Benzodiazepines acting on ventral surface of medulla cause airway dilation.
Benzodiazepines acting on ventral surface of medulla cause airway dilation.
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苯二氮卓类药物作用于延髓腹面引起气道扩张。
DOI：
10.1152/ajpregu.1989.257.4.r810
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Deal,EC
中科院分区：
文献类型：
--
作者：
Haxhiu,MA;vanLunteren,E;Cherniack,NS;Deal,EC
苯二氮卓类药物具有抗焦虑、抗惊厥、肌肉松弛和镇静催眠作用，可能通过作用于γ-氨基丁酸（GABA）能受体来影响呼吸。本研究调查了苯二氮卓类药物（地西泮和咪达唑仑）局部应用或显微注射到腹外侧髓质表面（VMS）下方对α-氯醛糖麻醉、瘫痪和人工通气猫气道张力的影响。通过测量放置在气管旁路喙段的气球中的压力变化来评估气管平滑肌张力。在 21 只使用 7% CO2 氧气进行通气的猫中，表面应用苯二氮卓类药物导致气管张力显着降低。与局部应用类似，在六只猫的腹侧髓质（距离表面 0.1-0.2 毫米）显微注射咪达唑仑（1 微克），使气管压力降低了 13.2 +/- 2.1 cmH2O（P 小于 0.01）。此外，在使用 12% O2 N2 通气的动物 (n = 5) 的 VMS 上应用苯二氮卓类药物可将气管压力从 15.9 +/- 2.2 降低至 5.2 +/- 2.7 cmH2O（P 小于 0.05）。此外，在所有研究的猫（n = 6）中，在髓质腹侧表面施用苯二氮卓类药物后，肺通气引起的气管收缩程度降低（从 11.4 +/- 1.6 到 2.2 +/- 0.9 cmH2O；P 小于 0.01）。 Ro 15-1788（一种特定的苯二氮卓类拮抗剂）的应用可逆转并阻断苯二氮卓类药物对气管张力的影响。然而，当阿托品消除副交感神经活动并用 5-羟色胺恢复气管张力时，VMS 上应用的苯二氮卓类药物对气管压力没有影响。这些结果表明，苯二氮卓类药物集中作用于 VMS 附近的结构，可以通过减少投射到气道的副交感神经元的活动来导致气道平滑肌张力降低。
The benzodiazepines that have anxiolytic, anticonvulsant, muscle-relaxant, and sedative-hypnotic properties affect respiration possibly by acting on gamma-aminobutyric acid (GABA)ergic receptors. This study investigated the effects of benzodiazepines diazepam and midazolam) applied topically to or microinjected just beneath the ventrolateral medullary surface (VMS) on airway tone in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated cats. Trachealis smooth muscle tension was assessed by measuring the changes in pressure in a balloon placed in a bypassed rostral segment of the trachea. In 21 cats ventilated with 7% CO2 in O2, surface application of benzodiazepines caused a significant decrease in tracheal tone. Similar to topical application, microinjection of midazolam (1 microgram) in the ventral medulla (0.1-0.2 mm from the surface) in six cats decreased tracheal pressure by 13.2 +/- 2.1 cmH2O (P less than 0.01). In addition, application of benzodiazepines on the VMS in animals ventilated with 12% O2 in N2 (n = 5) decreased tracheal pressure from 15.9 +/- 2.2 to 5.2 +/- 2.7 cmH2O (P less than 0.05). Furthermore, in all cats studied (n = 6), the magnitude of lung deflation-induced tracheal contraction was reduced after application of benzodiazepines on the ventral surface of the medulla (from 11.4 +/- 1.6 to 2.2 +/- 0.9 cmH2O; P less than 0.01). The effects of benzodiazepines on tracheal tone were reversed and blocked by application of Ro 15-1788, a specific benzodiazepines antagonist. However, when parasympathetic activity was abolished by atropine and tracheal tone was restored with 5-hydroxytryptamine, benzodiazepines applied on the VMS had no effect on tracheal pressure. These results suggest that benzodiazepines acting centrally, on structures located near the VMS, can cause a decrease in airway smooth muscle tone by diminishing the activity of parasympathetic neurons which project to the airways.