Fletcher D R, Shulkes A, Hardy K J
Aust N Z J Med. 1985 Aug;15(4):417-20. doi: 10.1111/j.1445-5994.1985.tb02763.x.
Smoking leads to a higher incidence of peptic ulcer and delays healing of those ulcers. Possible mechanisms include increased gastric acid secretion, reduced gastric mucosal blood flow, and reduced duodenal bicarbonate production. In six subjects we determined the effect of one hour of cigarette smoking on gastric mucosal blood flow (14C-aminopyrine clearance), acid secretion (triple lumen perfused oro-gastric tube), and plasma levels of gastrin and pancreatic polypeptide. Smoking reduced acid secretion from a median of 433 (range 160-707) mumol/min to 166 (47-340) mumol/min (p less than 0.05) and blood flow from 66 (40-70) ml/min to 36 (22-58) ml/min (p less than 0.05). There was no change in plasma gastrin and the small rise in pancreatic polypeptide would be insufficient to affect duodenal bicarbonate production. We conclude that cigarette smoking decreased gastric acid secretion and gastric mucosal blood flow. The increased incidence of gastric ulcers seen in smokers may be related to this reduction in gastric mucosal blood flow.
吸烟会导致消化性溃疡的发病率升高,并延缓溃疡的愈合。可能的机制包括胃酸分泌增加、胃黏膜血流量减少以及十二指肠碳酸氢盐生成减少。我们对6名受试者测定了吸烟1小时对胃黏膜血流量(14C-氨基比林清除率)、胃酸分泌(三腔灌注经口胃管)以及胃泌素和胰多肽血浆水平的影响。吸烟使胃酸分泌从中位数433(范围160 - 707)μmol/分钟降至166(47 - 340)μmol/分钟(p < 0.05),血流量从66(40 - 70)毫升/分钟降至36(22 - 58)毫升/分钟(p < 0.05)。血浆胃泌素无变化,胰多肽的小幅升高不足以影响十二指肠碳酸氢盐的生成。我们得出结论,吸烟会减少胃酸分泌和胃黏膜血流量。吸烟者中胃溃疡发病率增加可能与此胃黏膜血流量减少有关。