Cherbut C, Aubé A C, Blottière H M, Pacaud P, Scarpignato C, Galmiche J P
Human Nutrition Research Centre, INRA, Laboratory of Nutrition and Applied Technology, Nantes, France.
Gut. 1996 Jan;38(1):53-8. doi: 10.1136/gut.38.1.53.
Short chain fatty acids (SCFAs), produced in the gut by bacterial fermentation of carbohydrates, change intestinal motility by mechanisms as yet unknown. This study examined the mechanism(s) of action of SCFAs on contractility using isolated rat terminal ileum segments and isolated ileal smooth muscle cells. Strip contractions were recorded under isometric conditions. Intracellular calcium concentration ([Ca2+]i) was measured in single cells loaded with indo-1 penta-acetoxymethyl ester (indo-1 AM). SCFAs (10(-9) to 10(-2) mol/l) induced concentration dependent contractions. The effect was not different among the individual SCFAs. Exogenous acids (namely tartaric and citric acids) caused similar responses as SCFAs, whereas sodium acetate had no effect. The contraction was not blocked by tetrodotoxin, atropine or hexamethonium, showing that it was not mediated through a cholinergic pathway. Moreover, removal of the mucosa or addition of procaine (a local anaesthetic) to the bath did not change the SCFA induced contraction, while verapamil (a calcium-channel antagonist) completely suppressed it. In addition, application of SCFAs to isolated ileal myocytes evoked peaks in [Ca2+]i inhibited by D 600 (a blocker of voltage dependent calcium channels). Taken together, these results suggest that the contractile response stimulated by SCFAs in the rat terminal ileum could result from an acid sensitive calcium dependent myogenic mechanism.
短链脂肪酸(SCFAs)由肠道内碳水化合物的细菌发酵产生,其改变肠道蠕动的机制尚不清楚。本研究使用分离的大鼠回肠末端段和分离的回肠平滑肌细胞,研究了SCFAs对收缩性的作用机制。在等长条件下记录条带收缩情况。使用indo-1五乙酰氧基甲基酯(indo-1 AM)加载的单细胞测量细胞内钙浓度([Ca2+]i)。SCFAs(10^(-9)至10^(-2) mol/l)诱导浓度依赖性收缩。不同的SCFAs之间的作用无差异。外源性酸(即酒石酸和柠檬酸)引起与SCFAs相似的反应,而醋酸钠无作用。收缩不受河豚毒素、阿托品或六甲铵的阻断,表明其不是通过胆碱能途径介导的。此外,去除黏膜或向浴槽中添加普鲁卡因(一种局部麻醉剂)不会改变SCFAs诱导的收缩,而维拉帕米(一种钙通道拮抗剂)可完全抑制它。另外,将SCFAs应用于分离的回肠肌细胞会引起[Ca2+]i峰值,该峰值受D 600(电压依赖性钙通道阻滞剂)抑制。综上所述,这些结果表明,SCFAs在大鼠回肠末端刺激的收缩反应可能源于酸敏感的钙依赖性肌源性机制。