Niebel W, Beglinger C, Singer M V
Department of Medicine, University of Essen, Federal Republic of Germany.
Am J Physiol. 1988 Mar;254(3 Pt 1):G436-43. doi: 10.1152/ajpgi.1988.254.3.G436.
In two sets of dogs with gastric and pancreatic fistulas, we studied the effect of atropine on pancreatic bicarbonate output and release of secretin in response to intraduodenal HCl before and after stepwise removal of the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy alone and truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Ganglionectomy alone did not alter the incremental bicarbonate response to HCl. Truncal vagotomy alone significantly (P less than 0.05) decreased the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high (6 to 24 mmol/h) loads of HCl. Additional ganglionectomy restored the bicarbonate response to prevagotomy levels. With the extrinsic nerves intact and after ganglionectomy, but not after truncal vagotomy and truncal vagotomy plus ganglionectomy, intravenous atropine (14 nmol.kg-1.h-1) significantly reduced the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high loads of HCl. Neither the different surgical procedures nor atropine significantly altered plasma levels of secretin basally and in response to intestinal HCl. We conclude that 1) cholinergic fibers within the vagus nerves but not the splanchnic nerves are important mediators of the pancreatic bicarbonate response to low loads of HCl and 2) release of secretin by intestinal HCl is not under cholinergic and splanchnic control.
在两组患有胃瘘和胰瘘的狗中,我们研究了阿托品对胰液碳酸氢盐分泌量以及在逐步切除胰腺的外在神经(即单独进行腹腔神经节和肠系膜上神经节切除术,或单独进行迷走神经干切断术,以及迷走神经干切断术加腹腔神经节和肠系膜上神经节切除术)前后,十二指肠内注入盐酸后促胰液素释放的影响。单独进行神经节切除术并未改变对盐酸的碳酸氢盐分泌量增加反应。单独进行迷走神经干切断术显著(P<0.05)降低了对低剂量(1.5和3 mmol/h)而非高剂量(6至24 mmol/h)盐酸负荷的碳酸氢盐分泌量增加反应。额外的神经节切除术使碳酸氢盐反应恢复到迷走神经切断术前的水平。在外在神经完整时以及神经节切除术后,但在迷走神经干切断术以及迷走神经干切断术加神经节切除术后则不然,静脉注射阿托品(14 nmol·kg-1·h-1)显著降低了对低剂量(1.5和3 mmol/h)而非高剂量盐酸负荷的碳酸氢盐分泌量增加反应。不同的手术操作和阿托品均未显著改变基础状态下以及对肠道盐酸反应时的血浆促胰液素水平。我们得出结论:1)迷走神经而非内脏神经中的胆碱能纤维是胰腺对低剂量盐酸负荷产生碳酸氢盐反应的重要介质;2)肠道盐酸引起的促胰液素释放不受胆碱能和内脏神经控制。