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外在神经和内在神经在空肠移行性运动复合波激素诱导中的作用。

Role of extrinsic and intrinsic nerves in hormonal induction of the migrating motor complex in the jejunum.

作者信息

Hakim N S, Soper N J, Spencer M P, Sarr M G

机构信息

Department of Surgery, Mayo Medical School, Rochester, MN 55905.

出版信息

J Invest Surg. 1989;2(4):437-46. doi: 10.3109/08941938909018269.

Abstract

The mechanism of induction of the migrating motor complex (MMC) by neural or humoral agents and their role in the control of fasting motility are not well understood. Our aim was to determine the role of extrinsic and intrinsic nerves in mediating the induction of the MMC by motilin. Three groups of dogs were studied. Group I consisted of neurally intact control dogs. In group II, intrinsic neural continuity between the duodenum and the jejunum was interrupted by transection and reanastomosis of the distal duodenum. Dogs in group III underwent disruption of all intrinsic and extrinsic neural input to the entire jejunoileum. Serosal electrodes were sewn to duodenum and jejunum in all dogs. After a 2-week recovery, fasting myoelectric activity was recorded on four or more occasions. Motilin (0.1 microgram/kg iv) was given 30 min after a spontaneous duodenal phase III. In group I (controls), motilin induced a premature MMC, which originated in the duodenum and migrated along the small intestine. In group II (intrinsic neural disruption), motilin induced a premature MMC, which began simultaneously in the proximal duodenum and proximal jejunum. In group III (intrinsic and extrinsic neural disruption), motilin induced a premature MMC in the duodenum but not in the jejunum; rather, a short, nonmigrating burst of spike potentials occurred simultaneously in all jejunal electrodes. These observations suggest that extrinsic innervation is necessary for motilin to induce phase III activity in the jejunum. Extrinsic neural pathways appear to mediate motilin-induced MMC activity in the jejunum.

摘要

神经或体液因子诱导移行性运动复合波(MMC)的机制及其在空腹运动控制中的作用尚未完全明确。我们的目的是确定外在神经和内在神经在介导胃动素诱导MMC中的作用。研究了三组犬。第一组为神经完整的对照犬。第二组,十二指肠和空肠之间的内在神经连续性通过横断远端十二指肠并重新吻合而中断。第三组犬的整个空肠回肠的所有内在和外在神经输入均被破坏。所有犬的十二指肠和空肠均缝上浆膜电极。经过2周的恢复后,在四个或更多时间点记录空腹肌电活动。在十二指肠自发出现Ⅲ期30分钟后静脉注射胃动素(0.1微克/千克)。在第一组(对照组)中,胃动素诱导了一个提前出现的MMC,其起源于十二指肠并沿小肠移行。在第二组(内在神经破坏)中,胃动素诱导了一个提前出现的MMC,其在十二指肠近端和空肠近端同时开始。在第三组(内在和外在神经破坏)中,胃动素在十二指肠诱导了一个提前出现的MMC,但在空肠未诱导;相反,所有空肠电极同时出现一阵短暂的、不移行的棘波电位。这些观察结果表明,外在神经支配对于胃动素诱导空肠Ⅲ期活动是必要的。外在神经通路似乎介导了胃动素诱导的空肠MMC活动。

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