Colombel J F, Sutton A, Chayvialle J A, Modigliani R
INSERM U 290, Hôpital Saint-Lazare, Paris, France.
Gut. 1988 Sep;29(9):1158-66. doi: 10.1136/gut.29.9.1158.
The aim of this study was to measure the role of the duodenal loop in biliopancreatic secretion in man by infusing various stimuli at the ampulla of Vater and collecting duodenal contents at the ligament of Treitz, above an occluding balloon. Perfusion at 10 ml/min of a first mixture of aminoacids - phenylalanine (47.2 mmol), methionine (38.2 mmol), tryptophan (11 mmol), valine (61.6 mmol) - increased cholecystokinin (CCK) plasma concentrations and duodenal bile salt output (p less than 0.005) as compared with a control electrolyte solution, but did not change pancreatic enzyme secretion significantly; duodenal infusion of another aminoacid mixture - arginine (32.4 mmol), histidine (14.1 mmol), leucine (36 mmol), isoleucine (21.5 mmol), lysine (31 mmol), threonine (23 mmol) - did not change CCK plasma concentrations, bile salt or pancreatic enzyme output. The respective role of duodenal distension and endogenous CCK was investigated by perfusing the first aminoacid solution and the control solution at 2, 5, and 10 ml/min. Changing the perfusion rate of control solution from 2 to 5 ml/min led to a significant increase (p less than 0.01) in pancreatic secretion with no further increase at 10 ml/min. Bile salt output was not influenced by the perfusion rate of control solution. During the perfusion of the aminoacid solution, despite a stepwise increase in CCK release, the only significant change in pancreatic secretion was an increase of lipase output (p less than 0.05) when the infusion rate was raised from 2 to 5 ml/min. Our results suggest that duodenal CCK release (1) depends on the nature of aminoacids (2) has predominant role in the regulation of pancreatic secretion at low perfusion rate but is less effective when superimposed on a mechanical stimulus caused by duodenal distension (3) is a major stimulus for gall bladder contraction which is not influenced by duodenal distension.
本研究的目的是通过在 Vater 壶腹注入各种刺激物，并在 Treitz 韧带处、高于阻塞球囊处收集十二指肠内容物，来测定十二指肠袢在人体胆胰分泌中的作用。以 10 ml/min 的速度灌注第一种氨基酸混合物——苯丙氨酸（47.2 mmol）、蛋氨酸（38.2 mmol）、色氨酸（11 mmol）、缬氨酸（61.6 mmol）——与对照电解质溶液相比，可使血浆胆囊收缩素（CCK）浓度和十二指肠胆汁盐输出增加（p<0.005），但对胰腺酶分泌无显著影响；十二指肠注入另一种氨基酸混合物——精氨酸（32.4 mmol）、组氨酸（14.1 mmol）、亮氨酸（36 mmol）、异亮氨酸（21.5 mmol）、赖氨酸（31 mmol）、苏氨酸（23 mmol）——对血浆 CCK 浓度、胆汁盐或胰腺酶输出无影响。通过以 2、5 和 10 ml/min 的速度灌注第一种氨基酸溶液和对照溶液，研究了十二指肠扩张和内源性 CCK 的各自作用。将对照溶液的灌注速度从 2 ml/min 提高到 5 ml/min 导致胰腺分泌显著增加（p<0.01），而在 10 ml/min 时无进一步增加。对照溶液的灌注速度不影响胆汁盐输出。在灌注氨基酸溶液期间，尽管 CCK 释放逐步增加，但胰腺分泌中唯一的显著变化是当输注速度从 2 ml/min 提高到 5 ml/min 时脂肪酶输出增加（p<0.05）。我们的结果表明，十二指肠 CCK 释放（1）取决于氨基酸的性质（2）在低灌注速度下对胰腺分泌的调节起主要作用，但当叠加在十二指肠扩张引起的机械刺激上时效果较差（3）是胆囊收缩的主要刺激因素，不受十二指肠扩张的影响。
