Waterfall W E
Surgery. 1983 Aug;94(2):186-90.
Postprandial symptoms that occur in some patients following operation for duodenal ulcer are generally attributed to disruption of normal controlled gastric emptying resulting from vagotomy, enterostomy, or pyloroplasty. The notion that disturbances of small bowel motility could be caused by vagotomy and contribute to these symptoms led the author to examine the myoelectrical patterns of the small intestine in duodenal ulcer patients undergoing elective surgery for control of symptoms. These patients underwent either partial interruption of their vagus nerves by proximal gastric vagotomy (PGV) or complete section by truncal vagotomy (TV). Their records were compared with those of an equal number of control subjects with intact vagus nerves undergoing laparotomy for either gallstones or colonic cancer. Postoperative recordings were obtained without sedation via electrodes implanted at laparotomy and led out of the abdomen through a drain in the right upper quadrant. Observations were made on days 6 through 9 after reestablishment of normal gastrointestinal function. Three patterns of electrical activity were recorded--electrical control activity, electrical response activity, and migrating myoelectrical complexes (MMCs). No observable differences were seen among PGV, TV, and control procedure during fasting or fed conditions. A key to an understanding of the origin of the MMCs was provided by the finding of disruption of the normal cycling of the complex by a premature cycle whenever morphine was given. Release of acetylcholine in the myenteric plexus of the intestine by an intrinsic opioid agonist may be the initiating event of the intrinsic MMC. Exogenous morphine may have caused a premature MMC by mimicking the stimulus produced by endogenous opioid. The morphine response was similar in persons with or without vagus nerves, suggesting that the initiation of cycling of the complex is entirely under local control of the intestine and not exercised through the parasympathetic division of the autonomic nervous system.
一些十二指肠溃疡患者术后出现的餐后症状通常归因于迷走神经切断术、肠造口术或幽门成形术导致的正常受控胃排空紊乱。迷走神经切断术可能导致小肠运动障碍并促成这些症状的观点,促使作者研究择期手术治疗十二指肠溃疡以控制症状患者的小肠肌电模式。这些患者要么接受近端胃迷走神经切断术(PGV)部分切断迷走神经,要么接受迷走神经干切断术(TV)完全切断迷走神经。将他们的记录与同等数量迷走神经完整、因胆结石或结肠癌接受剖腹手术的对照受试者的记录进行比较。术后记录在未使用镇静剂的情况下,通过剖腹手术时植入的电极获得,并通过右上腹的引流管引出腹腔。在恢复正常胃肠功能后的第6至9天进行观察。记录了三种电活动模式——电控制活动、电反应活动和移行性肌电复合波(MMC)。在禁食或进食状态下,PGV、TV和对照手术之间未观察到明显差异。每当给予吗啡时,MMC正常循环被过早循环破坏这一发现为理解MMC的起源提供了关键线索。内源性阿片类激动剂在肠肌间神经丛释放乙酰胆碱可能是内源性MMC发生的起始事件。外源性吗啡可能通过模拟内源性阿片类产生的刺激导致MMC过早出现。有无迷走神经的人的吗啡反应相似,这表明复合波循环的起始完全受肠道局部控制,而非通过自主神经系统的副交感神经分支发挥作用。