Epithelial responses evoked by stimulation of submucosal neurons in guinea pig distal colon.
Epithelial responses evoked by stimulation of submucosal neurons in guinea pig distal colon.
复制标题
刺激豚鼠远端结肠粘膜下神经元引起的上皮反应。
DOI：
10.1152/ajpgi.1987.252.5.g667
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Cooke,HJ
中科院分区：
文献类型：
--
作者：
Kuwahara,A;Bowen,S;Wang,J;Condon,C;Cooke,HJ
在ususe通量室中建立粘膜下层粘膜肌剥离片，观察粘膜下神经元对豚鼠远端结肠离子转运的影响。电位差（PD）和短路电流的自发变化范围从与管腔负电位相关的正电流到与管腔正电位相关的负电流。粘膜阿米洛利降低了两组的基础电流。在有正或负短路电流的组织中，单向的粘膜到浆膜的钠通量大于浆膜到粘膜的钠通量，并且存在小的净吸收通量。很少或没有氯化物分泌通量。电刺激粘膜下神经元在正或负短路电流的组织中引起河豚毒素敏感的短路电流增加。这是由于净氯化物通量增加，而净钠通量或剩余通量变化不大。净氯化物通量的增加几乎完全是由于血清到粘膜氯化物通量的增加，并与总组织电导的增加有关。阿托品可降低刺激诱发反应。这些结果表明，刺激支配远端结肠上皮的粘膜下神经元可引起大量氯离子分泌反应，部分原因是在神经-肠细胞连接处释放乙酰胆碱。
The influence of submucosal neurons on ion transport in the guinea pig distal colon was examined in muscle-stripped sheets of submucosa-mucosa set up in Ussing flux chambers. Spontaneous variations in potential differences (PD) and short-circuit current occurred ranging from positive currents associated with luminal negative PDs to negative currents with luminal positive PDs. Basal current in both groups was reduced by mucosal amiloride. In tissues with positive or negative short-circuit currents, unidirectional mucosal-to-serosal sodium fluxes were greater than serosal-to-mucosal fluxes and small net absorptive fluxes were present. Little or no chloride secretory flux was present. Electrical stimulation of submucosal neurons evoked a tetrodotoxin-sensitive increase in short-circuit current in tissues with positive or negative short-circuit currents. This was due to an increase in net chloride flux and little change in net sodium flux or residual flux. The increase in net chloride flux was due almost entirely to an increase in serosal-to-mucosal chloride flux and was associated with an increase in total tissue conductance. The stimulus-evoked response was reduced by atropine. These results suggest that stimulation of submucosal neurons that innervate the distal colonic epithelium evokes a large chloride secretory response that is due in part to release of acetylcholine at neuro-enterocyte junctions.