Glad H, Svendsen P, Olsen O, Schaffalitzky de Muckadell O B
Department of Medical Gastroenterology, Odense University Hospital, Denmark.
Am J Physiol. 1997 Jan;272(1 Pt 1):G154-60. doi: 10.1152/ajpgi.1997.272.1.G154.
During the cephalic phase of gastric acid secretion, vagally mediated synchronous stimulation of bicarbonate provides protection against the acid. The purpose of this study was to determine simultaneously the effect of electrical vagal stimulation (EVS) on pancreatic, hepatic, and duodenal mucosal bicarbonate secretion, thereby estimating their relative importance in vagally induced duodenal acid neutralization. Splanchnicotomy increased vagally induced pancreaticobiliary bicarbonate secretion, whereas duodenal mucosal bicarbonate secretion was unchanged. After splanchnicotomy, EVS (10 ms, 15 mA, 12 Hz) significantly increased pancreatic bicarbonate secretion (0-4.17 mmol/h), hepatic bicarbonate secretion (0.16 to 0.22 mmol/h), and duodenal mucosal bicarbonate secretion (0.17 to 0.31 mmol/h). Pancreaticobiliary bicarbonate secretion was atropine resistant, whereas vagally induced duodenal mucosal bicarbonate secretion was diminished by atropine (2.0 mg/kg). After splanchnicotomy, EVS (10 ms, 15 mA, 12 Hz) had no effect on portal plasma concentration of secretin, whereas vasoactive intestinal peptide was increased (14-29 pM). EVS at 12 Hz with varying duration (3 or 10 ms) and amplitude (3-50 mA) had no further effect on the bicarbonate secretion from the three organs. In addition, biliary [14C]mannitol clearance was shown not to be a reliable marker of canalicular bile secretion in pigs. These results suggest that in the anesthetized pig 1) vagal stimulation is only of minor importance to hepatic bicarbonate secretion; 2) vagal stimulation activates pancreatic bicarbonate secretion through both cholinergic muscarinic and noncholinergic transmission; and 3) vagal stimulation induces duodenal mucosal bicarbonate secretion mainly through cholinergic muscarinic transmission. In conclusion, these results suggest that only pancreatic and duodenal bicarbonate production play a role in vagally induced duodenal acid neutralization.
在胃酸分泌的头期，迷走神经介导的碳酸氢盐同步刺激可提供抗酸保护。本研究的目的是同时确定电迷走神经刺激（EVS）对胰腺、肝脏和十二指肠黏膜碳酸氢盐分泌的影响，从而评估它们在迷走神经诱导的十二指肠酸中和中的相对重要性。内脏神经切断术增加了迷走神经诱导的胰胆管碳酸氢盐分泌，而十二指肠黏膜碳酸氢盐分泌未改变。内脏神经切断术后，EVS（10毫秒，15毫安，12赫兹）显著增加了胰腺碳酸氢盐分泌（0 - 4.17毫摩尔/小时）、肝脏碳酸氢盐分泌（0.16至0.22毫摩尔/小时）和十二指肠黏膜碳酸氢盐分泌（0.17至0.31毫摩尔/小时）。胰胆管碳酸氢盐分泌对阿托品有抗性，而迷走神经诱导的十二指肠黏膜碳酸氢盐分泌可被阿托品（2.0毫克/千克）减少。内脏神经切断术后，EVS（10毫秒，15毫安，12赫兹）对门静脉血浆中促胰液素浓度无影响，而血管活性肠肽增加（14 - 29皮摩尔）。12赫兹、不同持续时间（3或10毫秒）和幅度（3 - 50毫安）的EVS对这三个器官的碳酸氢盐分泌没有进一步影响。此外，胆汁[14C]甘露醇清除率在猪中不是胆小管胆汁分泌的可靠标志物。这些结果表明，在麻醉的猪中：1）迷走神经刺激对肝脏碳酸氢盐分泌的重要性较小；2）迷走神经刺激通过胆碱能毒蕈碱和非胆碱能传递激活胰腺碳酸氢盐分泌；3）迷走神经刺激主要通过胆碱能毒蕈碱传递诱导十二指肠黏膜碳酸氢盐分泌。总之，这些结果表明，只有胰腺和十二指肠产生的碳酸氢盐在迷走神经诱导的十二指肠酸中和中起作用。
