Effect of ethanol on the motility of the sphincter of Oddi

Background: The role of the sphincter of Oddi (SO) in ethanol (ETOH)-induced pancreatitis is controversial. Our aim was to characterise the effect of ETOH on basal and stimulated rabbit SO motility.

Methods: SOs removed from white rabbits were placed in an organ bath containing Krebs solution. The effects of 0.2, 0.4, 0.6 and 0.8% of ETOH on the contractile responses of the SO were determined. The SOs were stimulated with either 0.1µM carbachol (C), 1µM erythromycin (E) or 0.1µM CCK.

Results: (1) ETOH at a dose of 0.4% significantly decreased the baseline contractile amplitude from 11.98±0.05 mN to 11.19±0.07 mN, however, no significant changes in the contractile frequency were observed. 0.6% of ETOH significantly decreased both the baseline amplitude and the frequency compared to the control group (10.50±0.01 mN, 12.13±0.10 mN and 3.53±0.13 c/min, 5.5±0.13 c/min, respectively). Moreover, 0.8% of ETOH resulted in complete relaxation of the SO. (2) 0.1µM C or 1µM E stimulated the baseline amplitudes (by 82% and 75%, respectively) and the contractile frequencies (by 150% and 106%, respectively). The C or E-stimulated groups 0.2–0.6% of ETOH significantly inhibited both the amplitude and the frequency. 0.6% of ETOH completely relaxed the SO. (3) 0.1µM CCK stimulated the baseline amplitudes and the frequencies. 0.4–0.6% of ETOH inhibited both the amplitudes and the frequencies in the CCK-stimulated group, while 0.8% of ETOH immediately and completely relaxed the SO.

Conclusions: ETOH strongly inhibits the basal, C, E and CCK-stimulated rabbit SO motility. Therefore, it is possible that during alcohol-intake the relaxed SO opens the way for pancreatic fluid to flow out into the duodenum in rabbit. This relaxation of the SO may protect the pancreas against alcohol-induced damage.