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体外由大肠杆菌STa肠毒素和环核苷酸激活的营养不良大鼠肠道中的神经维持性分泌亢进。

Neurally maintained hypersecretion in undernourished rat intestine activated by E. coli STa enterotoxin and cyclic nucleotides in vitro.

作者信息

Nzegwu H C, Levin R J

机构信息

Department of Biomedical Science, University of Sheffield.

出版信息

J Physiol. 1994 Aug 15;479 ( Pt 1)(Pt 1):159-69. doi: 10.1113/jphysiol.1994.sp020285.

Abstract
  1. The electrogenic secretory responses of stripped jejuna and ilea from chronically undernourished rats (50% control diet for 21 days) to the bacterial enterotoxin Escherichia coli STa, measured as the short-circuit current in vitro, show an enhanced maximum secretion (ISC, max) with a prolonged duration compared with fed intestine. 2. The ISC, max is unaffected by pretreatment of the intestine in vitro with hexamethonium, atropine, procaine or indomethacin, or by desensitization to 5-hydroxytryptamine (5-HT), while the prolonged duration is unaffected by atropine, indomethacin or 5-HT desensitization but is reduced by hexamethonium and procaine. 3. Both 8-bromo-cyclic GMP and dibutyryl cyclic AMP added serosally activate the enhanced ISC, max and its maintenance. Pretreatment with tetrodotoxin had no effect on the initial ISC, max but prevented its maintenance. 4. Bethanechol, dimethyl phenyl piperazinium, vasoactive intestinal polypeptide, 5-HT and luminal propionate all induced the characteristic hypersecretory activity in the undernourished intestine compared with the fed state, but none could activate the maintenance circuit to prolong their transient responses. 5. Maintenance of the induced hypersecretory activity is the first example of induction of the neural control of intestinal secretion by the dietary intake level and illustrates the plasticity of the enteric nervous system.
摘要
  1. 以体外短路电流衡量,长期营养不良大鼠(给予50%对照饮食21天)空肠和回肠对细菌肠毒素大肠杆菌STa的电分泌反应显示,与喂食状态的肠道相比,最大分泌量(ISC,max)增加且持续时间延长。2. 体外对肠道用六甲铵、阿托品、普鲁卡因或吲哚美辛预处理,或对5-羟色胺(5-HT)脱敏,均不影响ISC,max,而持续时间不受阿托品、吲哚美辛或5-HT脱敏的影响,但六甲铵和普鲁卡因可使其缩短。3. 经浆膜面添加8-溴环鸟苷酸和二丁酰环腺苷酸均可激活增强的ISC,max及其维持。用河豚毒素预处理对初始ISC,max无影响,但可阻止其维持。4. 与喂食状态相比,氨甲酰甲胆碱、二甲基苯基哌嗪、血管活性肠肽、5-HT和腔内丙酸盐均在营养不良的肠道中诱导出特征性的高分泌活性,但均不能激活维持回路来延长其短暂反应。5. 诱导的高分泌活性的维持是饮食摄入水平对肠道分泌神经控制诱导的首个实例,说明了肠神经系统的可塑性。

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