Helm J F, Bro S L, Dodds W J, Sarna S K, Hoffmann R G
Department of Medicine, Medical College of Wisconsin, Milwaukee 53226.
Am J Physiol. 1992 Dec;263(6 Pt 1):G953-9. doi: 10.1152/ajpgi.1992.263.6.G953.
We studied the propagation of phasic contractions initiated by tetraethylammonium (TEA, 1-10 mM), high K+ concentration (10-30 mM), and bethanechol (10(-6) to 10(-2) M) in a whole organ in vitro preparation of the opossum smooth muscle esophagus. TEA initiated phasic contractions that began at all sites along the smooth muscle esophagus and propagated in both directions with a velocity similar to that of primary peristalsis. Blockade of neural transmission by tetrodotoxin (TTX, 10(-7) M) did not prevent contraction propagation. Although a majority of contractions initiated by TEA did not propagate the full length of the esophageal specimen, with the addition of TTX most contractions initiated by TEA did propagate the full specimen length in either direction. High K+ concentration and bethanechol elicited propagated contractions similar to those initiated by TEA. We conclude that 1) a myogenic mechanism exists for propagation of contractions along the smooth muscle esophagus and 2) intramural inhibitory nerves modulate the extent of myogenic propagation in the ascending as well as descending direction. We suggest that esophageal peristalsis may occur by myogenic propagation of contractions that are normally initiated in the proximal smooth muscle esophagus by excitatory nerves. Intramural inhibitory nerves may inhibit retrograde propagation as well as mediate descending inhibition in advance of the peristaltic wave.
我们研究了在负鼠平滑肌食管的全器官体外制备中，由四乙铵（TEA，1 - 10 mM）、高钾浓度（10 - 30 mM）和氨甲酰甲胆碱（10⁻⁶至10⁻² M）引发的阶段性收缩的传播情况。TEA引发的阶段性收缩在平滑肌食管的所有部位开始，并以与原发性蠕动相似的速度双向传播。河豚毒素（TTX，10⁻⁷ M）阻断神经传递并不能阻止收缩的传播。虽然由TEA引发的大多数收缩并没有传播到食管标本的全长，但加入TTX后，由TEA引发的大多数收缩确实在任一方向上传播到了标本的全长。高钾浓度和氨甲酰甲胆碱引发的传播性收缩与TEA引发的相似。我们得出结论：1）沿着平滑肌食管存在一种收缩传播的肌源性机制；2）壁内抑制性神经在收缩向上和向下传播的方向上调节肌源性传播的程度。我们认为食管蠕动可能是由通常由兴奋性神经在近端平滑肌食管引发的收缩的肌源性传播引起的。壁内抑制性神经可能抑制逆行传播，并在蠕动波之前介导下行抑制。
