猫气道平滑肌松弛的神经控制。

R J Altiere, J L Szarek, L Diamond
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引用次数: 25

摘要

采用电场刺激(EFS)技术对猫气管和支气管分离段气道平滑肌的功能神经支配进行了研究。电场刺激引起静息张力下组织的收缩和5-羟色胺(5-HT)预收缩组织的双相反应(收缩后松弛)。10(-6) M阿托品可消除宫缩。抑制反应依赖于脉冲电压、持续时间和频率。在低电压(小于或等于10 V)和脉冲持续时间(小于或等于0.3 ms)下,3 × 10(-6) M河豚毒素(TTX)消除了EFS诱导的弛缓。更大的刺激参数引起ttx抗性松弛。用10(-6)M心得安和10(-5)M胍乙啶预处理后,松弛频率响应曲线向右偏移。这些发现表明猫气道受兴奋性胆碱能神经、抑制性肾上腺素能神经和抑制性非肾上腺素能非胆碱能神经(NANC)支配。用六甲铵、西咪替丁、吲哚美辛或去甲二氢愈创木酸预处理组织不影响NANC松弛反应。由此得出结论,猫气道平滑肌的NANC抑制反应是通过内在神经节后神经纤维介导的,并且独立于组胺h2受体的激活而发生,不涉及花生四烯酸代谢的环加氧酶或脂加氧酶产物。
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Neural control of relaxation in cat airways smooth muscle.

Functional innervation of cat airways smooth muscle was examined in isolated segments of trachea and bronchi using electrical field stimulation (EFS) techniques. Field stimulation caused contraction in tissues at resting tone and biphasic responses (contraction followed by relaxation) in tissues precontracted with 5-hydroxytryptamine (5-HT). Contractions were abolished by 10(-6) M atropine. Inhibitory responses were dependent on impulse voltage, duration, and frequency. At low voltages (less than or equal to 10 V) and pulse durations (less than or equal to 0.3 ms), EFS induced relaxations were abolished by 3 X 10(-6) M tetrodotoxin (TTX). Greater stimulus parameters elicited TTX-resistant relaxations. Pretreatment of the tissues with 10(-6) M propranolol and 10(-5) M guanethidine caused rightward shifts in relaxation frequency-response curves. These findings indicate that cat airways are innervated by excitatory cholinergic, inhibitory adrenergic, and inhibitory nonadrenergic noncholinergic (NANC) nerves. Pretreatment of the tissues with hexamethonium, cimetidine, indomethacin, or nordihydroguaiaretic acid did not affect NANC relaxation responses. It is concluded that NANC inhibitory responses in cat airway smooth muscle are mediated through intrinsic postganglionic nerve fibers and occur independently of histamine H2-receptor activation and without involvement of cyclooxygenase or lipoxygenase products of arachidonic acid metabolism.

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