Otsuka H
Department of Anesthesiology, Hokkaido University School of Medicine, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1998 Mar;73(2):117-36.
To elucidate the various actions of volatile anesthetics on respiratory activity and chemosensitivity, we have studied the activities of the respiration-related structures in the medulla of the in vitro brainstem-spinal cord preparation of the newborn rat. Halothane decreased respiratory burst frequency (fR), inspiratory duration (Ti), integrated ventral C4 root activity (integral of C4) and respiratory minute activity (RMA) in a concentration-dependent fashion. Bicuculline counteracted the depressive effect of halothane on fR, integral of C4, and RMA. Inspiratory neuronal activity recorded at the rostral ventrolateral medulla (RVL) corresponded to these changes. Activities of Pre-Inspiratory (Pre-I) neurons and expiratory neurons in the RVL were also inhibited by halothane. The C4 activity did not always correspond to Pre-I neurons' discharge. In this comparative study of three volatile anesthetics, the inhibitory effect on fR appeared to be greater with enflurane than with halothane or isoflurane. The reversal effects of bicuculline on decreases in fR, integral of C4, and RMA also seemed to be greater with enflurane than with halothane or isoflurane. Hypercapnia (pH 7.0) induced a significant increase in fR and RMA, and a significant decrease in Ti. Although halothane inhibited overall activities, chemo-responsiveness to hypercapnia changed similarly even during halothane application. Hypocapnia (pH 7.8) significantly decreased fR, and increased integral of C4 and Ti. Hypocapnia during halothane application also induced a significant decrease in fR and RMA. These results suggest that the modification of GABAA receptor-mediated neurotransmission is in part responsible for the respiratory depression by volatile anesthetics, affecting especially fR, integral of C4, and RMA. Low respiratory rate by enflurane is associated with GABAergic modification. Prolongation of Ti by enflurane, seen clinically, does not seem to be either central or GABAergic. These findings demonstrate the responsiveness to CO2 and the respiratory compensation mechanism via respiratory frequency in the isolated preparation. It is, furthermore, indicated that halothane preserves the central chemosensitivity while its concentration is high enough to reduce the respiratory activities.
为阐明挥发性麻醉剂对呼吸活动和化学敏感性的各种作用，我们研究了新生大鼠体外脑干 - 脊髓制备物延髓中与呼吸相关结构的活动。氟烷以浓度依赖性方式降低呼吸爆发频率（fR）、吸气持续时间（Ti）、腹侧C4神经根综合活动（C4积分）和呼吸分钟活动（RMA）。荷包牡丹碱可抵消氟烷对fR、C4积分和RMA的抑制作用。在延髓头端腹外侧（RVL）记录的吸气神经元活动与这些变化相对应。RVL中吸气前（Pre - I）神经元和呼气神经元的活动也受到氟烷的抑制。C4活动并不总是与Pre - I神经元的放电相对应。在对三种挥发性麻醉剂的这项比较研究中，恩氟烷对fR的抑制作用似乎比氟烷或异氟烷更大。荷包牡丹碱对fR、C4积分和RMA降低的逆转作用似乎恩氟烷也比氟烷或异氟烷更大。高碳酸血症（pH 7.0）导致fR和RMA显著增加，Ti显著降低。尽管氟烷抑制总体活动，但即使在使用氟烷期间，对高碳酸血症的化学敏感性变化也相似。低碳酸血症（pH 7.8）显著降低fR，并增加C4积分和Ti。氟烷应用期间的低碳酸血症也导致fR和RMA显著降低。这些结果表明，GABAA受体介导的神经传递的改变部分导致了挥发性麻醉剂引起的呼吸抑制，尤其影响fR、C4积分和RMA。恩氟烷导致的低呼吸频率与GABA能改变有关。临床上观察到的恩氟烷引起的Ti延长似乎既不是中枢性的也不是GABA能的。这些发现证明了在离体制备物中对CO2的反应性以及通过呼吸频率的呼吸补偿机制。此外，表明当氟烷浓度高到足以降低呼吸活动时，它仍保留中枢化学敏感性。
