuraba Shigeki, Kashiwagi Masanori, Hatori Eiki, Tsujita Miki, Hosokawa Yuki, Takeda Junzo, Kuwana Shun-Ichi
Department of Anesthesiology, Keio University School of Medicine, Japan.
Anesthesiology. 2008 Aug;109(2):233-42. doi: 10.1097/ALN.0b013e31817f5baf.
Sevoflurane-induced respiratory depression has been reported to be due to the action on medullary respiratory and phrenic motor neurons. These results were obtained from extracellular recordings of the neurons. Here, the authors made intracellular recordings of respiratory neurons and analyzed their membrane properties during sevoflurane application. Furthermore, they clarified the role of gamma-aminobutyric acid type A receptors in sevoflurane-induced respiratory depression.
In the isolated brainstem-spinal cord of newborn rat, the authors recorded the C4 nerve burst as an index of inspiratory activity. The preparation was superfused with a solution containing sevoflurane alone or sevoflurane plus the gamma-aminobutyric acid type A receptor antagonist picrotoxin or bicuculline. Neuronal activities were also recorded using patch clamp techniques.
Sevoflurane decreased C4 burst rate and amplitude. Separate perfusion of sevoflurane to the medulla and to the spinal cord decreased C4 burst rate and amplitude, respectively. Both picrotoxin and bicuculline attenuated the reduction of C4 burst rate. Sevoflurane reduced both intraburst firing frequency and membrane resistance of respiratory neurons except for inspiratory neurons.
Under the influence of sevoflurane, the region containing inspiratory neurons, i.e., the pre-Bötzinger complex, may determine the inspiratory rhythm, because reduced C4 bursts were still synchronized with the bursts of inspiratory neurons within the pre-Bötzinger complex. In contrast, the sevoflurane-induced decrease in C4 burst amplitude is mediated through the inhibition of phrenic motor neurons. gamma-Aminobutyric acid type A receptors may be involved in the sevoflurane-induced respiratory depression within the medulla, but not within the spinal cord.
据报道，七氟醚诱导的呼吸抑制是由于其对延髓呼吸神经元和膈运动神经元的作用。这些结果是通过对神经元的细胞外记录获得的。在此，作者对呼吸神经元进行了细胞内记录，并分析了七氟醚作用期间它们的膜特性。此外，他们阐明了A型γ-氨基丁酸受体在七氟醚诱导的呼吸抑制中的作用。
在新生大鼠的离体脑干-脊髓中，作者记录C4神经冲动爆发作为吸气活动的指标。制备物用单独含七氟醚或七氟醚加A型γ-氨基丁酸受体拮抗剂印防己毒素或荷包牡丹碱的溶液进行灌流。还使用膜片钳技术记录神经元活动。
七氟醚降低了C4冲动爆发的频率和幅度。分别向延髓和脊髓灌流七氟醚分别降低了C4冲动爆发的频率和幅度。印防己毒素和荷包牡丹碱均减弱了C4冲动爆发频率的降低。除吸气神经元外，七氟醚降低了呼吸神经元的爆发内放电频率和膜电阻。
在七氟醚的影响下，包含吸气神经元的区域，即前包钦格复合体，可能决定吸气节律，因为C4冲动爆发的减少仍与前包钦格复合体内吸气神经元的冲动爆发同步。相比之下，七氟醚诱导的C4冲动爆发幅度降低是通过抑制膈运动神经元介导的。A型γ-氨基丁酸受体可能参与了七氟醚在延髓内而非脊髓内诱导的呼吸抑制。
