Zhang H Q, Lai Y L
Division of Pharmacology and Experimental Therapeutics, University of Kentucky College of Pharmacy, Lexington 40536.
Respir Physiol. 1993 Dec;94(3):285-95. doi: 10.1016/0034-5687(93)90024-5.
To study the role of vagal afferent C-fibers in resiniferatoxin (RTX)-induced bronchoconstriction in vivo, 30 guinea pigs weighing 347 +/- 28 g were evenly and randomly divided into five groups: Group 1, control; 2, chronic vagotomy; 3, local capsaicin (acute); 4, local capsaicin (chronic); and 5, systemic capsaicin. Each animal was anesthetized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All animals were pretreated with atropine and phenoxybenzamine. Immediately after RTX was intravenously injected, each animal in the control group exhibited profound decreases in maximal expiratory flow, dynamic respiratory compliance, and total lung capacity, as well as an increase in functional residual capacity, indicating severe airway constriction. Animals in Groups 2-4 exhibited partial abolishment, while those in Group 5 showed complete abolishment of the RTX-induced bronchoconstriction. In 12 additional animals (6 animals each in control and chronic vagotomy groups), chronic vagotomy caused also suppressive effects on capsaicin-induced airway constriction. At one min, our data demonstrate that 36-51% of noncholinergic bronchoconstriction is due to the vagal component while the remaining constriction is due to the nonvagal component. Thus, the nonvagal component plays a significant role in this type of tachykinin-mediated airway constriction.
为研究迷走传入C纤维在体内树脂毒素（RTX）诱导的支气管收缩中的作用，将30只体重为347±28 g的豚鼠均匀随机分为五组：第1组为对照组；第2组为慢性迷走神经切断组；第3组为局部应用辣椒素（急性）组；第4组为局部应用辣椒素（慢性）组；第5组为全身应用辣椒素组。每只动物用戊巴比妥钠麻醉，插入气管插管和静脉导管，用三碘季铵酚使其麻痹，并进行人工通气。所有动物均用阿托品和酚苄明预处理。静脉注射RTX后，对照组的每只动物均出现最大呼气流量、动态呼吸顺应性和肺总量显著降低，功能残气量增加，表明气道严重收缩。第2 - 4组动物的RTX诱导的支气管收缩部分被消除，而第5组动物则完全消除。在另外12只动物（对照组和慢性迷走神经切断组各6只）中，慢性迷走神经切断对辣椒素诱导的气道收缩也有抑制作用。在1分钟时，我们的数据表明，36 - 51%的非胆碱能支气管收缩是由迷走神经成分引起的，而其余的收缩是由非迷走神经成分引起的。因此，非迷走神经成分在这种速激肽介导的气道收缩中起重要作用。
