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负鼠奥迪括约肌的壁内神经控制。

Intramural neural control of opossum sphincter of Oddi.

作者信息

Helm J F, Dodds W J, Christensen J, Sarna S K

机构信息

Digestive System Research Center, Medical College of Wisconsin, Milwaukee 53226.

出版信息

Am J Physiol. 1989 Dec;257(6 Pt 1):G925-9. doi: 10.1152/ajpgi.1989.257.6.G925.

Abstract

We evaluated the intramural neural control of the opossum sphincter of Oddi (SO) in an in vitro preparation. Force transducers were used to record contractions at four sites along the sphincter segment. To stimulate intramural nerves, 10- to 120-s trains of pulses (4-10 V amplitude, 0.5 ms duration, and 5 Hz frequency) were delivered to one of three electrode pairs implanted along the SO. Electrical stimulation in the proximal, mid, or distal SO elicited phasic contractions that invariably originated in the proximal SO and propagated antegrade along the entire length of the sphincter segment. Stimulus-evoked contractions resembled spontaneous antegrade peristaltic contractions, but occurred at a higher rate (12-20/min). Atropine completely blocked this excitatory response to nerve stimulation. After atropine, nerve stimulation in the proximal, mid, or distal SO abolished spontaneous contractions at and distal to the site of stimulation for the duration of the stimulus. The inhibitory response to nerve stimulation was completely blocked by tetrodotoxin but was unaffected by phenoxybenzamine, tolazoline, or propranolol. We conclude that 1) the opossum SO is innervated by intramural cholinergic excitatory nerves and nonadrenergic noncholinergic inhibitory nerves; 2) cholinergic excitatory nerves are organized in ascending neural pathways, whereas nonadrenergic noncholinergic inhibitory nerves descend along the length of the SO; and 3) these neural pathways may modulate SO peristalsis in vivo and participate in ascending excitatory and descending inhibitory reflexes.

摘要

我们在体外实验中评估了负鼠奥迪括约肌(SO)的壁内神经控制。使用力传感器记录括约肌段四个部位的收缩情况。为了刺激壁内神经,将10至120秒的脉冲串(幅度4至10伏,持续时间0.5毫秒,频率5赫兹)施加到沿SO植入的三对电极中的一对。在SO近端、中部或远端进行电刺激可引发相性收缩,这些收缩总是起源于SO近端,并沿括约肌段全长顺行传播。刺激诱发的收缩类似于自发性顺行蠕动收缩,但频率更高(12至20次/分钟)。阿托品完全阻断了这种对神经刺激的兴奋性反应。阿托品处理后,在刺激期间,对SO近端、中部或远端的神经刺激消除了刺激部位及其远端的自发性收缩。对神经刺激的抑制反应完全被河豚毒素阻断,但不受酚苄明、妥拉唑啉或普萘洛尔的影响。我们得出结论:1)负鼠SO由壁内胆碱能兴奋性神经和非肾上腺素能非胆碱能抑制性神经支配;2)胆碱能兴奋性神经以升行神经通路组织,而非肾上腺素能非胆碱能抑制性神经沿SO全长下行;3)这些神经通路可能在体内调节SO蠕动,并参与升行兴奋性和下行抑制性反射。

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