Effects of ethanol on the sphincter of Oddi: an endoscopic manometric study.

The effects of ethanol, given either intragastrically or intravenously, on the sphincter of Oddi was evaluated by endoscopic manometry. In 12 subjects intragastric ethanol (150 ml of 32%) was given over 10 minutes. In five control subjects saline solution (150 ml of 0.9%) was given intragastrically instead of ethanol. In five other subjects ethanol was infused intravenously (6 ml/kg of 10%) for 36 minutes. Ethanol given intragastrically produced a significant inhibitory effect on sphincter of Oddi pressure. Peak pressure fell from a control value of 75.7 +/- 26.35 mmHg to 39 +/- 15.39 mmHg (p less than 0.001) at 35 minutes. Basal pressure fell from a control value of 30.17 +/- 19.47 mmHg to 11.83 +/- 6.35 mmHg (p less than 0.01) at 35 minutes. Wave height fell from a control value of 41.33 +/- 15.4 mmHg to 27.16 +/- 11.25 mmHg (p less than 0.02) at 35 minutes. No effects on sphincter of Oddi wave frequency were observed. No significant modifications of sphincter motor activity were observed after intragastric saline infusion. Ethanol given intravenously also produced an appreciable inhibitory effect on sphincter of Oddi pressure, without affecting its wave frequency.     

Influence of cholangiography on biliary sphincter of Oddi manometric parameters

BACKGROUND: When sphincter of Oddi manometry (SOM) and endoscopic retrograde cholangiopancreatography are performed at the same session, SOM is usually performed immediately before ductography because of concern about the accuracy of the manometric recording after contrast medium injection. However, it would be preferable to inject contrast medium first to identify other causes for a patient's symptoms, allowing selective use of SOM. The aim of this study was to evaluate the effect of cholangiography on sphincter of Oddi (SO) basal pressure. METHODS: Twenty-five patients with suspected SO dysfunction were prospectively studied. Conventional station pull-through manometry of the biliary part of the sphincter was performed before and after cholangiography. The intraductal pressure and basal sphincter pressure were evaluated. RESULTS: The mean intraductal pressure was 8+/-5.5 mm Hg before and 13.3+/-6.8 mm Hg after contrast medium injection (p< 0.01). However, the basal sphincter pressure was not significantly altered (52.9+/-42.1 mm Hg vs. 55.1+/-38.1 mm Hg, p = 0.52). Concordance (normal vs. abnormal) between the basal sphincter pressure before and after ductography was seen in 24 of 25 patients (96%). CONCLUSIONS: Intraductal installation of contrast medium immediately before SOM infrequently alters SO basal pressure in a clinically significant manner. We therefore believe that this sequence can be utilized in clinical practice.     

Influence of cholecystectomy on sphincter of Oddi motility

Background—Gall bladder and sphincter of Oddi (SO)function are coordinated by hormonal and neuronal mechanisms. Nervefibres pass between the gall bladder and the SO via the cystic duct. Itis therefore possible that cholecystectomy may alter SO motility.
Aim—To investigate the effect of cholecystectomyon SO function
Methods—SO manometry was performed in five women(median age 52 years), a few days before and six months afterlaparoscopic cholecystectomy which was undertaken for uncomplicatedcholelithiasis. Basal and post-cholecystokinin (CCK) SO motility were measured.
Results—All patients were symptom free afterlaparoscopic cholecystectomy. Prior to surgery common bile ductpressure, and tonic and phasic SO motility were normal and phasiccontractions were inhibited by intravenous CCK (1 Ivy Dog Unit/kg). Sixmonths later, common bile duct pressure and baseline tonic and phasic activity were unchanged but CCK failed to suppress phasic activity.
Conclusion—Cholecystectomy, at least in the shortterm, suppresses the normal inhibitory effect of pharmacological dosesof CCK on the SO. The mechanism of this effect is unknown but it couldbe due to SO denervation.

