Sarna S, Condon R E, Cowles V
Gastroenterology. 1983 Apr;84(4):814-22.
The enteric mechanisms governing initiation of migrating myoelectric complexes were studied in 6 conscious dogs, each implanted with a set of 12 bipolar electrodes on the small intestine. The small intestine was transected and reanastomosed at three sites to give four isolated segments of equal length. Each segment had three implanted electrodes. All four isolated segments generated migrating myoelectric complexes which were, initially, totally independent of each other in time. The most proximal segment had the longest mean migrating myoelectric complex time period (106.2 +/- 10.1 SEM min) and the second segment had the shortest mean migrating myoelectric complex time period (66.8 +/- 6.7 SEM min). Distal to the second segment, the mean migrating myoelectric complex time period increased progressively (83.1 +/- 11.2 SEM min and 95.8 +/- 7.6 SEM min, respectively). Isolation of the small intestine into segments did not significantly change migrating myoelectric complex propagation characteristics such as velocity and direction of propagation within each segment. The mean duration of phase 3 activity was not affected in the first segment but increased significantly in the distal three segments (p less than 0.05). The propagation of migrating myoelectric complexes across the sites of transection and reanastomosis started recovering 45-60 days after surgery and recovered fully by 98-108 days. The study findings show that enteric mechanisms control the initiation of migrating myoelectric complexes. Each small segment of the small intestine is capable of initiating migrating myoelectric complexes of its own and behaves as a relaxation oscillator. In the intact small intestine, regional migrating myoelectric complex oscillators are coupled by the intrinsic neurons so that the proximal oscillators drive the distal oscillators. Recovery of migrating myoelectric complex propagation across sites of transection and reanastomosis suggest that intrinsic nerves regenerate after transection.
在6只清醒犬中研究了控制移行性肌电复合波起始的肠道机制,每只犬在小肠上植入一组12个双极电极。小肠在三个部位横断并重新吻合,形成四个等长的孤立节段。每个节段有三个植入电极。所有四个孤立节段均产生移行性肌电复合波,最初,它们在时间上完全相互独立。最近端节段的移行性肌电复合波平均周期最长(106.2±10.1标准误分钟),第二个节段的移行性肌电复合波平均周期最短(66.8±6.7标准误分钟)。在第二个节段的远端,移行性肌电复合波平均周期逐渐增加(分别为83.1±11.2标准误分钟和95.8±7.6标准误分钟)。将小肠分离成节段并未显著改变移行性肌电复合波的传播特性,如每个节段内的传播速度和方向。第一段的3期活动平均持续时间未受影响,但在远端三个节段显著增加(p<0.05)。移行性肌电复合波在横断和重新吻合部位的传播在术后45 - 60天开始恢复,并在98 - 108天完全恢复。研究结果表明,肠道机制控制移行性肌电复合波的起始。小肠的每个小节段都能够启动自身的移行性肌电复合波,并表现为一个松弛振荡器。在完整的小肠中,局部移行性肌电复合波振荡器通过内在神经元耦合,使得近端振荡器驱动远端振荡器。移行性肌电复合波在横断和重新吻合部位传播的恢复表明,横断后内在神经会再生。