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。A组(n=9)：造好胃瘘后，经胃管注入乙醇2.0g·kg~(-1)·d~(-1)。O组(n=7)：结扎小胰管后，切开十二指肠，在主胰管内插入聚乙烯管。AO组(n=9)：A、O两组均采用手法治疗。C组(n=9)：单纯剖腹手术。每组在3个月后再次开腹，O组仅见轻度导管周围纤维化，未见实质细胞损伤。在AO组，纤维化进一步扩展到导管周围和小叶间区，可见实质细胞损伤，并伴有慢性炎症细胞浸润。促胰液素试验显示，与对照Gloup组相比，AO组的尿流率、碳酸氢盐浓度和淀粉酶产量显著降低。与对照组相比，O组的流量和淀粉酶产量显著降低。与正常对照组相比，AO组大鼠胰腺血流量明显减少，提示胰管梗阻加重了酒精对胰腺实质细胞的损伤，血流减少对慢性酒精性胰腺炎的损伤有加重作用。该模型具有很强的人类CAP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.