Keywords:sphincter of Oddi; cholecystectomy; cholecystokinin

     

Effect of pirenzepine on motility of Oddi's sphincter]

Pirenzepine (Gastrozepin) has a proven positive effect in the treatment of peptic ulcers by blocking the so called muscarinic acetylcholine receptors of the gastric glands. Reports of positive results with pirenzepine in the treatment of acute pancreatitis led to new discussions about its biological effects. It is thought that there are three ways by which pirenzepine acts in the pancreas. It decreases enzymatic secretion and it increases the secretion of sodium bicarbonate and water. Furthermore, it is said to have a spasmolytic effect on the sphincter of Oddi. To prove this spasmolytic effect we performed endoscopic manometry at the sphincter of Oddi with intubation of the pancreatic duct in 12 healthy patients. After two minutes of manometric registration of the normal sphincter activity 6 patients received 10 mg pirenzepine i.v. while a control group of 6 patients received 2 ml of 0.9% NaCl i.v. During the next 5 minutes the basal pressure of the sphincter, the amplitude of concentrations, as well as their frequency and duration were monitored. There were no changes noticed in the placebo group. However, pirenzepine caused a considerable decrease of the 4 manometric parameters of the sphincter of Oddi in all patients. Within 5 minutes the basal tonus fell from 14.3 +/- 5.1 mm of mercury to 9.0 +/- 6.0 (p less than 0.01). The frequency of contractions dropped from 5.8 +/- 2.7 per minute to 2.0 +/- 2.1 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

A controlled study of the effect of midazolam on abnormal sphincter of Oddi motility

BACKGROUND: The effect of a medication on sphincter of Oddi motility should be characterized if it is to be used during sphincter of Oddi manometry. Controversy exists as to whether midazolam influences sphincter of Oddi motility. This study assessed the effect of midazolam on the hypertensive sphincter of Oddi. METHODS: The study population consisted of 36 patients who presented with recurrent abdominal pain resulting from sphincter of Oddi dysfunction. The study was nonrandomized, prospective, and placebo controlled. Patient allocation was consecutive. Sphincter of Oddi manometry was performed in standard fashion. Manometric tracings were interpreted while the investigator was blinded to treatment allocation. Eighteen patients in the test group received 2 mg of midazolam intravenously whereas the 18 patients in the control group received saline solution intravenously. Manometric parameters were measured before and 3 minutes after the intravenous infusion. Changes in manometric findings before and after the administration of saline solution and midazolam were compared. RESULTS: Midazolam caused a significant reduction in basal sphincter of Oddi pressure (24 mm Hg) as compared with saline solution (p < 0.001). Diagnostic concordance (normal vs. abnormal) between the basal sphincter pressure before and after midazolam was seen in only 77% of patients. CONCLUSIONS: Midazolam significantly altered sphincter of Oddi motility. The decrease in sphincteric pressures would have altered diagnosis and management in 4 of 18 patients. Midazolam should not be used during sphincter of Oddi manometry.     

Effects of sphincter of Oddi motility on the formation of cholesterol gallstones

AIM: To investigate the mechanisms and effects of sphincter of Oddi (SO) motility on cholesterol gallbladder stone formation in guinea pigs.METHODS: Thirty-four adult male Hartley guinea pigs were divided randomly into two groups, the control group (n = 10) and the cholesterol gallstone group (n = 24), which was sequentially divided into four subgroups with six guinea pigs each according to time of sacrifice. The guinea pigs in the cholesterol gallstone group were fed a cholesterol lithogenic diet and sacrificed after 3, 6, 9, and 12 wk. SO manometry and recording of myoelectric activity were obtained by a multifunctional physiograph at each stage. Cholecystokinin-A receptor (CCKAR) expression levels in SO smooth muscle were detected by quantitative real-time PCR (qRT-PCR) and serum vasoactive intestinal peptide (VIP), gastrin, and cholecystokinin octapeptide (CCK-8) were detected by enzyme-linked immunosorbent assay at each stage in the process of cholesterol gallstone formation.RESULTS: The gallstone formation rate was 0%, 0%, 16.7%, and 83.3% in the 3, 6, 9, and 12 wk groups, respectively. The frequency of myoelectric activity in the 9 wk group, the amplitude of myoelectric activity in the 9 and 12 wk groups, and the amplitude and the frequency of SO in the 9 wk group were all significantly decreased compared to the control group. The SO basal pressure and common bile duct pressure increased markedly in the 12 wk group, and the CCKAR expression levels increased in the 6 and 12 wk groups compared to the control group. Serum VIP was elevated significantly in the 9 and 12 wk groups and gastrin decreased significantly in the 3 and 9 wk groups. There was no difference in serum CCK-8 between the groups.CONCLUSION: A cholesterol gallstone-causing diet can induce SO dysfunction. The increasing tension of the SO along with its decreasing activity may play an important role in cholesterol gallstone formation. Expression changes of CCKAR in SO smooth muscle and serum VIP and CCK-8 may be important causes of SO dysfunction.     

