Takeuchi K, Ohuchi T, Okabe S
Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.
Dig Dis Sci. 1994 Dec;39(12):2543-6. doi: 10.1007/BF02087688.
The role of capsaicin-sensitive sensory neurons in the healing of HCl-induced gastric lesions was investigated in rats. Rats fasted for 18 hr were given 0.6 N HCl orally for induction of gastric lesions, and they were fed normally from 1 hr later. On various days after HCl treatment, area of lesions, acid secretion, mucosal H+ permeability, and blood flow responses were measured. Functional ablation of capsaicin-sensitive sensory neurons was performed two weeks before the experiment by subcutaneous injections of high-dose capsaicin. Sensory deafferentation did not affect the development of gastric damage in response to HCl but significantly delayed the healing of these lesions. The mucosa damaged by HCl secreted less acid but showed significant rise in H+ permeability, resulting in acid back-diffusion accompanied by an increase of mucosal blood flow. Sensory deafferentation had no effect on acid secretion and mucosal permeability changes in the damaged stomach but completely blocked the hyperemic response caused by acid back-diffusion. Capsaicin-sensitive sensory neurons may contribute to healing of gastric lesions, probably by mediating the mucosal hyperemic responses associated with acid back-diffusion and by facilitating acid disposal in the mucosa.
在大鼠中研究了辣椒素敏感感觉神经元在盐酸诱导的胃损伤愈合中的作用。禁食18小时的大鼠口服0.6N盐酸以诱导胃损伤，1小时后开始正常进食。在盐酸处理后的不同天数，测量损伤面积、酸分泌、粘膜H⁺通透性和血流反应。在实验前两周通过皮下注射高剂量辣椒素对辣椒素敏感感觉神经元进行功能切除。感觉传入神经切断不影响对盐酸的胃损伤发展，但显著延迟这些损伤的愈合。盐酸损伤的粘膜分泌较少的酸，但H⁺通透性显著升高，导致酸反向扩散并伴有粘膜血流增加。感觉传入神经切断对受损胃中的酸分泌和粘膜通透性变化没有影响，但完全阻断了酸反向扩散引起的充血反应。辣椒素敏感感觉神经元可能有助于胃损伤的愈合，可能是通过介导与酸反向扩散相关的粘膜充血反应以及促进粘膜中的酸处理。
