Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 1, 2004; 10(23): 3470-3474
Published online Dec 1, 2004. doi: 10.3748/wjg.v10.i23.3470
Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro
Réka Sári, Attila Pálvölgyi, Zoltán Rakonczay Jr, Tamás Takács, János Lonovics, László Czakó, Zoltán Szilvássy, Péter Hegyi
Réka Sári, Attila Pálvölgyi, Zoltán Rakonczay Jr, Tamás Takács, János Lonovics, László Czakó, Peter Hegyi, First Department of Medicine, Faculty of Medicine, University of Szeged H-6720, Koranyi fasor 10, Hungary
Zoltán Szilvássy, Department of Pharmacology, Medical University of Debrecen H-4032, Nagyerdei krt, 98, Hungary
Author contributions: All authors contributed equally to the work.
Supported by The Wellcome Trust (Grant No. 022618), and by the Hungarian Scientific Research Fund (D42188, T43066 and T042589)
Correspondence to: Péter Hegyi, M.D., Ph.D., First Department of Medicine, University of Szeged, H-6701, PO Box 469, Hungary. hep@in1st.szote.u-szeged.hu
Telephone: +36-62-545200 Fax: +36-62-545185
Received: April 10, 2004
Revised: May 12, 2004
Accepted: May 25, 2004
Published online: December 1, 2004
Abstract

AIM: 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 SO motility.

METHODS: SOs removed from white rabbits were placed in an organ bath (Krebs solution, pH7.4, 37 °C). The effects of 2 mL/L, 4 mL/L, 6 mL/L and 8 mL/L of ETOH on the contractile responses of the sphincter were determined. SOs were stimulated with either 0.1 μmol/L carbachol, 1 μmol/L erythromycin or 0.1 μmol/L cholecystokinin (CCK).

RESULTS: ETOH at a dose of 4 mL/L 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. ETOH (0.6%) 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 cycles(c)/min, respectively). Moreover, 0.8% of ETOH resulted in complete relaxation of the SO. Carbachol (0.1 μmol/L) or erythromycin (1 μmol/L) stimulated the baseline amplitudes (by 82% and 75%, respectively) and the contractile frequencies (by 150% and 106%, respectively). In the carbachol or erythromycin-stimulated groups 2-6 mL/L of ETOH significantly inhibited both the amplitude and the frequency. Interestingly, a 4-5 min administration of 6 mL/L ETOH suddenly and completely relaxed the SO. CCK (0.1 μmol/L) stimulated the baseline amplitude from 12.37 ± 0.05 mN to 27.40 ± 1.82 mN within 1.60 ± 0.24 min. After this peak, the amplitude decreased to 17.17 ± 0.22 mN and remained constant during the experiment. The frequency peaked at 12.8 ± 0.2 c/min, after which the constant frequency was 9.43 ± 0.24 c/min throughout the rest of the experiment. ETOH at a dose of 4 mL/L significantly decreased the amplitude from 16.13 ± 0.23 mN to 14.93 ± 0.19 mN. However, no significant changes in the contractile frequency were observed. ETOH at a dose of 6 mL/L inhibited both the amplitudes and the frequencies in the CCK-stimulated group, while 8 mL/L of ETOH completely relaxed the SO.

CONCLUSION: ETOH strongly inhibits the basal, carbachol, erythromycin, 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 rabbits. This relaxation of the SO may protect the pancreas against alcohol-induced damage.

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