Cyclic motility of the sphincter of Oddi

The sphincter of Oddi has a cyclic motility that is closely associated with the duodenal migrating motor complex during fasting. This close association affects the bile flow mechanism and may play several roles in keeping the intestine clean and maintaining the migrating motor complex. The cyclic motility of the sphincter of Oddi changes after surgery and abnormal motility causes biliary dyskinesia. In this article, the gastrointestinal migrating motor complex and cyclic motility of the sphincter of Oddi are reviewed for better understanding of biliary and gastrointestinal physiology and the relationship between the two phenomena.     

生长抑素对Oddi括约肌功能的影响

天然生长抑素(somatostatin,SST)是一种胃肠激素及神经肽,主要分布于神经和消化系统中,具有广泛的生物学效应. 消化系SST大多由胰腺和胃肠黏膜中的D细胞分泌,能抑制胃肠运动及多种激素分泌. SST调节作用由G蛋白偶联受体,即生长抑素受体(somatostatin receptor,SSTR)介导. Oddi括约肌(sphincter of Oddi,SO)位于十二指肠乳头周围,是一结构和功能相对独立的器官,其运动主要受神经、激素、Cajal间质细胞的调节. SST对SO的作用尚存在争议,本文就生长抑素对SO功能的影响进行综述.     

Prospective evaluation of droperidol on sphincter of Oddi motility

BACKGROUND: Droperidol increasingly is used as an effective adjunct for conscious sedation during endoscopic procedures. Given the concern for the effects of narcotics and benzodiazepines on sphincter of Oddi motility, and the potential difficulty in sedating patients undergoing sphincter of Oddi manometry, droperidol could be an ideal agent in this setting. METHODS: Over a 43-month period, consecutive patients undergoing sphincter of Oddi manometry were studied prospectively. Sphincter of Oddi manometry was performed under general anesthesia in all but 10 patients. Standard retrograde pull-through techniques were used to examine the biliary and/or pancreatic sphincter, depending on the indication for sphincter of Oddi manometry. After the initial two pull-throughs, 5 mg of droperidol were given intravenously and measurements were repeated 5 minutes later. RESULTS: A total of 55 patients were studied (42 women [76%], 13 men; mean age 43 years). The basal biliary sphincter pressures measured in 35 patients before and after droperidol were, respectively, 56 mm Hg and 48 mm Hg (p = 0.02); the basal pancreatic sphincter pressures measured in 22 patients before and after droperidol were, respectively, 92 mm Hg and 67 mm Hg (p = 0.29). By using a definition for sphincter of Oddi dysfunction of a basal pressure greater than 40 mm Hg, droperidol would have resulted in a change in diagnosis in 5 patients undergoing biliary manometry (one misclassified as sphincter of Oddi dysfunction, 4 misclassified as normal), and 6 patients undergoing pancreatic sphincter manometry (5 misclassified as sphincter of Oddi dysfunction, one misclassified as normal) (total 19% of procedures). No complication was associated with droperidol use. CONCLUSIONS: Droperidol alters basal sphincter pressures, which in some patients was clinically significant and would have resulted in misclassification. Although safe and well tolerated, droperidol appears to have subtle but clinically significant effects on the sphincter of Oddi.     

加贝酯对犬胰腺移植后Oddi括约肌及外分泌功能的影响

目的研究加贝酯对膀胱引流式犬胰腺移植后移植物Oddi括约肌(SO)和外分泌功能的影响。方法正常犬和膀胱引流式胰腺移植后犬应用加贝酯前后进行SO测压,检测移植后犬应用加贝酯前后尿中胰蛋白原激活肽(TAP)和淀粉酶水平。结果正常犬SO有规律收缩,基础压为(19．4±3．2)mmHg,收缩频率为(9．9±1．6)次／min,收缩幅度为(45．1±6．5)mmHg,动力指数为355．4±31．3。应用加贝酯后SO收缩频率和动力指数分别下降为(4．8±0．9)次／min和206．5±21．4,与用药前相比,差异均有统计学意义(P<0．01)。基础压和收缩幅度无明显变化(P>0．05)。胰腺移植后,犬移植物SO基础压和收缩频率分别升高为(27．2±5．6)mmHg和(13．8±2．5)次／min,收缩幅度缩小为(8．6±2．5) mmHg,动力指数无明显变化。移植犬应用加贝酯后,SO基础压、收缩频率、收缩幅度和动力指数分别降低为(18．6±2．9)mmHg、(8．6±2．5)次／min、(5．4±0．9)mmHg和136．9±3．5,与用药前相比,差异均有统计学意义(P<0．01)。用加贝酯后尿淀粉酶和TAP水平分别为(6 000±290)IU／L和(16．7±3．8) nom／L,与用药前相比,有显著性差异(P<0．01)。结论加贝酯可抑制犬SO运动,尤其胰腺移植后,抑制作用更加显著。加贝酯还可以降低膀胱引流式犬胰腺移植后尿中的胰蛋白酶原激活肽和尿淀粉酶水平,从而有助于防治移植物胰腺炎。     

