Sandler A D, Schlegel J F, Maher J W, Olinde A J, McGuigan J E
Department of Surgery, University of Iowa, Iowa City.
Surgery. 1989 Apr;105(4):529-34.
Acidification of the gastric cardia has been shown to increase lower esophageal sphincter pressure (LESP). The mechanism by which this phenomenon occurs remains unknown. This study was undertaken to examine the effect and mechanism of action of proximal gastric acidification on LESP in the dog model. In long-term studies, acidification resulted in a significant increase in mean LESP (23.2 cm H2O). Pretreatment with either topical lidocaine or subcutaneous atropine blocked the sphincteric response to acidification. Neither truncal vagotomy and pyloroplasty, proximal gastric vagotomy, antral vagotomy and pyloroplasty, nor circumferential gastric myotomy significantly altered the sphincteric response to acid. Pretreatment with 6-hydroxydopamine or somatostatin also failed to alter the increase in LESP in response to acid. In short-term studies, after gastric transection 5 cm distal to the gastroesophageal junction, acidification of a vagally innervated distal gastric pouch produced a slight decrease in LESP, whereas acidification of the proximal (orad) section of gastric mucosa still resulted in a significant increase in LESP. These studies suggest that the increase in LESP observed with acidification of the gastric cardia is a local mechanism mediated by an intrinsic neural pathway dependent on cholinergic neurotransmission. This phenomenon of local reflex excitation may be another contributing mechanism to the barrier against gastroesophageal reflux.
胃贲门酸化已被证明可增加食管下括约肌压力（LESP）。这种现象发生的机制尚不清楚。本研究旨在探讨犬模型中胃近端酸化对LESP的影响及其作用机制。在长期研究中，酸化导致平均LESP显著增加（23.2 cm H₂O）。局部利多卡因或皮下阿托品预处理可阻断括约肌对酸化的反应。全腹迷走神经切断术和幽门成形术、胃近端迷走神经切断术、胃窦迷走神经切断术和幽门成形术，以及环形胃肌切开术均未显著改变括约肌对酸的反应。6-羟基多巴胺或生长抑素预处理也未能改变酸刺激引起的LESP增加。在短期研究中，在胃食管交界处远端5 cm处切断胃后，支配迷走神经的胃远端小袋酸化导致LESP略有下降，而胃黏膜近端（口腔侧）酸化仍导致LESP显著增加。这些研究表明，胃贲门酸化时观察到的LESP增加是一种由依赖胆碱能神经传递的内在神经通路介导的局部机制。这种局部反射兴奋现象可能是抗胃食管反流屏障的另一个促成机制。
