Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro

Réka Sári, Attila Pálvölgyi, Z. Rakonczay, T. Takács, J. Lonovics, L. Czakó, Z. Szilvássy, P. Hegyi

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Pages (from-to)3470-3474
Number of pages5
JournalWorld Journal of Gastroenterology
Volume10
Issue number23
Publication statusPublished - Dec 1 2004

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Sphincter of Oddi
Ethanol
Rabbits
Cholecystokinin
Carbachol
Erythromycin
Alcohols
In Vitro Techniques
Baths
Duodenum
Pancreatitis
Pancreas
Control Groups

ASJC Scopus subject areas

  • Gastroenterology

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Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro. / Sári, Réka; Pálvölgyi, Attila; Rakonczay, Z.; Takács, T.; Lonovics, J.; Czakó, L.; Szilvássy, Z.; Hegyi, P.

In: World Journal of Gastroenterology, Vol. 10, No. 23, 01.12.2004, p. 3470-3474.

Research output: Contribution to journalArticle

@article{003689067fd342ebaaa5d54f125a3f3e,
title = "Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro",
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.",
author = "R{\'e}ka S{\'a}ri and Attila P{\'a}lv{\"o}lgyi and Z. Rakonczay and T. Tak{\'a}cs and J. Lonovics and L. Czak{\'o} and Z. Szilv{\'a}ssy and P. Hegyi",
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TY - JOUR

T1 - Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro

AU - Sári, Réka

AU - Pálvölgyi, Attila

AU - Rakonczay, Z.

AU - Takács, T.

AU - Lonovics, J.

AU - Czakó, L.

AU - Szilvássy, Z.

AU - Hegyi, P.

PY - 2004/12/1

Y1 - 2004/12/1

N2 - 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.

AB - 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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