Tabatabai M, Kitahata L M, Kawahara M, Collins J G
Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut 06510.
Proc Soc Exp Biol Med. 1990 Oct;195(1):79-83. doi: 10.3181/00379727-195-43122.
The effect of enflurane on the firing activity (spikes/sec) of the inspiratory neurons of the dorsal respiratory group (DRG) of the medulla oblongata was studied in decerebrate, paralyzed, mechanically ventilated cats before and after bilateral cervical vagotomy. Inspiratory neuronal activity, phrenic neurogram, arterial blood pressure, tracheal pressure, and end tidal CO2 concentration were recorded. Cells whose firing activity was in phase with that of the phrenic nerve were considered inspiratory neurons. Administration of 1 and 2% enflurane in oxygen produced gradual, significant, and dose-dependent depression of the cell activity with cervical vagi either intact or severed. Recovery of the cell activity occurred after termination of enflurane administration. In cats with intact vagi, 10 min after introduction of 1 and 2% enflurane, the cell activity (mean +/- SE) expressed as percentage of the control was 70 +/- 6% (P less than 0.05) and 48 +/- 5% (P less than 0.01), respectively. Bilateral cervical vagotomy did not affect the degree of cell depression due to enflurane. Hypercarbia induced by inhalation of 5% CO2 increased cell activity, but it did not block enflurane-induced cell depression, although it reduced it. It may be concluded that enflurane depresses the activity of the inspiratory neurons of the DRG. The results also suggest that the respiratory depressant effect of enflurane has a central component and that the DRG region may serve as a site to mediate the enflurane-induced respiratory depression.
在双侧颈迷走神经切断前后,对去大脑、麻痹、机械通气的猫,研究了恩氟烷对延髓背侧呼吸组(DRG)吸气神经元放电活动(每秒放电次数)的影响。记录了吸气神经元活动、膈神经电图、动脉血压、气管压力和呼气末二氧化碳浓度。其放电活动与膈神经同步的细胞被视为吸气神经元。无论颈迷走神经完整与否,吸入1%和2%的恩氟烷均能使细胞活动逐渐、显著且呈剂量依赖性地受到抑制。停止给予恩氟烷后,细胞活动恢复。在迷走神经完整的猫中,引入1%和2%恩氟烷10分钟后,以对照值的百分比表示的细胞活动(平均值±标准误)分别为70±6%(P<0.05)和48±5%(P<0.01)。双侧颈迷走神经切断并不影响恩氟烷所致的细胞抑制程度。吸入5%二氧化碳引起的高碳酸血症增加了细胞活动,但虽能减轻恩氟烷所致的细胞抑制,却不能阻断其作用。可以得出结论,恩氟烷可抑制DRG吸气神经元的活动。结果还提示,恩氟烷的呼吸抑制作用有中枢成分,且DRG区域可能是介导恩氟烷所致呼吸抑制的部位。