Anagnostides A, Chadwick V S, Selden A C, Maton P N
Gastroenterology. 1984 Jul;87(1):109-14.
The cephalic phase of pancreatic secretion in humans was investigated using modified sham feeding and a duodenal perfusion system. Studies performed in 5 normal volunteers were designed so that trypsin and bicarbonate outputs during sham feeding, with or without pretreatment with atropine, were compared to "maximal" pancreatic secretory response to exogenous stimulation with caerulein and secretin. The role of gastric acid entry to the duodenum in mediating cephalic responses was assessed by a comparison between outputs observed when gastric aspiration (congruent to 80% efficient) was used alone and when acid entry was completely abolished by combining gastric aspiration with cimetidine pretreatment. To evaluate the role, if any, of gut hormone release in the pancreatic secretory response to sham feeding, plasma gastrin and cholecystokinin concentrations were monitored throughout. Trypsin outputs during sham feeding were 31.9 +/- 10.45 kallikrein inactivator units per 30 min, equivalent to four times basal output and 92% of maximal, but were only 54% maximal in subjects pretreated with cimetidine. Atropine suppressed basal trypsin output and abolished the response to sham feeding (4.98 +/- 3.89 kallikrein inactivator units per 30 min). A modest increase in bicarbonate secretion during sham feeding (3.30 +/- 1.97 mmol/30 min versus basal of 0.68 +/- 0.74 mmol/30 min, p = 0.5) was not influenced by atropine but was abolished by cimetidine pretreatment. No significant changes in plasma gastrins were observed in these studies and plasma cholecystokinins remained undetectable throughout. We conclude that there is tonic vagal stimulation of trypsin secretion, and that sham feeding markedly increases trypsin output, which is augmented further by acid entry into the duodenum. There is no direct effect of cephalic stimulation on bicarbonate secretion or on gastrin or cholecystokinin release.
利用改良的假饲法和十二指肠灌注系统，对人类胰腺分泌的头期进行了研究。在5名正常志愿者身上进行的研究设计如下：将假饲期间（无论是否用阿托品预处理）胰蛋白酶和碳酸氢盐的分泌量，与用蛙皮素和促胰液素进行外源性刺激时的“最大”胰腺分泌反应进行比较。通过比较单独使用胃抽吸术（效率约为80%）时和胃抽吸术与西咪替丁预处理联合使用使胃酸进入完全消除时观察到的分泌量，评估胃酸进入十二指肠在介导头期反应中的作用。为了评估肠道激素释放在胰腺对假饲分泌反应中的作用（如果有作用的话），全程监测血浆胃泌素和胆囊收缩素浓度。假饲期间胰蛋白酶的分泌量为每30分钟31.9±10.45激肽释放酶灭活单位，相当于基础分泌量的4倍，为最大分泌量的92%，但在用西咪替丁预处理的受试者中仅为最大分泌量的54%。阿托品抑制基础胰蛋白酶分泌量，并消除对假饲的反应（每30分钟4.98±3.89激肽释放酶灭活单位）。假饲期间碳酸氢盐分泌量有适度增加（3.30±1.97 mmol/30分钟，而基础分泌量为0.68±0.74 mmol/30分钟，p = 0.5），不受阿托品影响，但被西咪替丁预处理消除。在这些研究中未观察到血浆胃泌素有显著变化，且全程未检测到血浆胆囊收缩素。我们得出结论，存在对胰蛋白酶分泌的紧张性迷走神经刺激，假饲显著增加胰蛋白酶分泌量，胃酸进入十二指肠会进一步增强该分泌量。头期刺激对碳酸氢盐分泌、胃泌素或胆囊收缩素释放没有直接影响。