Vector manometric study of the sphincter of Oddi in the dog: Functional and morphological correlation

The relationship between sphincter of Oddi pressure and the morphological structure of the sphincter was studied in eight dogs prepared with a duodenal cannula. Sphincter of Oddi manometry was performed in awake animals in three directions, ventral, left dorsal, and right dorsal, using a catheter with three radial side holes for recording at one level. The pressure in the ventral direction (26.6 ± 1.06 mmHg) (mean ± SEM) was significantly lower than that in the left and right dorsal directions (30.6 ± 1.42 and 31.2 ± 1.23 mmHg, respectively). This functional manometric difference in the three directions correlated closely with the morphological structure of the sphincter of Oddi; the sum of the thickness of the sphincter of Oddi muscle and duodenal proper muscle was greater on the dorsal than on the ventral side. To our knowledge, this is the first report of axial asymmetry in sphincter of Oddi pressure. (Received May 27, 1997; accepted April 24, 1998)     

Effect of nalbuphine on the motility of the sphincter of Oddi in patients with suspected sphincter of Oddi dysfunction

BACKGROUND: Nalbuphine is an ideal supplementary analgesic drug for midazolam-induced conscious sedation during operative endoscopy because it has no cardiovascular effect and only a moderate depressive effect on respiration. However, no data are available as to whether nalbuphine is suitable as an analgesic drug during endoscopic sphincter of Oddi manometry. The aim of the present study was to investigate the effect of nalbuphine on the sphincter of Oddi motility in patients with a suspected sphincter of Oddi dysfunction. METHODS: Seventeen patients who were suspected clinically to have SOD after cholecystectomy were prospectively investigated. Five mg of midazolam was administered intravenously before the procedure to induce conscious sedation. After approximately 5 minutes of stationary sphincter of Oddi manometry recording (baseline), either 10 mg of nalbuphine or saline solution (placebo) was administered intravenously in random fashion and pressure was recorded for a further 5 minutes. Maximum sphincter of Oddi basal pressure and average phasic contraction amplitude and frequency were measured before and after the infusion of the drug or saline solution. RESULTS: Nalbuphine administration effectively enhanced the sedation obtained with midazolam without any adverse effect. When the sphincter of Oddi manometric periods before and after the administration of nalbuphine versus placebo were compared, there was a significantly increased basal sphincter of Oddi pressure only in the nalbuphine group: respectively, 49 (18) and 77 (29) mm Hg (p = 0.003) versus 51 (24) and 49 (23) mm Hg (p = 0.9). The phasic contraction amplitude did not change in response to nalbuphine, but the phasic contraction frequency increased significantly, from 5 (3) to 8 (4) per minute (p = 0.04). CONCLUSIONS: Nalbuphine has a stimulatory effect on sphincter of Oddi motility in patients with a suspected sphincter of Oddi dysfunction. Nalbuphine should not be used as premedication before endoscopic ERCP if sphincter of Oddi manometry is to be performed.     

Effect of glyceryl trinitrate on the sphincter of Oddi motility and baseline pressure.

