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Perfusion manometry of the sphincter of Oddi (SO) using a pneumohydraulic capillary infusion system records phasic wave activity superimposed on basal pressure. A triple-lumen catheter allows the recording of propagation of the phasic waves. Microtransducer manometry is an alternative that permits prolonged recording of biliary pressure without the need for infusion. A cyclic change is recognized in SO motility in coordination with the migrating motor complex (MMC) of the duodenum during fasting. SO contractions occur at maximal frequency and amplitude during phase 3 of the duodenal MMC. Using two microtransducer catheters placed by duodenoscopy, a cyclic elevation of biliary pressure can be recorded in concert with phase 3. These findings indicate that human SO contractions impede bile flow. SO dysfunction causing biliary-type pain can be diagnosed by manometry. The pressure elevation during phase 3 may contribute to the development of pain in patients with biliary dyskinesia. Gastrectomy and proximal duodenal transection were proven to affect sphincter motility, as evidenced by the paradoxical response to cholecystokinin. Choledocholithiasis and hepatolithiasis are associated with low basal pressure, presumably due to repeated injury to the sphincter by passing stones. SO and biliary manometry leads to better understanding of biliary dynamics and the pathophysiology of biliary diseases.

A comparative ultrasound and radiological investigation of gallbladder and hepatic tree function was made in patients after operation with creation of artificial stomach, Billroth I and Roux operations. The control group consisted of 30 unoperated patients. Scintigraphy discovered gallbladder dyskinesia in 12 (18.7%) patients of the study group and in 6 (20%) controls. Ultrasonography--in 15 (33.3%) patients of the study group, 5 (25%) patients after distal resection of the stomach with pyloriform gastroduodenoanastomosis, 18 (51.47%) patients operated by Roux and 5 (16.6%) controls, respectively. It is shown that normal transduodenal passage of food has a positive effect on gallbladder and liver functions.

Objective: The objective of the study was to study gall bladder volume in fasting and 45 minutes post-prandial, by real time ultrasound in healthy controls and diabetic patients with and without autonomic neuropathy and to compare them., Method: Age, Sex and body mass index (BMI) matched 50 healthy subjects and 10 patients with insulin dependent diabetes mellitus and 40 patients with noninsulin dependent diabetes mellitus were evaluated according to National diabetes Data Group of National Institute of Health (1979) criteria: 1. Fasting (overnight) venous plasma glucose concentration of > 140 mg/dl on two separate occasions. 2. Following ingestion of 75 gms of glucose, venous plasma glucose concentration of > 200 mg/dl at second hour and at one other occasion during two hour test. Autonomic neuropathy was assessed by the presence of symptoms like dysphagia, abdominal fullness, nausea, vomiting, diarrhea +/- nocturnal, faecal incontinence or constipation, dysuria, urinary incontinence, the gustatory sweating, impotence etc. and were confirmed by standing test for orthostatic hypotension, hand grip test, Valsalva test and deep breaths test., Result: The study showed that: 1. Patients of diabetes mellitus had statistically significant larger fasting gall bladder volumes and these values were highly significant amongst patients with autonomic neuropathy. 2. Patients of diabetes mellitus and statistically significant larger post fatty meal gall bladder volume and these values were highly significant in patients with autonomic neuropathy., Conclusions: We therefore conclude that impaired gall bladder contraction was found amongst patients of diabetes mellitus with autonomic neuropathy. The mechanism responsible for cholecystoparesis is attributed to vagal neuropathy. Incomplete gall bladder emptying leads to sequestration of cholesterol and nidus formation. Therefore gall bladder functions should be evaluated routinely in such patients and early intervention is recommended.

Background: Correlation between various gastrointestinal events and particular aspects of the migrating motor complex has been reported. This study correlates postcholecystectomy pain to variations in biliary pressure associated with the duodenal motor cycle., Methods: In 18 patients with postcholecystectomy pain and 10 control subjects, biliary and duodenal pressures were recorded simultaneously with microtransducers. After recording a spontaneous cycle, morphine was administered to induce a premature phase III and spasm of the sphincter of Oddi, and then cerulein was administered to stop the spasm., Results: Transient but significant elevations of biliary pressure occurred at duodenal phase III in both groups, but a greater percentage of the patients developed pain during phase III (89% vs. 20%, p<0.01). Morphine produced premature phase III and biliary pressure elevation, which were accompanied by pain more frequently in the patients than in the control subjects (78% vs. 30%, p<0.05). Biliary pressure dropped after the cerulein injection, relieving the pain in 13 of 14 patients and in 2 of 3 control subjects who had morphine-induced pain. The phase III-related pain was relieved by endoscopic sphincterotomy in 14 of 15 patients., Conclusions: The cyclic elevation of biliary pressure in coordination with phase III of the duodenal motor cycle may contribute to the development of pain in patients with postcholecystectomy biliary dyskinesia.

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.

