Owyang C, Dozois R R, DiMagno E P, Go V L
Gastroenterology. 1977 Nov;73(5):1046-9.
We have developed a canine model which allows simultaneous quantification of pancreatic enzyme outputs, duodenal volume flow, and pancreatic and duodenal pressures under physiological circumstances. Twelve studies on 4 conscious healthy dogs demonstrated that mean fasting pancreatic pressure was 5 to 10 cm H2O higher than mean fasting duodenal pressure. Furthermore, 8 min after ingestion of a meal, both the pancreatic and the duodenal pressure increased. Surprisingly, the mean duodenal pressure was higher than the mean pancreatic pressure 20 min after feeding. This relationship lasted for 30 min. Lastly, elevation of postprandial pancreatic pressure occurred concomitantly with increased pancreatic enzyme output, and duodenal pressure increased with increased duodenal volume flow. The observed large postprandial duodenal volume flows associated with duodenal pressures greater than pancreatic duct pressures may favor reflux of duodenal contents into the pancreatic duct. These relationships may be important in the pathogenesis of postprandial pancreatitis and in the induction of pancreatic cancer.
我们开发了一种犬类模型,该模型能够在生理情况下同时对胰腺酶输出量、十二指肠容积流量以及胰腺和十二指肠压力进行量化。对4只清醒健康犬进行的12项研究表明,空腹时胰腺平均压力比十二指肠平均压力高5至10厘米水柱。此外,进食后8分钟,胰腺和十二指肠压力均升高。令人惊讶的是,进食后20分钟,十二指肠平均压力高于胰腺平均压力。这种关系持续了30分钟。最后,餐后胰腺压力升高与胰腺酶输出量增加同时发生,十二指肠压力则随十二指肠容积流量增加而升高。观察到的餐后十二指肠容积流量大且十二指肠压力高于胰管压力,可能有利于十二指肠内容物反流至胰管。这些关系可能在餐后胰腺炎的发病机制以及胰腺癌的诱发中具有重要意义。