It is widely accepted that glyceryl trinitrate (GTN) effectively dilates the smooth muscles of blood vessels. A similar effect has been postulated on the smooth muscles in the gastrointestinal tract. In this study the motility of the sphincter of Oddi and the common bile duct pressure as determined by endoscopic manometry was investigated in nine patients before and after sublingual application of 1.2 mg GTN (nitro group). Eight untreated patients served as controls. Three minutes after application of GTN the papillary contraction amplitude decreased from 69.3 +/- 4.3 mmHg to 36.8 +/- 5.1 mmHg (p less than 0.005) and the papillary baseline pressure fell from 8.9 +/- 0.6 mmHg to 2.9 +/- 0.2 mmHg (p less than 0.005) respectively. The contraction frequency in the nitro group and all motility parameters in the control group remained unchanged. These results indicate that GTN does not influence the sphincter of Oddi motility, but it relaxes very effectively the sphincter of Oddi muscle. Thus, GTN should be taken into account for the treatment of biliary colic. In our endoscopic unit GTN proved to be useful as premedication for endoscopic examinations, particularly for the removal of small and medium size common bile duct stones through the intact papilla.     

加贝酯对犬胰腺移植后Oddi括约肌及外分泌功能的影响

目的 研究加贝酯对膀胱引流式犬胰腺移植后移植物Oddi括约肌(SO)和外分泌功能的影响.方法 正常犬和膀胱引流式胰腺移植后犬应用加贝酯前后进行SO测压,检测移植后犬应用加贝酯前后尿中胰蛋白原激活肽(TAP)和淀粉酶水平.结果 正常犬SO有规律收缩,基础压为(19.4 ± 3.2)mmHg,收缩频率为(9.9 ± 1.6)次/min,收缩幅度为(45.1 ± 6.5)mmHg,动力指数为355.4 ± 31.3.应用加贝酯后SO收缩频率和动力指数分别下降为(4.8 ± 0.9)次/min和206.5 ± 21.4,与用药前相比,差异均有统计学意义(P＜0.01).基础压和收缩幅度无明显变化(P＞0.05).胰腺移植后,犬移植物SO基础压和收缩频率分别升高为(27.2 ± 5.6)mmHg和(13.8 ± 2.5)次/min,收缩幅度缩小为(8.6 ± 2.5)mmHg,动力指数无明显变化.移植犬应用加贝酯后,SO基础压、收缩频率、收缩幅度和动力指数分别降低为(18.6 ± 2.9)mmHg、(8.6 ± 2.5)次/min、(5.4 ± 0.9)mmHg和136.9 ± 3.5,与用药前相比,差异均有统计学意义(P＜0.01).用加贝酯后尿淀粉酶和TAP水平分别为(6 000 ± 290)IU/L和(16.7 ± 3.8)nom/L,与用药前相比,有显著性差异(P＜0.01).结论 加贝酯可抑制犬SO运动,尤其胰腺移植后,抑制作用更加显著.加贝酯还可以降低膀胱引流式犬胰腺移植后尿中的胰蛋白酶原激活肽和尿淀粉酶水平,从而有助于防治移植物胰腺炎.     

Effects of morphine on the human sphincter of Oddi.

The effects of morphine on intraluminal pressures recorded from the sphincter of Oddi (SO) at endoscopic retrograde cholangiopancreatography in 19 patients who were without evidence of biliary or pancreatic disease were studied. Morphine was given in four successive doses of 2.5, 2.5, 5, and 10 micrograms/kg iv at five minute intervals. Morphine in subanalgesic doses increased the frequency of SO phasic pressure waves to a maximum of 10-12/min, caused the phasic waves to occur simultaneously along the sphincter segment, increased phasic wave amplitude from 72 (26) (SE) to 136 (31) mmHg, and increased SO basal pressure from 10 (1) to 29 (9) mmHg (p less than 0.05). The effects of morphine on the SO are mediated by more than one opioid receptor type, as naloxone competitively antagonised the increase in phasic wave frequency induced by morphine, but did not affect the increase in SO basal pressure elicited by morphine. When given after naloxone, morphine decreased phasic wave amplitude, an inhibitory effect that is normally masked by morphine's dominant naloxone sensitive excitatory effect. Mu receptors do not appear to be involved in control of spontaneous SO motor function, as naloxone alone did not affect SO motor activity. The excitatory effects of morphine on the SO are not mediated by cholinergic nerves, as they were not blocked by atropine. Cholinergic nerves, however, may have a role in regulating spontaneous SO motor function because atropine alone depressed phasic wave activity and basal pressure. Although morphine does cause 'spasm' of the human SO, its effects are more complex than is commonly believed.     

