Experimental study for pathogenesis of chronic alcoholic pancreatitis

慢性酒精性胰腺炎（CAP）的发病机制尚不清楚。然而，胰管阻塞和缺血在cap中起重要作用。A组（n=9）：在制备胃瘘后，通过胃插管给予2.0 g kg^<-1> day^<-1>乙醇。O组（n=7）：小胰管结扎后，切开十二指肠，将聚乙烯管置入大胰管。AO组（n=9）： A、O组手法均应用于本组。C组（n=9）：仅开腹手术。3个月后再次开腹。O组可见轻度管周纤维化，无实质细胞损伤。AO组纤维化进一步扩展至导管周围和小叶间区，可见实质细胞损伤伴慢性炎症细胞浸润。分泌素试验显示，与对照组相比，AO组的流量、碳酸氢盐浓度和淀粉酶输出量均显著降低。与对照组相比，0组的流速和淀粉酶产量显著降低。与对照组相比，AO组胰腺血流量明显减少。我们的结论是，胰管阻塞增加了酒精引起的实质细胞损伤，血流减少对慢性酒精性胰腺炎病变有加重作用。这个模型非常具有人类CAP的代表性。

Pathogenesis of chronic alcoholic pancreatitis (CAP) has been unclear. However, pancreatic duct obstruction and ischemia play an important role in CAP.We prepared the following four groups.Group A (n=9) : after preparing a gastric fistula, 2.0 g kg^<-1> day^<-1> of ethanol was administered via a gastric cannula. Group O (n=7) : after ligation of the minor pancreatic duct, the duodenum was incised to insert a polyethylene tube into the major duct. Group AO (n=9) : both manipulations used in group A and O were applied to this group. Group C (n=9) : laparotomy only. Laparotomy was reperformed 3 months later in each group.In group O,mild periductal fibrosis was recognizad without parenchymal cell damage. In group AO,fibrosis extended further into the peri-ductal and inter-lobular regions, and parenchymal cell damage with chronic inflammatory cell infiltration was seen. The secretin test revealed a significantly decreased flow rate, bicarbonate concentration and amylase output in group AO when conpared to the control gloup. In group O,flow rate and amylase output were significantly reduced in comparison to that in control. In group AO,pancreatic blood flow was decreased significantly in comparison to that in control.We concluded that pancreatic duct obstruction increased the parenchymal cell damage induced by alcohol administration, and that decrease of blood flow has an aggravating effect on the chronic alcoholic pancreatitis lesion. This model was very representative of human CAP.