Boden G, Shore L S, Essa-Koumar N, Landor J H
Am J Dig Dis. 1976 Nov;21(11):974-7. doi: 10.1007/BF01071910.
The effect of nicotine (100 mug/kg hr-1) on serum secretin and pancreatic secretions was studied in dogs with chronic pancreatic fistulas. Release of immunoreactive secretin (IRS) was stimulated by intraduodenal infusion of HCl (9.6 mEq/30 min). Pancreatic flow rate and bicarbonate and protein secretions were stimulated either by intestinal acidification or infusion of exogenous secretin (1.0 IU/kg hr-1). It was found that nicotine delayed the appearance of peak IRS concentrations in response to intraduodenal HCl by about 20 min. However, nicotine had no effect on the total amount of IRS released nor was this delay accompanied by a similar delay in the appearance of peak bicarbonate output. Furthermore, nicotine did not affect pancreatic secretory function stimulated by either HCl or exogenous secretin. These data do not support the thesis that nicotine plays an important role in the pathogenesis of duodenal ulcers in smokers by inhibiting the pancreatic secretion of bicarbonate.
在患有慢性胰瘘的犬中,研究了尼古丁(100微克/千克·小时-1)对血清促胰液素和胰腺分泌的影响。通过十二指肠内输注HCl(9.6毫当量/30分钟)刺激免疫反应性促胰液素(IRS)的释放。通过肠道酸化或输注外源性促胰液素(1.0国际单位/千克·小时-1)刺激胰液流速以及碳酸氢盐和蛋白质分泌。发现尼古丁使十二指肠内HCl刺激后IRS浓度峰值的出现延迟约20分钟。然而,尼古丁对释放的IRS总量没有影响,并且这种延迟并未伴随着碳酸氢盐输出峰值出现的类似延迟。此外,尼古丁不影响由HCl或外源性促胰液素刺激的胰腺分泌功能。这些数据不支持尼古丁通过抑制胰腺碳酸氢盐分泌在吸烟者十二指肠溃疡发病机制中起重要作用这一论点。