Grönroos J M
Department of Pathology, University of Turku, Finland.
Eur Surg Res. 1991;23(3-4):222-7. doi: 10.1159/000129156.
Recently we indicated that pancreatic secretory stimulation with pancreozymin superimposed on chronic alcohol intake increases the tissue necrosis in rat pancreas caused by intraductal bile salt administration, and proposed a new theory of the pathogenesis of acute alcoholic pancreatitis. The purpose of the present work was to study whether secretin and alcohol have a similar damage-expanding coeffect in this experimental model of acute pancreatitis. Though secretin treatment seemed to increase the pancreatic necrosis slightly in both alcoholic animals (four groups, n = 5 in each group) and control animals (four groups, n = 5 in each group), no difference was found in the amount of tissue necrosis between alcohol-treated and control animals after secretin treatment and intraductal taurocholate. The mean percentages of necrosis in pancreatic parenchyma were 21.7, 16.1 and 16.3% in alcoholic groups and 15.9, 19.9 and 17.6% in control groups, when secretin was given 15, 45 and 90 min before sodium taurocholate. When preceding secretin stimulation was not given, the mean percentage of necrosis caused by taurocholate was 13.3% in alcoholic animals and 12.0% in control animals. Taken together with our earlier studies the results suggest that the synergism between chronic alcohol intake and pancreozymin formerly reported is neither due to a different response of alcoholic animals from that of control animals to increased flow of pancreatic juice during taurocholate-induced experimental acute pancreatitis nor caused by malnutrition often associated with chronic alcoholism. These results give indirectly further support to the theory that alcohol-induced alterations in the pancreozymin pathway, particularly, may play a crucial role in the pathogenesis of acute alcoholic pancreatitis.
最近我们指出，在长期饮酒的基础上，用促胰液素刺激胰腺分泌会增加大鼠胰腺因导管内注入胆盐而导致的组织坏死，并提出了急性酒精性胰腺炎发病机制的新理论。本研究的目的是探讨在这个急性胰腺炎实验模型中，促胰液素和酒精是否具有类似的损伤扩大协同效应。尽管促胰液素治疗似乎在酒精处理组动物（四组，每组n = 5）和对照组动物（四组，每组n = 5）中都使胰腺坏死略有增加，但在促胰液素治疗和导管内注入牛磺胆酸盐后，酒精处理组和对照组动物的组织坏死量没有差异。当在注入牛磺胆酸钠前15、45和90分钟给予促胰液素时，酒精处理组胰腺实质坏死的平均百分比分别为21.7%、16.1%和16.3%，对照组分别为15.9%、19.9%和17.6%。当不给予促胰液素刺激时，牛磺胆酸盐导致的酒精处理组动物坏死平均百分比为13.3%，对照组为12.0%。结合我们早期的研究结果表明，先前报道的长期饮酒和促胰液素之间的协同作用，既不是由于在牛磺胆酸盐诱导的实验性急性胰腺炎期间，酒精处理组动物与对照组动物对胰液流量增加的反应不同，也不是由常与慢性酒精中毒相关的营养不良引起的。这些结果间接进一步支持了这样一种理论，即酒精引起的促胰液素途径改变，尤其可能在急性酒精性胰腺炎的发病机制中起关键作用。
