Kalloo A N, Pasricha P J
Section of Therapeutic Endoscopy, Johns Hopkins Hospital, Baltimore, Maryland 21287-4461, USA.
Dig Dis Sci. 1995 Apr;40(4):745-8. doi: 10.1007/BF02064972.
Although sphincter of Oddi (SO) dysfunction has been implicated in the pathogenesis of postcholecystectomy syndrome and pancreatitis, little is known about normal physiologic stimuli, such as intraduodenal fat on human SO motility. Furthermore, gastric distension that frequently accompanies endoscopic manometry has been shown in animal studies to affect SO motility. We evaluated the effects of intraduodenal fat and gastric distension on SO basal pressure. Asymptomatic volunteers had SO manometry performed while sequentially performing gastric distension and intraduodenal fat perfusion. Five subjects (ages 29.8 +/- 4.8 years, range 22-35 years) had a mean basal sphincter of Oddi pressure of 23.4 +/- 5 mm Hg (range 17-31 mm Hg). Injection of air into the stomach caused no appreciable change in either intragastric pressure or SO pressure. Intraduodenal fat infusion resulted in a decrease in mean SO basal pressure from 23.4 +/- 5.0 to 4.4 +/- 4.4 mm Hg (P = 0.004). These results demonstrate that gastric distension does not affect SO basal pressure and that intraduodenal fat infusion reduces SO basal pressure.
尽管Oddi括约肌(SO)功能障碍被认为与胆囊切除术后综合征及胰腺炎的发病机制有关,但对于正常生理刺激,如十二指肠内脂肪对人体SO运动的影响却知之甚少。此外,动物研究表明,内镜测压时常伴随的胃扩张会影响SO运动。我们评估了十二指肠内脂肪和胃扩张对SO基础压力的影响。对无症状志愿者进行SO测压的同时,依次进行胃扩张和十二指肠内脂肪灌注。5名受试者(年龄29.8±4.8岁,范围22 - 35岁)的Oddi括约肌基础压力平均为23.4±5 mmHg(范围17 - 31 mmHg)。向胃内注入空气对胃内压力或SO压力均未产生明显变化。十二指肠内注入脂肪导致SO基础压力平均值从23.4±5.0 mmHg降至4.4±4.4 mmHg(P = 0.004)。这些结果表明,胃扩张不影响SO基础压力,而十二指肠内注入脂肪会降低SO基础压力。