Failure of secretin to increase sodium taurocholate-induced pancreatic necrosis in alcoholic rats.

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.