Hall K E, Greenberg G R, El-Sharkawy T Y, Diamant N E
Gastroenterology. 1984 Jul;87(1):76-85.
Both the vagus nerve and motilin have been implicated in the initiation of phase III of the fasting migrating motor complex. To investigate the contribution of each, the effects of intravenous porcine motilin, vagosympathetic nerve blockade, and atropine were assessed. Intralumenal pressures of the lower esophageal sphincter, stomach, and upper small intestine, and plasma motilin levels were monitored. Porcine and canine motilin in plasma were distinguished by radioimmunoassay using two different antibodies. Injection of porcine motilin (75-370 pmol), initiated dose-dependent phase III-like motor activity in the lower esophageal sphincter, stomach, and small bowel if the vagi were intact; if the vagi were blocked, activity was initiated in the small bowel only. Moreover , a significant (p less than 0.001), dose-dependent peak in canine plasma motilin was observed after the onset of the induced motor activity when the vagi were intact or blocked, with plasma motilin peaks comparable to those occurring spontaneously. In both intact and vagally blocked dogs, atropine abolished both the spontaneous motor activity and associated rise in motilin level, and also abolished porcine motilin-induced activity. However, a diminished, but significant (p less than 0.01) peak in porcine motilin-induced canine motilin persisted in the presence of atropine. These results in dogs indicate that while spontaneous phase II motility in the upper gastrointestinal tract and phase III activity in the lower esophageal sphincter and stomach are dependent on vagally mediated excitatory pathways, spontaneous and induced phase III motor activity in the small intestine are dependent on nonvagal cholinergic innervation. Canine motilin release induced by porcine motilin is mediated primarily by a nonvagal cholinergic (muscarinic) pathway, with minor contributions from vagal noncholinergic, and nonvagal noncholinergic mechanisms. Because spontaneous or induced motilin release peaks well after the onset of phase III motor activity, it is unlikely that motilin is the primary factor responsible for initiation of the migrating motor complex in the dog. Motilin may, however, modulate motility produced by preexisting neural excitation.
迷走神经和胃动素均与空腹移行性运动复合波的Ⅲ期启动有关。为研究各自的作用，评估了静脉注射猪胃动素、迷走交感神经阻滞及阿托品的效果。监测了食管下括约肌、胃和小肠上段的腔内压力以及血浆胃动素水平。使用两种不同抗体通过放射免疫分析法区分血浆中的猪胃动素和犬胃动素。若迷走神经完整，注射猪胃动素（75 - 370 pmol）可在下食管括约肌、胃和小肠引发剂量依赖性的Ⅲ期样运动活动；若迷走神经被阻滞，则仅在小肠引发活动。此外，在迷走神经完整或被阻滞时，诱导的运动活动开始后，犬血浆胃动素出现显著的（p < 0.001）剂量依赖性峰值，血浆胃动素峰值与自发出现的峰值相当。在迷走神经完整和被阻滞的犬中，阿托品均消除了自发运动活动及相关的胃动素水平升高，也消除了猪胃动素诱导的活动。然而，在阿托品存在的情况下，猪胃动素诱导的犬胃动素仍出现降低但显著的（p < 0.01）峰值。犬的这些结果表明，虽然上消化道的自发Ⅱ期运动以及食管下括约肌和胃的Ⅲ期活动依赖于迷走神经介导的兴奋性通路，但小肠的自发和诱导Ⅲ期运动活动依赖于非迷走胆碱能神经支配。猪胃动素诱导的犬胃动素释放主要由非迷走胆碱能（毒蕈碱）途径介导，迷走非胆碱能和非迷走非胆碱能机制也有较小作用。由于自发或诱导的胃动素释放在Ⅲ期运动活动开始后很久才达到峰值，胃动素不太可能是犬移行性运动复合波启动的主要因素。然而，胃动素可能调节由先前神经兴奋产生的运动。
