Hemlin M, Mellander A
Department of Physiology, University of Göteborg, Sweden.
Acta Physiol Scand. 1992 Jul;145(3):239-51. doi: 10.1111/j.1748-1716.1992.tb09361.x.
The aim of this study was to evaluate the mechanism behind neurogenic fluid secretion in the rat jejunum. In vitro, short-circuit current (SCC) and potential difference (PD) were measured with the conventional Ussing technique. In vivo, electric parameters and net fluid transport (NFT) were simultaneously recorded with two different techniques. In separate in vivo experiments alkaline secretion (As) was estimated. In vitro, the chloride channel blocking substance 5-nitro-2(-3-phenylpropyl-amino)benzoic acid (NPPB) and the loop diuretic substance furosemide (F) inhibited SCC, whereas the carbonic anhydrase inhibitor acetazolamide (Ace) lacked effect. Noradrenaline inhibited SCC and this effect was antagonized by NPPB and F. In vivo, cholera toxin induced a parallel increase in PD/SCC and fluid secretion. Conversely, mesenteric nerve stimulation (MNS) or administration of the nicotinic antagonist hexamethonium (Hx), concomitantly inhibited PD/SCC and fluid secretion. However, there was a poor correlation between the magnitudes of these effects. F inhibited SCC in vivo and also the SCC-effect of MNS. However, F had no effect on fluid secretion in vivo, nor on the NFT-effect of MNS. Jejunal As was stimulated by cholera toxin and MNS significantly inhibited As. The present results challenge the current view on the role of electrogenic chloride secretion in intestinal secretion. Alternative mechanisms are tentatively discussed.
本研究的目的是评估大鼠空肠神经源性液体分泌背后的机制。在体外，采用传统的Ussing技术测量短路电流（SCC）和电位差（PD）。在体内，用两种不同的技术同时记录电参数和净液体转运（NFT）。在单独的体内实验中，估计碱性分泌（As）。在体外，氯通道阻断物质5-硝基-2-（3-苯丙基-氨基）苯甲酸（NPPB）和袢利尿剂速尿（F）抑制SCC，而碳酸酐酶抑制剂乙酰唑胺（Ace）无作用。去甲肾上腺素抑制SCC，且该作用被NPPB和F拮抗。在体内，霍乱毒素诱导PD/SCC和液体分泌平行增加。相反，肠系膜神经刺激（MNS）或给予烟碱拮抗剂六甲铵（Hx），同时抑制PD/SCC和液体分泌。然而，这些作用的大小之间相关性较差。F在体内抑制SCC以及MNS的SCC效应。然而，F对体内液体分泌无作用，对MNS的NFT效应也无作用。空肠As受霍乱毒素刺激，MNS显著抑制As。目前的结果对当前关于电中性氯分泌在肠分泌中作用的观点提出了挑战。初步讨论了替代机制。
