Suppr超能文献

乙醇在体外抑制兔奥迪括约肌的运动。

Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro.

作者信息

Sári Réka, Pálvölgyi Attila, Rakonczay Zoltán, Takács Tamás, Lonovics János, Czakó László, Szilvássy Zoltán, Hegyi Péter

机构信息

First Department of Medicine, Faculty of Medicine, University of Szeged, H-6701, Koranyi fasor 10, Hungary.

出版信息

World J Gastroenterol. 2004 Dec 1;10(23):3470-4. doi: 10.3748/wjg.v10.i23.3470.

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 degrees). 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 mumol/L carbachol, 1 mumol/L erythromycin or 0.1 mumol/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 micromol/L) or erythromycin (1 micromol/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 0.6% ETOH suddenly and completely relaxed the SO. CCK (0.1 micromol/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.

摘要

目的

奥迪括约肌(SO)在乙醇(ETOH)诱导的胰腺炎中的作用存在争议。我们的目的是描述乙醇对基础状态及刺激状态下SO运动的影响。

方法

从白兔身上取出的SO置于器官浴槽中(Krebs溶液,pH7.4,37摄氏度)。测定2 mL/L、4 mL/L、6 mL/L和8 mL/L乙醇对括约肌收缩反应的影响。用0.1 μmol/L卡巴胆碱、1 μmol/L红霉素或0.1 μmol/L胆囊收缩素(CCK)刺激SO。

结果

4 mL/L的乙醇显著降低基线收缩幅度,从11.98±0.05 mN降至11.19±0.07 mN。然而,未观察到收缩频率有显著变化。与对照组(分别为10.50±0.01 mN、12.13±0.10 mN和3.53±0.13次/分钟、5.5±0.13次/分钟)相比,0.6%的乙醇显著降低了基线幅度和频率。此外,0.8%的乙醇导致SO完全松弛。0.1 μmol/L卡巴胆碱或1 μmol/L红霉素刺激基线幅度(分别增加82%和75%)和收缩频率(分别增加150%和106%)。在卡巴胆碱或红霉素刺激组中,2 - 6 mL/L的乙醇显著抑制幅度和频率。有趣的是,给予0.6%乙醇4 - 5分钟会突然使SO完全松弛。0.1 μmol/L CCK在1.60±0.24分钟内将基线幅度从12.37±0.05 mN刺激至27.40±1.82 mN。在此峰值后,幅度降至17.17±0.22 mN,并在实验期间保持恒定。频率在12.8±0.2次/分钟达到峰值,此后在实验剩余时间内恒定频率为9.43±0.24次/分钟。4 mL/L的乙醇显著降低幅度,从16.13±0.23 mN降至14.93±0.19 mN。然而,未观察到收缩频率有显著变化。6 mL/L的乙醇抑制CCK刺激组的幅度和频率,而8 mL/L的乙醇使SO完全松弛。

结论

乙醇强烈抑制基础状态、卡巴胆碱、红霉素及CCK刺激的兔SO运动。因此,在兔子摄入酒精期间,松弛的SO可能为胰液流入十二指肠开辟了道路。SO的这种松弛可能保护胰腺免受酒精诱导的损伤。

相似文献

1
Ethanol inhibits the motility of rabbit sphincter of Oddi in vitro.
World J Gastroenterol. 2004 Dec 1;10(23):3470-4. doi: 10.3748/wjg.v10.i23.3470.
2
The effect of ethanol on sphincter of Oddi motility in vitro.
J Surg Res. 1997 Jan;67(1):58-61. doi: 10.1006/jsre.1996.4939.
3
Effect of four medications associated with gastrointestinal motility on Oddi sphincter in the rabbit.
Pancreatology. 2009;9(5):615-20. doi: 10.1159/000212095. Epub 2009 Aug 4.
4
Interplay between nitric oxide and VIP in CCK-8-induced phasic contractile activity in the rabbit sphincter of Oddi.
World J Gastroenterol. 2005 Jun 7;11(21):3264-6. doi: 10.3748/wjg.v11.i21.3264.
5
Oddi sphincter function after canine auto-pancreas transplantation with bladder drainage.
World J Gastroenterol. 2003 Dec;9(12):2849-52. doi: 10.3748/wjg.v9.i12.2849.
6
The effect of peroxynitrite on sphincter of Oddi motility.
J Surg Res. 1999 Jan;81(1):55-8. doi: 10.1006/jsre.1998.5436.
7
Effect of hydroxyl radical (OH.) on sphincter of Oddi motility.
Digestion. 1997;58(5):452-7. doi: 10.1159/000201482.
9
Influence of motilin and cholecystokinin on sphincter of Oddi and duodenal mobility.
Am J Physiol. 1987 Nov;253(5 Pt 1):G679-83. doi: 10.1152/ajpgi.1987.253.5.G679.
10
Rabbit sphincter of Oddi and duodenal pressure and slow-wave activity. Effects of cholecystokinin.
Scand J Gastroenterol. 1994 Jun;29(6):537-44. doi: 10.3109/00365529409092469.

本文引用的文献

1
Duodenoscopy in treatment of acute gallstone pancreatitis.
Hepatobiliary Pancreat Dis Int. 2002 Nov;1(4):608-10.
3
Induction of duodenal motility activates the sphincter of Oddi (SO)-duodenal reflex in the Australian possum in vitro.
Auton Autacoid Pharmacol. 2002 Apr;22(2):109-17. doi: 10.1046/j.1474-8673.2002.00251.x.
4
Animal models in alcoholic pancreatitis--what can we learn?
Pancreatology. 2002;2(3):189-203. doi: 10.1159/000058033.
7
Acute pancreatitis.
J Am Osteopath Assoc. 2001 Apr;101(4 Suppl Pt 1):S6-9.
8
The effects of somatostatin and octreotide on the human sphincter of Oddi.
Eur J Gastroenterol Hepatol. 1999 Aug;11(8):897-901. doi: 10.1097/00042737-199908000-00015.
10
Effect of hydroxyl radical (OH.) on sphincter of Oddi motility.
Digestion. 1997;58(5):452-7. doi: 10.1159/000201482.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验