促胰液素在犬餐后胰腺分泌负反馈调节中的作用。

Imamura M, Lee K Y, Song Y, Moriyasu M, Chang T M, Chey W Y

Department of Medicine, University of Rochester Medical Center, New York.

Gastroenterology. 1993 Aug;105(2):548-53. doi: 10.1016/0016-5085(93)90733-s.

BACKGROUND

A negative feedback regulation of pancreatic exocrine secretion has been observed in fasting rats, pigs, and humans, but this phenomenon could not be found in fasting dogs. The aims of the present study were to investigate whether or not postprandial pancreatic secretion is regulated by a negative feedback mechanism and to determine if the mechanism is mediated by secretion and/or cholecystokinin (CCK) in dogs.

METHODS

In eight dogs prepared with gastric and Herrera's pancreatic cannulas, pancreatic juice was collected for 3 hours after feeding a mixed meal to measure volume, bicarbonate, and trypsin output. Peripheral venous blood was obtained to determine plasma immunoreactive secretin and CCK levels. Four groups of experiments were performed while pancreatic juice was diverted from the duodenum: (1) diversion of pancreatic juice alone, (2) intraduodenal infusion of fresh pancreatic juice while pancreatic juice was diverted, (3) intraduodenal infusion of 150 mg/h of trypsin and 300 mg/h of chymotrypsin, and (4) intraduodenal infusion of 0.1 mol/L NaHCO3.

RESULTS

Pancreatic secretion during diversion of pancreatic juice was significantly greater than that obtained while pancreatic juice was returned. Diversion-induced pancreatic hypersecretion was significantly suppressed by intraduodenal administration of pancreatic proteases, but it was not influenced significantly by 0.1 mol/L NaHCO3. The suppression by either pancreatic juice or proteases paralleled the decrease in plasma secretin response, whereas the CCK response remained unchanged. The inhibitory effect of pancreatic proteases on pancreatic secretion was blocked by a physiological dose of exogenous secretin, 0.06 clinical U.kg-1.h-1.

CONCLUSIONS

In dogs, postprandial pancreatic secretion is controlled by a negative feedback mechanism mediated mainly by the release of secretin, but not by CCK.

背景

在禁食的大鼠、猪和人类中观察到胰腺外分泌存在负反馈调节，但在禁食的狗中未发现此现象。本研究的目的是调查餐后胰腺分泌是否受负反馈机制调节，并确定该机制是否由狗的分泌物和/或胆囊收缩素（CCK）介导。

方法

对8只制备了胃和赫雷拉胰腺插管的狗，喂食混合餐后收集3小时的胰液，以测量其体积、碳酸氢盐和胰蛋白酶输出量。采集外周静脉血以测定血浆免疫反应性促胰液素和CCK水平。在胰液从十二指肠分流时进行了四组实验：（1）仅胰液分流；（2）胰液分流时十二指肠内输注新鲜胰液；（3）十二指肠内输注150mg/h的胰蛋白酶和300mg/h的糜蛋白酶；（4）十二指肠内输注0.1mol/L的NaHCO₃。

结果

胰液分流期间的胰腺分泌明显大于胰液回输时的分泌量。十二指肠内给予胰腺蛋白酶可显著抑制分流诱导的胰腺分泌亢进，但0.1mol/L的NaHCO₃对其无显著影响。胰液或蛋白酶的抑制作用与血浆促胰液素反应的降低平行，而CCK反应保持不变。生理剂量的外源性促胰液素（0.06临床单位·kg⁻¹·h⁻¹）可阻断胰腺蛋白酶对胰腺分泌的抑制作用。