胆源性胰腺炎大鼠胰腺胆囊收缩素受体变化的实验研究

目的　探讨胆源性胰腺炎（biliarypancreatitis，BP）大鼠胰腺胆囊收缩素受体（cholecystokininreceptor，CCK-R）和血浆胆囊收缩素八肽（cholecystokininoctapeptide，CCK-OP）的变化及其之间的关系。　方法　采用放射受体分析法检测36只BP大鼠及36只对照组大鼠胰腺组织膜CCK-R和竞争性酶联免疫法检测其血浆CCK-OP的含量。　结果　胆胰管结扎后3h、6h及24h胰腺组织膜CCK-R的最大结合容量（Bmax）值为179.0±1.1、119.0±1.8、及114.0±1.4fmol/ml；平衡解离常数Kd值为0.26±0.01、0.13±0.07、0.14±0.01nM；6h及24hBmax值和Kd值与对照大鼠存在显著差异(P均＜0.05)。BP大鼠血浆CCK-OP含量各为12.55±2.10、0.81±0.16、0.79±0.24PM/L；与正常大鼠相比，胰腺CCK-R在术后6h及24h期间结合位点数减少，亲合力增大（P＜0.05）；血浆CCK-OP含量仅在术后3h与对照组大鼠差异有显著性意义（P＜0.05）。　结论　BP大鼠发病过程中，胰腺CCK-R及血浆CCK-OP均发生了明显的变化。

The alteration of cholecystokinin receptors in the pancreas in rats with experimental biliary pancreatitis

Objective　 To evaluate the alteration of cholecystokinin-receptor in the pancreas and plasma cholecystokinin-octapeptide in rats with biliary pancreatitis (BP), and the relation between cholecystokinin-octapeptide and cholecystokinin-receptor.　 Method　 By means of radioligand binding assay and competitive enzyme immunoassay, the pancreatic cholecystokinin-receptor and plasma cholecystokinin-octapeptide were investigated in rats with biliary pancreatitis reproduced by pancreatic bile duct ligation.　 Results　At 3 hr., 6 hr., 24 hr. after the ligation, the maximal binding capacity (Bmax) of CCK-R was 179.0±1.1, 119.0±1.8, and 114.0±1.4 fmol/ml in BP rats respectively. The dissociation constant(Kd) was 0.26±0.01, 0.13±0.07, and 0.14±0.01 nM in BP rats respectively. Compared with normal rats the Bmax and Kd in BP rats were significantly different at 6 h and 24 h (all P＜0.05). The contents of cholecystokinin-octapeptide in plasma were 12.55±2.10, 0.81±0.16, 0.79±0.24 PM/L in BP rats respectively, which was statistically different from control at 3 h (P＜0.05).　Conclusions　 Significant decrease of Bmax and Kd was observed in BP rats. The content of pancreas cholecystokinin-octapeptide in plasma increased in BP rats at 3hr(P＜0.05). These results suggest that alteration of pancreatic cholecystokinin-receptor and plasma cholecystokinin-octapeptide may play an important role in the pathogenesis of biliary pancreatitis.