Pabst M A, Schöninkle E, Holzer P
Department of Histology and Embryology, University of Graz, Austria.
Gut. 1993 Jul;34(7):897-903. doi: 10.1136/gut.34.7.897.
Capsaicin sensitive afferent neurones have previously been reported to play a part in gastric mucosal protection. The aim of this study was to investigate whether these nociceptive neurones strengthen mucosal defence against injury or promote rapid repair of the damaged mucosa, or both. This hypothesis was examined in anaesthetised rats whose stomachs were perfused with ethanol (25 or 50% in saline, wt/wt) for 30 minutes. The gastric mucosa was inspected 0 and 180 minutes after ethanol had been given at the macroscopic, light, and scanning electron microscopic level. Rapid repair of the ethanol injured gastric mucosa (reduction of deep injury, partial re-epithelialisation of the denuded surface) took place in rats anaesthetised with phenobarbital, but not in those anaesthetised with urethane. Afferent nerve ablation as a result of treating rats with a neurotoxic dose of capsaicin before the experiment significantly aggravated ethanol induced damage as shown by an increase in the area and depth of mucosal erosions. Rapid repair of the injured mucosa, however, as seen in rats anesthetised with phenobarbital 180 minutes after ethanol was given, was similar in capsaicin and vehicle pretreated animals. Ablation of capsaicin sensitive afferent neurones was verified by a depletion of calcitonin gene related peptide from the gastric corpus wall. These findings indicate that nociceptive neurones control mechanisms of defence against acute injury but are not required for rapid repair of injured mucosa.
辣椒素敏感传入神经元此前已被报道在胃黏膜保护中发挥作用。本研究的目的是调查这些伤害性神经元是增强黏膜对损伤的防御能力，还是促进受损黏膜的快速修复，或者两者皆有。在麻醉大鼠中对这一假设进行了检验，这些大鼠的胃用乙醇（25%或50%的生理盐水，重量/重量）灌注30分钟。在给予乙醇后0和180分钟，从宏观、光学和扫描电子显微镜水平检查胃黏膜。在用苯巴比妥麻醉的大鼠中，乙醇损伤的胃黏膜出现了快速修复（深度损伤减轻，裸露表面部分重新上皮化），但在用乌拉坦麻醉的大鼠中未出现。实验前用神经毒性剂量的辣椒素处理大鼠导致传入神经切除，这显著加重了乙醇诱导的损伤，表现为黏膜糜烂面积和深度增加。然而，在用乙醇后180分钟用苯巴比妥麻醉的大鼠中观察到的受损黏膜快速修复，在辣椒素预处理和载体预处理的动物中是相似的。通过胃体壁降钙素基因相关肽的消耗证实了辣椒素敏感传入神经元的切除。这些发现表明，伤害性神经元控制着针对急性损伤的防御机制，但受损黏膜的快速修复并不需要它们。
