The effect of ethanol on the pancreatic duct sphincter of Oddi

Alcohol ingestion causes pancreatitis to develop in some people, but the mechanism(s) by which alcohol causes pancreatitis are unclear. The effect of alcohol on the pancreatic duct sphincter of Oddi (PD-SO) may play a significant role. To better understand the effects of alcohol on the PD-SO, we studied 24 alcoholic subject's PD-SO before and after 80 g of alcohol was instilled into their stomachs. Seventeen of the subjects had a prior history of pancreatitis. The mean maximal alcohol level achieved by 30 min after the instillation was 98.1 +/- 47.9 mg/dl. The only prealcohol differences between the pancreatitis group and the nonpancreatitis group were higher mean basal PD-SO pressures and higher mean phasic contraction amplitudes (8.7 and 20.2 mm Hg higher, respectively) in the pancreatitis group. The acute change in the subjects' blood alcohol levels produced similar changes in both groups. A non-statistically significant fall in the mean basal PD-SO pressure of 2.7 mm Hg was observed. The phasic contraction mean amplitude decreased by 24.1 mm Hg (p < 0.001) and the mean duration decreased by 0.6 s (p = 0.0064). The frequency of phasic contractions did not change after ingestion of alcohol. There was a significant fall in the percentage of antegrade phasic contractions (-15.8%, p = 0.016), which was compensated for by nearly equal increases in the percentage of retrograde and simultaneous contractions. We conclude that acute alcohol ingestion in subjects with a history of chronic alcohol consumption changes the PD-SO motor activity in a way that could predipose to duodenopancreatic reflux. Thus, reflux of bile, activated enzymes, or other substances into the pancreatic duct might occur more readily and predispose one to pancreatitis after alcohol ingestion.