Effects of splanchnic nerve stimulation and of clonidine on gastric and duodenal HCO3- secretion in the anaesthetized cat.
Effects of splanchnic nerve stimulation and of clonidine on gastric and duodenal HCO3- secretion in the anaesthetized cat.
复制标题
内脏神经刺激和可乐定对麻醉猫胃和十二指肠 HCO3- 分泌的影响。
DOI：
10.1111/j.1748-1716.1987.tb08135.x
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
O. Nylander
中科院分区：
文献类型：
--
作者：
L. Fändriks;C. Jönson;O. Nylander
在结扎肾上腺的氯醛糖麻醉猫上进行了实验。切断迷走神经和内脏神经并安排外周电刺激。用等渗盐水灌注胃腔，并根据灌注液中的 pH/pCO2 测量值计算胃 H+ 和 HCO3- 分泌物。胃动力被记录为灌注回路中静水压力的变化。通过pH-stat滴定原位监测粘膜HCO3-分泌到十二指肠中。迷走神经刺激（10 Hz，10 分钟）增加胃和十二指肠 HCO3- 分泌，以及胃运动活动和 H+ 分泌。内脏神经刺激（10 Hz，10 分钟）不影响胃 H+ 和 HCO3- 分泌，但往往会降低胃运动张力和十二指肠基础 HCO3- 分泌。内脏神经刺激与迷走神经刺激同时进行，可抑制胃收缩以及单独对迷走神经刺激的反应中观察到的胃H+和十二指肠HCO3-分泌物的增加，但对胃HCO3-分泌物的增加几乎没有影响。然而，在存在α2-肾上腺素受体阻滞剂育亨宾的情况下，这种迷走神经内脏刺激诱导胃收缩、H+分泌和十二指肠HCO3-分泌反应，其程度与单独迷走神经刺激诱导的反应相似，而胃HCO3-分泌反应比单独迷走神经刺激更大。 α2-肾上腺素受体激动剂可乐定（50微克kg-1h-1，静脉注射）抑制胃收缩并增加胃和十二指肠响应迷走神经刺激的HCO3-分泌，但不影响迷走神经刺激胃H+分泌。结果表明存在对涉及α2-肾上腺素受体的胃和十二指肠HCO3-分泌的外周交感神经抑制作用。还可能存在对胃和十二指肠 HCO3- 分泌的内脏神经刺激作用。
Experiments were performed on chloralose-anaesthetized cats with ligated adrenals. The vagal and splanchnic nerves were cut and arranged for peripheral electric stimulation. The gastric lumen was perfused with isotonic saline and gastric H+ and HCO3- secretions were calculated from pH/pCO2 measurements in the perfusate. Gastric motility was recorded as changes in hydrostatic pressure in the perfusion circuit. Mucosal HCO3- secretion into the duodenum was monitored in situ by pH-stat titration. Vagal stimulation (10 Hz for 10 min) increased gastric and duodenal HCO3- secretions, as well as gastric motor activity and H+ secretion. Splanchnic nerve stimulation (10 Hz for 10 min) did not affect gastric H+ and HCO3- secretions, but tended to decrease gastric motor tone and basal duodenal HCO3- secretion. Splanchnic nerve stimulation simultaneously with vagal stimulation inhibited gastric contractions and the rise in gastric H+ and duodenal HCO3- secretions observed in response to vagal stimulation alone, but had little effect on the rise in gastric HCO3- secretion. However, such vago-splanchnic stimulation in the presence of the alpha 2-adrenoceptor blocker yohimbine induced gastric contractions, H+ secretory and duodenal HCO3- secretory responses with magnitudes similar to those induced by vagal stimulation alone, whereas the gastric HCO3- secretory response was larger than by vagal stimulation alone. The alpha 2-adrenoceptor agonist clonidine (50 micrograms kg-1 h-1, i.v.) inhibited the gastric contractions and increases in gastric and duodenal HCO3- secretion in response to vagal stimulation, but did not influence vagal stimulation of gastric H+ secretion. The results suggest the existence of a peripheral sympatho-inhibitory action on gastric and duodenal HCO3- secretion involving alpha 2-adrenoceptors. Also splanchnic neural stimulatory effects on gastric and duodenal HCO3- secretion may exist.