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。
Effects of splanchnic nerve stimulation and of clonidine on gastric and duodenal HCO3- secretion in the anaesthetized cat.
作者信息
Fändriks L, Jönson C, Nylander O
出版信息
Acta Physiol Scand. 1987 Jun;130(2):251-8. doi: 10.1111/j.1748-1716.1987.tb08134.x.
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.
在氯醛糖麻醉且肾上腺结扎的猫身上进行了实验。切断迷走神经和内脏神经，并安排进行外周电刺激。用等渗盐水灌注胃腔，根据灌注液中的pH/pCO₂测量值计算胃H⁺和HCO₃⁻分泌量。胃动力记录为灌注回路中静水压力的变化。通过pH稳态滴定原位监测十二指肠黏膜HCO₃⁻分泌。迷走神经刺激（10Hz，持续10分钟）增加了胃和十二指肠HCO₃⁻分泌，以及胃运动活性和H⁺分泌。内脏神经刺激（10Hz，持续10分钟）不影响胃H⁺和HCO₃⁻分泌，但倾向于降低胃运动张力和基础十二指肠HCO₃⁻分泌。与迷走神经刺激同时进行的内脏神经刺激抑制了胃收缩以及单独迷走神经刺激时观察到的胃H⁺和十二指肠HCO₃⁻分泌增加，但对胃HCO₃⁻分泌增加影响不大。然而，在α₂肾上腺素能受体阻滞剂育亨宾存在的情况下进行这种迷走-内脏神经刺激会诱发胃收缩、H⁺分泌和十二指肠HCO₃⁻分泌反应，其幅度与单独迷走神经刺激诱导的相似，而胃HCO₃⁻分泌反应比单独迷走神经刺激时更大。α₂肾上腺素能受体激动剂可乐定（50微克/千克·小时⁻¹，静脉注射）抑制了迷走神经刺激引起的胃收缩以及胃和十二指肠HCO₃⁻分泌增加，但不影响迷走神经对胃H⁺分泌的刺激。结果表明存在一种涉及α₂肾上腺素能受体的对胃和十二指肠HCO₃⁻分泌的外周交感抑制作用。此外，内脏神经对胃和十二指肠HCO₃⁻分泌可能存在神经刺激作用。
Zotero 插件