Isaacs P E, Corbett C L, Riley A K, Hawker P C, Turnberg L A
J Clin Invest. 1976 Sep;58(3):535-42. doi: 10.1172/JCI108498.
The possibility that the autonomic nervous system may influence the function of intestinal mucosa was investigated by assessing the effect of acetyl choline on ion transport in human intestine. Isolated pieces of stripped ileal mucosa were mounted in Perspex flux-chambers and bathed in isotonic glucose Ringer's solution. Acetyl choline caused a rise in mean potential difference (8.8-12.3 mV, P less than 0.002) and short circuit current (287.7-417.2 muA-cm-2, P less than 0.01) (n = 12), observable at a concentration of 0.01 mM and maximal at 0.1 mM. This effect was enhanced by neostigmine and blocked by atropine. Isotopic flux determinations revealed a change from a small mean net Cl absorption (58) to a net Cl secretion (-4.3mueq-cm-2-h-1P less than 0.001) due predominantly to an increase in the serosal to mucosal unidirectional flux of Cl (10.63-14.35 mueq-cm-2-h-1P less than 0.05) and a smaller reduction in the mucosal to serosal flux (11.22 to 10.02 mueq-cm-2-h-1P less than 0.05). Unidirectional and net Na transport was unaffected. A similar electrical and ion transport response was observed in a single study of two pieces of jejunal mucosa. In the absence of glucose net chloride secretion was produced and again an insignificant effect on net sodium transport was noted. Acetyl choline did not provoke a sustained effect on mucosal cyclic adenine nucleotide levels although a short-lived cyclic adenine nucleotide response was seen in some tissues 20-30 s after drug addition. These studies demonstrate that acetyl choline does influence human intestinal ion transport by stimulating chloride secretion and suggest a possible mechanism by which the parasympathetic nervous system could be concerned in the control of ion transport.
通过评估乙酰胆碱对人体肠道离子转运的影响,研究了自主神经系统可能影响肠黏膜功能的可能性。将分离的去黏膜回肠片段置于有机玻璃通量室中,并用等渗葡萄糖林格氏液进行灌注。乙酰胆碱可引起平均电位差升高(8.8 - 12.3 mV,P<0.002)和短路电流升高(287.7 - 417.2 μA·cm⁻²,P<0.01)(n = 12),在浓度为0.01 mM时即可观察到这种效应,在0.1 mM时达到最大。新斯的明可增强此效应,阿托品则可阻断此效应。同位素通量测定显示,主要由于氯离子从浆膜向黏膜的单向通量增加(10.63 - 14.35 μeq·cm⁻²·h⁻¹,P<0.05)以及从黏膜向浆膜通量的较小减少(11.22至10.02 μeq·cm⁻²·h⁻¹,P<0.05),导致平均净氯离子吸收从少量(58)转变为净氯离子分泌(-4.3 μeq·cm⁻²·h⁻¹,P<0.001)。单向和净钠转运未受影响。在对两片空肠黏膜的单次研究中观察到了类似的电和离子转运反应。在无葡萄糖的情况下产生了净氯离子分泌,并且再次观察到对净钠转运的影响不显著。乙酰胆碱虽在给药后20 - 30秒在一些组织中引起了短暂的环磷酸腺苷反应,但并未对黏膜环磷酸腺苷水平产生持续影响。这些研究表明,乙酰胆碱确实通过刺激氯离子分泌来影响人体肠道离子转运,并提示了副交感神经系统可能参与离子转运控制的一种可能机制。