Konturek S J, Krzyzek E, Bilski J
Institute of Physiology, Academy of Medicine, Krakow, Poland.
Regul Pept. 1991 Oct 1;36(1):85-97. doi: 10.1016/0167-0115(91)90197-o.
Previous studies demonstrated that pancreatic enzyme secretion in rats is stimulated by the diversion of pancreatic juice from the duodenum or by the inhibition of pancreatic proteinases in the intestinal lumen but little attention has been paid to the role of gastric secretion in this stimulation. This study, carried out on conscious rats with large gastric (GF) and pancreatic fistulas, confirms that diversion of pancreatic juice in rats with the GF closed results in the progressive stimulation of pancreatic secretion reaching the maximum similar to that induced by exogenous CCK. When the GF was kept open, the diversion resulted in only small increment in pancreatic secretion and this was accompanied by progressive increase in gastric acid outputs. Similar amounts of HCl (25-400 mumol/h) instilled intraduodenally (i.d.) in rats with the GF open fully reproduced the increase in pancreatic secretion observed after the diversion of pancreatic juice and this effect was completely abolished by the pretreatment with L-364,718, a specific CCK receptor antagonist. Pretreatment with omeprazole to suppress completely gastric acid secretion in the diverted state resulted in a decline in pancreatic secretion similar to that observed after opening the GF. Camostate given in graded doses (6-200 mg/kg) either i.d. or s.c. in rats with pancreatic juice returned to the duodenum caused a dose-dependent increase in pancreatic secretion, but after opening the GF or after omeprazole this increase was reduced by about 50% while after L-364,718 it was abolished. This study provides evidence that gastric secretion plays an important role in the pancreatic response to diversion of pancreatic juice or inhibition of luminal proteinases (but not to feeding) and the elimination of gastric acid reduces this response.
以往的研究表明，大鼠胰酶分泌可通过将胰液从十二指肠引流或抑制肠腔内的胰蛋白酶来刺激，但胃分泌在这种刺激中的作用却很少受到关注。本研究在具有大胃瘘（GF）和胰瘘的清醒大鼠身上进行，证实了在GF关闭的大鼠中，胰液引流会导致胰分泌逐渐受到刺激，达到与外源性CCK诱导的最大值相似的水平。当GF保持开放时，引流仅导致胰分泌有少量增加，同时胃酸分泌量逐渐增加。在GF完全开放的大鼠中，向十二指肠内（i.d.）注入相似量的HCl（25 - 400 μmol/h），完全再现了胰液引流后观察到的胰分泌增加，并且这种效应被特异性CCK受体拮抗剂L - 364,718预处理完全消除。用奥美拉唑预处理以在引流状态下完全抑制胃酸分泌，导致胰分泌下降，类似于打开GF后观察到的情况。在胰液回流到十二指肠的大鼠中，以分级剂量（6 - 200 mg/kg）经十二指肠内（i.d.）或皮下（s.c.）给予卡莫司他，会导致胰分泌呈剂量依赖性增加，但打开GF后或给予奥美拉唑后，这种增加减少了约50%，而给予L - 364,718后则被消除。本研究提供了证据表明，胃分泌在胰腺对胰液引流或肠腔蛋白酶抑制（但不是对进食）的反应中起重要作用，并且消除胃酸会降低这种反应。
