Ainsworth M A, Fenger C, Svendsen P, Schaffalitzky de Muckadell O B
Dept. of Medical Gastroenterology S, Odense University, Denmark.
Scand J Gastroenterol. 1993 Dec;28(12):1091-7. doi: 10.3109/00365529309098315.
The effect of stimulation of duodenal mucosal bicarbonate secretion with vasoactive intestinal peptide (VIP) on acid-induced damage to the duodenal mucosa was studied in anaesthetized pigs in which bile and pancreatic juice were diverted from the duodenum. Mucosal damage was quantitatively assessed histologically, and mucosal blood flow was determined by means of radioactively labelled microspheres. Compared with placebo, intravenous infusion of VIP (500 pmol/kg/h) significantly stimulated duodenal mucosal bicarbonate secretion (47 +/- 13 versus 249 +/- 53 mumol/h) without concomitant changes in mucosal blood flow (51.5 +/- 7.8 versus 48.5 +/- 9.1 ml/min/100 g) or arterial bicarbonate concentration (24.2 +/- 1.1 versus 23.4 +/- 0.9 mM). The same dose of VIP increased the acid disappearance rate in the duodenum (2.2 +/- 0.14 versus 3.3 +/- 0.09 mmol/h) and reduced the extent of damage to the duodenal surface (16 +/- 2% versus 7 +/- 2%) during duodenal infusion of 0.03 M HCl but not 0.1 M HCl. We conclude that the protection offered by VIP against the small dose of acid is most likely secondary to the effect of VIP on mucosal bicarbonate secretion. Thus, this study suggests that duodenal mucosal bicarbonate secretion, independent of mucosal blood flow, is an integral factor in duodenal mucosal defence.
在麻醉猪身上进行研究,这些猪的胆汁和胰液已从十二指肠分流,以探讨血管活性肠肽(VIP)刺激十二指肠黏膜碳酸氢盐分泌对酸诱导的十二指肠黏膜损伤的影响。通过组织学方法对黏膜损伤进行定量评估,并借助放射性标记微球测定黏膜血流量。与安慰剂相比,静脉输注VIP(500 pmol/kg/h)显著刺激十二指肠黏膜碳酸氢盐分泌(47±13对249±53 μmol/h),而黏膜血流量(51.5±7.8对48.5±9.1 ml/min/100 g)或动脉碳酸氢盐浓度(24.2±1.1对23.4±0.9 mM)无伴随变化。相同剂量的VIP在十二指肠输注0.03 M HCl期间增加了十二指肠内酸的消失率(2.2±0.14对3.3±0.09 mmol/h)并减少了十二指肠表面的损伤程度(16±2%对7±2%),但在输注0.1 M HCl时未出现此现象。我们得出结论,VIP对小剂量酸的保护作用很可能继发于VIP对黏膜碳酸氢盐分泌的影响。因此,本研究表明,独立于黏膜血流量的十二指肠黏膜碳酸氢盐分泌是十二指肠黏膜防御的一个重要因素。