Yoshinaga K, Washizuka M, Segawa Y
Department of Applied Research, Central Research Laboratories, Zeria Pharmaceutical Co., Ltd., 2512-1 Oshikiri, Kohnan-machi, Ohsato-gun, Saitama 360-0111, Japan.
Biol Pharm Bull. 2000 Nov;23(11):1318-22. doi: 10.1248/bpb.23.1318.
We evaluated the association between aggravation of pancreatitis and multiple factors enhancing pancreatic exocrine secretion using a rat model of pancreatic bile duct ligation (PBDL)-induced pancreatitis. Under fasting and non-fasting conditions, a PBDL group, a second group treated by hepatic bile duct ligation (BDL) and a third group treated by pancreatic duct ligation (PDL) were compared in terms of serum amylase (S-amylase) activity. The S-amylase activity in the PBDL group was higher than in the sham group. In the PDL group, the increase in S-amylase activity was lower than in the PBDL group. In the BDL group, no increase in S-amylase activity was observed. Diversion of pancreatic and/or bile juice in these groups resulted in no increase of S-amylase activity. Truncal vagotomy or injection of an anticholinergic drug or a cholecystokinin (CCK)1-receptor antagonist inhibited pancreatic exocrine secretion and S-amylase activity in the non-fasting PBDL group but not in the fasting PBDL group. These results suggest that retention of pancreatic juice in the pancreatic duct is necessary for the increase of S-amylase activity, and that dietary stimulation and impaired duodenal inflow of bile and pancreatic juice commonly enhance pancreatic exocrine secretion, acting synergistically as aggravating factors in pancreatitis. CCK and the vagus nerve system appears to be involved in enhancing pancreatic exocrine secretion with diet stimulation as an aggravating factor.
我们使用胰胆管结扎（PBDL）诱导的胰腺炎大鼠模型，评估了胰腺炎加重与多种增强胰腺外分泌的因素之间的关联。在禁食和非禁食条件下，比较了PBDL组、经肝胆管结扎（BDL）处理的第二组和经胰管结扎（PDL）处理的第三组的血清淀粉酶（S-淀粉酶）活性。PBDL组的S-淀粉酶活性高于假手术组。在PDL组中，S-淀粉酶活性的增加低于PBDL组。在BDL组中，未观察到S-淀粉酶活性增加。这些组中胰液和/或胆汁的改道未导致S-淀粉酶活性增加。在非禁食的PBDL组中，迷走神经干切断术、注射抗胆碱能药物或胆囊收缩素（CCK）1受体拮抗剂可抑制胰腺外分泌和S-淀粉酶活性，但在禁食的PBDL组中则不然。这些结果表明，胰管内胰液的潴留是S-淀粉酶活性增加所必需的，并且饮食刺激以及胆汁和胰液十二指肠流入受损通常会增强胰腺外分泌，作为胰腺炎的加重因素起协同作用。CCK和迷走神经系统似乎参与了以饮食刺激作为加重因素增强胰腺外分泌的过程。