Certain aspects of normal and abnormal motility of sphincter of Oddi

Applications of electromyographic and endoscopic manometric techniques in experimental and clinical studies have enhanced our knowledge of the normal physiology and motility disturbances of the sphincter of Oddi. The sphincter of Oddi has an active role in coordinating the time and rate of secretion of biliopancreatic juice into the duodenum. In the opossum, the sphincter of Oddi exhibits spontaneous contractions that migrate distally along the sphincter and expels its contents into the duodenum. Although the motor activity of the sphincter of Oddi is independent from that of the duodenum, there is a correlation between the frequency of bursts of spike potentials in the sphincter of Oddi and the migrating motor complex phases in the duodenum. Abnormal motility of the sphincter of Oddi has been reported during endoscopic manometric evaluation of patients with choledocholithiasis and sphincter of Oddi dyskinesia. Patients with common bile duct stones have an increase in the frequency of retrograde propagation of phasic waves. Elevation of basal pressure as well as an increase in the frequency and amplitude of sphincter of Oddi phasic waves and the common bile duct-duodenum gradient pressure may occur in patients with sphincter of Oddi dyskinesia. Endoscopic manometric studies of the sphincter of Oddi may become an important method to diagnose sphincter of Oddi dyskinesia.     

Distension of the gall bladder inhibits sphincter of Oddi motility in humans.

Studies in animals have suggested a neural reflex between the gall bladder and the sphincter of Oddi. The aim of this study was to investigate whether sphincter of Oddi motility is altered by distension of the gall bladder in humans. Sphincter of Oddi motility was recorded intraoperatively in 10 patients undergoing elective cholecystectomy for gall stones. The manometry was performed by a triple lumen constantly perfused catheter which was introduced through the cystic duct and positioned across the sphincter of Oddi to record sphincter basal pressure, wave amplitude, and frequency of contractions. In five patients a separate catheter was introduced into the gall bladder after ligation of the cystic duct. This catheter was used to distend the gall bladder. Sphincter of Oddi pressures were measured before, during, and after the distension. In a separate control group of patients (n = 5) basal sphincter of Oddi activity was recorded without distension of the gall bladder. Distension of the gall bladder decreased sphincter of Oddi basal pressure from (mean (SD] 22.8 (8.5) mmHg to 18.6 (6.5) mmHg (p = 0.01, paired t test) and frequency of sphincter of Oddi contractions decreased from 2.6 (1.6) to 1.1 (1.3) contractions/min (p = 0.003, paired t test). The results were significantly different from those of the control group (p less than 0.05, unpaired t test) during the same time period (four minutes). Pulse rate and blood pressure were not affected by the gall bladder distension. The results suggest a local reflex between the gall bladder and the sphincter of Oddi that might be important in the regulation of the pressure within the bile ducts and flow across the sphincter. This reflex is likely to be neurally mediated and injuries to it may be important in the aetiology of postcholecystectomy sphincter of Oddi dysfunction.     

Prospective evaluation of adjunctive ketamine on sphincter of Oddi motility in humans

Background and Aim:  Performance of sphincter of Oddi manometry (SOM) at endoscopic retrograde cholangio-pancreatogram (ERCP) is technically demanding and requires that the patient be well sedated. Droperidol is used as an adjunctive agent in patients who are difficult to sedate. Concerns regarding the safety profile of droperidol and its effects on sphincter of Oddi motility has resulted in the search for other potent sedative agents that do not influence SOM readings. Ketamine, a dissociative anesthetic, is increasingly being used as an adjunctive agent for conscious sedation. This study evaluates the effect of ketamine on sphincter of Oddi motility when used as an adjunctive sedative agent during ERCP.
Patients and Methods:  This is a prospective study of 30 consecutive patients undergoing SOM who were difficult to sedate and required adjunctive ketamine. Manometry was initially performed with intravenous administration of diazepam plus meperidine or a combination of diazepam plus meperidine and midazolam. After the initial two pull-throughs, 20 mg of ketamine was administered intravenously and the measurements were repeated 5 min later.
Results:  The basal pressures of the biliary sphincter and of the pancreatic sphincter were not significantly altered by ketamine. By using a definition for sphincter of Oddi dysfunction of a basal pressure ≥40 mmHg, concordance (normal vs abnormal) between the basal sphincter pressure before and after ketamine was seen in 28 patients (93%). Ketamine also did not lead to a difference in phasic wave amplitude, duration, or frequency. No complication was associated with ketamine use.
Conclusions:  Ketamine at 20 mg did not significantly affect SOM parameters. Further studies are required to confirm our preliminary findings before ketamine can be added to the armamentarium of agents used for performance of sphincter of Oddi manometry.