内脏神经激活可抑制大鼠十二指肠腔酸化诱导的HCO3-分泌增加。

Splanchnic nerve activation inhibits the increase in duodenal HCO3- secretion induced by luminal acidification in the rat.

作者信息

Jönson C, Tunbäck-Hanson P, Fändriks L

机构信息

Department of Physiology, University of Göteborg, Sweden.

出版信息

Gastroenterology. 1989 Jan;96(1):45-9. doi: 10.1016/0016-5085(89)90762-2.

DOI:10.1016/0016-5085(89)90762-2

PMID:2909437

Abstract

Acid exposure of the duodenal mucosa increased duodenal HCO3- secretion by approximately 60%. When the acid exposure was performed simultaneously with an arterial bleeding of 0.6 ml/100 g body wt (10% of the total blood volume), the increase in duodenal HCO3- secretion was totally abolished. When the acid exposure and bleeding procedures were performed at the same time in rats with bilaterally cut splanchnic nerves, alkaline secretion increased by 60%, as it did in the unbled rats. Direct electrical stimulation of the splanchnic nerves (10 Hz, supramaximal intensity) inhibited the stimulatory effect of duodenal acid exposure on alkaline secretion. Taken together, the data suggest that the sympathetic nervous system, because of splanchnic nerve activation, inhibits the acid-induced increase in duodenal HCO3- secretion.

摘要

十二指肠黏膜暴露于酸性环境会使十二指肠HCO₃⁻分泌增加约60%。当在以0.6毫升/100克体重（占总血容量的10%）进行动脉出血的同时进行酸性暴露时，十二指肠HCO₃⁻分泌的增加完全被消除。当在双侧切断内脏神经的大鼠中同时进行酸性暴露和出血操作时，碱性分泌增加了60%，与未出血的大鼠情况相同。直接电刺激内脏神经（10赫兹，超强强度）可抑制十二指肠酸性暴露对碱性分泌的刺激作用。综合来看，这些数据表明，由于内脏神经激活，交感神经系统会抑制酸性诱导的十二指肠HCO₃⁻分泌增加。