Sári Réka, Pálvölgyi Attila, Rakonczay Zoltán, Takács Tamás, Lonovics János, Czakó László, Szilvássy Zoltán, Hegyi Péter
First Department of Medicine, Faculty of Medicine, University of Szeged, H-6701, Koranyi fasor 10, Hungary.
World J Gastroenterol. 2004 Dec 1;10(23):3470-4. doi: 10.3748/wjg.v10.i23.3470.
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.
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).
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.
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.
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。
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。
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。
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。