Department of Pathophysiology, School of Medicine, Tongji University, Si Ping Road 1239, 200092, Shanghai, China.
Langenbecks Arch Surg. 2010 Apr;395(4):407-11. doi: 10.1007/s00423-010-0594-5. Epub 2010 Mar 24.
Postoperative ileus involves reflex inhibition of intestinal motility within hours after surgery and a subsequent intestinal inflammatory response that is characterized by efferent vagal modulation via acetylcholine receptors on intestinal macrophages. We aimed to characterize the role of vagal modulation of intestinal motility during the early hours after surgery.
C57BL6 mice underwent laparotomy and standardized small bowel manipulation to induce postoperative ileus. Subgroups were vagotomized 3-4 days prior to experiments or received pharmacological inhibition of the acetylcholine alpha7 subunit with the inhibitor alpha-bungarotoxin, while control animals were sham operated and remained otherwise untreated. Three hours later, a 2-cm jejunal segment was harvested with the mesentery attached. Mesenteric afferent nerve recordings were established in an organ bath generating a multiunit signal with subsequent computerized analysis. Intraluminal pressure was continuously recorded to assess intestinal motility. Afferent nerve responses were quantified at baseline and to chemical stimulation with bradykinin (0.5 microM) or serotonin (5-HT; 500 microM) and following mechanical stimulation by continuous ramp distension to 60 mmHg.
Peak amplitudes of intestinal motility and afferent nerve discharge at baseline were not different following chronic vagotomy, alpha-bungarotoxin or sham operation. Maximum afferent discharge to 5-HT following alpha-bungarotoxin was comparable to sham controls, while the response was reduced in chronically vagotomized animals (p < 0.05). Maximum afferent nerve discharge to bradykinin and peak firing during maximum distension at 60 mmHg was similar in the different subgroups. At luminal distension from 10 to 30 mmHg, afferent discharge was lower in vagotomized animals compared to sham controls (p < 0.05) but unchanged after alpha-bungarotoxin.
Sensitivity to low-threshold distension and 5-HT is mediated via vagal afferents during postoperative ileus, while sensitivity to high-threshold distension and bradykinin is independent of vagal afferent innervation. Early inhibition of intestinal motility at 3 h after onset of postoperative ileus does not appear to depend on vagal innervation.
术后肠麻痹涉及手术后数小时内肠道运动反射抑制和随后的肠道炎症反应，其特征是通过肠道巨噬细胞上的乙酰胆碱受体对传出迷走神经进行调制。我们旨在描述术后早期肠道运动的迷走神经调节作用。
C57BL6 小鼠行剖腹术和标准化小肠操作以诱导术后肠麻痹。亚组在实验前 3-4 天行迷走神经切断术或用抑制剂α-银环蛇毒素抑制乙酰胆碱α7 亚单位，而对照动物行假手术且不进行其他处理。3 小时后，带有肠系膜的 2cm 空肠段被采集。在器官浴中建立肠系膜传入神经记录，产生多单位信号，随后进行计算机分析。连续记录肠腔内压力以评估肠道运动。在基线和用缓激肽（0.5µM）或 5-羟色胺（5-HT；500µM）化学刺激以及持续增加至 60mmHg 的 ramp 扩张进行机械刺激后，定量传入神经反应。
慢性迷走神经切断术、α-银环蛇毒素或假手术后，基线时肠道运动和传入神经放电的峰值幅度没有差异。α-银环蛇毒素后 5-HT 的最大传入放电与假对照相似，而慢性迷走神经切断术动物的反应减少（p<0.05）。不同亚组中对缓激肽的最大传入神经放电和在 60mmHg 最大扩张时的峰值放电相似。在 10-30mmHg 的管腔扩张时，迷走神经切断术动物的传入放电低于假对照（p<0.05），但在用 α-银环蛇毒素处理后没有变化。
在术后肠麻痹期间，低阈值扩张和 5-HT 的敏感性通过迷走传入神经介导，而对高阈值扩张和缓激肽的敏感性则不依赖于迷走传入神经支配。术后肠麻痹发生后 3 小时早期抑制肠道运动似乎不依赖于迷走神经支配。
