Martin C J, Patrikios J, Dent J
Gastroenterology. 1986 Oct;91(4):890-6. doi: 10.1016/0016-5085(86)90691-8.
In the present study we have examined the hypothesis that transient lower esophageal sphincter relaxations are under vagal control. Fasting esophageal motor function was monitored with a manometric sleeve catheter passed via a cervical esophagostomy. Gastric insufflation with oxygen resulted in intermittent venting of gas into the esophagus during transient lower esophageal sphincter relaxations. Such venting of gas was associated with the occurrence of esophageal body common cavities and gas venting from the esophageal stoma, all of which increased with increasing rates of gastric insufflation. The optimal insufflation rate, 80 ml/min, produced stomal gas venting at a rate of 10.3 +/- 1.1/h (mean +/- SE). The time and pressure profiles of transient lower esophageal sphincter relaxations induced by gastric insufflation were similar to those relaxations seen with spontaneous postprandial gastroesophageal reflux and belching in dogs. Sphincteric relaxation started 10 s before the onset of common cavities. In all 4 dogs, cooling of cervical subcutaneous vagosympathetic loops abolished transient lower esophageal sphincter relaxations, common cavities, and stomal gas venting. Within 1-4 min of cessation of vagal cooling, all three markers of gastroesophageal gas venting returned. Atropine, 50 and 200 micrograms/kg i.v., did not block transient lower esophageal sphincter relaxations or gas reflux. Gastric gaseous distention is a potent and consistent trigger of transient lower esophageal sphincter relaxations in the dog. This effect can be used as a model for study of control mechanisms of transient sphincter relaxation-dependent gastroesophageal reflux. Our observations with this model indicate that transient lower esophageal sphincter relaxations are under vagosympathetic control, but that muscarinic mechanisms are not important mediators of this control.
在本研究中，我们检验了如下假设：食管下括约肌的短暂松弛受迷走神经控制。通过经颈部食管造口插入的测压套囊导管监测空腹时的食管运动功能。向胃内注入氧气导致在食管下括约肌短暂松弛期间气体间歇性排入食管。这种气体排放与食管体部共同腔隙的出现以及气体从食管造口排出有关，所有这些都随着胃内注气速率的增加而增加。最佳注气速率为80 ml/min，此时造口气体排放速率为10.3±1.1次/小时（平均值±标准误）。胃内注气诱发的食管下括约肌短暂松弛的时间和压力曲线与犬自发性餐后胃食管反流和嗳气时所见的松弛曲线相似。括约肌松弛在共同腔隙出现前10秒开始。在所有4只犬中，冷却颈部皮下迷走交感神经袢可消除食管下括约肌短暂松弛、共同腔隙和造口气体排放。在迷走神经冷却停止后1 - 4分钟内，胃食管气体排放的所有三个指标均恢复。静脉注射50和200微克/千克的阿托品并未阻断食管下括约肌短暂松弛或气体反流。胃内气体扩张是犬食管下括约肌短暂松弛的一种有效且持续的触发因素。这种效应可作为研究依赖于括约肌短暂松弛的胃食管反流控制机制的模型。我们用这个模型进行的观察表明，食管下括约肌短暂松弛受迷走交感神经控制，但毒蕈碱机制不是这种控制的重要介导因素。