It is shown in the article that the ultrasonic monitoring of the pancreas with dyskinesia of the gallbladder during different phases of interdigestive motility can be helpful in the diagnosis of early stages of pancreatitis, especially in the absence of clinical symptoms.

Background: Secretin administration induces a brief distinct dilatation of the main pancreatic duct in healthy persons, visible at ultrasonography. Several investigations have indicated that sonographic duct measurements before and after secretin injections are a useful tool in the diagnostic screening for pancreatic disease., Aims: Aim of this study was to evaluate the influence of aging on the test results., Methods: We examined prospectively two groups of patients with distinctly different mean age, measuring the pancreatic duct diameter sonographically before, 2, 4, 6 and 10 minutes after intravenous injection of 1 CU secretin per kilogram body weight. The examination was performed in all patients on account of abdominal complaints, and pancreatic disease could be excluded by further diagnostic procedures. Group 1 consisted of 22 patients, median age 30.5 years, Group 2: 21 patients, median age 68 years., Results: The younger patients (Group 1) had a mean basal pancreatic duct diameter of 1.6 mm. After secretin injection they showed dilatation reading 3. 1 mm, corresponding to 94% of the basal duct diameter. The older patients (Group 2), with a basal diameter of 1.9 mm, showed a duct enlargement of about 84% to 3.5 mm. There was no statistically significant difference between the two groups concerning extent and temporal development of secretin-induced pancreatic duct dilatation., Conclusions: The underlying mechanisms of response to secretin stimulation - hydrokinetic pancreatic function, sphincter of Oddi motor function, and extensibility of Wirsung's duct--do not seem to be impaired by aging. Thus, the ultrasound secretin test should be suitable for application in older patients.

After successful gallstone lithotripsy, biliary pain recurs in about one third of patients. However, gallstone recurrence can be shown in only 40-60% of these patients. Therefore, other causes, such as sphincter of Oddi dysfunction (SOD), may be suspected. Twenty-two consecutive patients with recurrent biliary pain after successful gallstone lithotripsy without evidence of gallstone recurrence at ultrasonography were enrolled. Liver tests were elevated in 13 patients and ERC showed a dilated bile duct in nine. All 22 patients underwent sphincter of Oddi (SO) manometry, bile sample analysis for microlithiasis, endoscopic sphincterotomy (ES), and bile duct exploration with a Dormia basket. Thereafter, the patients were clinically followed at bimonthly intervals. SO manometry revealed SOD in 15/22 patients. This was more often the case in patients with initially larger (>2 cm) or multiple stones than after lithotripsy for solitary small stones (P < 0.01). Microlithiasis was detected in one patient, another patient had small biliary calculi at bile duct exploration (both without SOD). After ES, 14/15 patients with biliary SOD but none of the five without SOD improved (median follow-up: two years; P < 0.01). The one patient with CBD stones became symptom-free after ES, while the patient with microlithiasis improved after additional cholecystectomy only. Overall, ES proved to be the adequate therapy in 15/22 patients (68%, median follow-up: 22 months). After gallstone lithotripsy, SOD is found in about two thirds of patients with recurrent symptoms but without gallstone recurrence. In this group CBD stones or microlithiasis are rare. Therefore, SOD has to be suspected in this situation and ES gives favorable results, even when performed on a clinical basis only (without SO manometry).

Impaired gallbladder motility plays an important role in the pathogenesis of benign gallbladder disorders. Defective gallbladder muscle contraction is associated with supersaturated bile with cholesterol and with pregnancy due to high circulating levels of progesterone. These abnormalities result in bile stasis that facilitates gallstone growth. A defective gallbladder muscle contraction may also contribute to the pathogenesis of acute and chronic cholecystitis. In addition, an impaired gallbladder contraction may be the source of recurrent biliary colicky pain in patients with acalculus gallbladder disease. The gallbladders of these patients have an abnormal ejection fraction of less than 35% in response to an intravenous infusion of cholecystokinin (CCK). Although histology of the gallbladder wall is grossly normal, the muscle cells are functionally abnormal, with an impaired response to agonists that act on membrane and cytosolic receptors.

Ultrasonic monitoring was conducted in patients with chronic cholecystitis, pancreatitis (n = 186) to study contractile and functional activities of the gallbladder, pancreas, duodenum. The motor and evacuatory function of the gallbladder and pancreas was found out to be dependable upon the phase dyskinesias of duodenum. An increased pressure in duodenal cavity tends to impair the processes of intracavitary digestion and motor and evacuatory function of the gallbladder, pancreas, and to affect the phase outflow of bile and pancreatic juice.

Bilification during the interdigestive period of duodenal motility was studied together with basal and stimulated duodenal intubation in healthy subjects and patients with chronic noncalculous cholecystitis, with a mode of medicamentous stimulation of the gallbladder contractile function being developed. An adequate response to the standard cholekinetic was recordable during the second phase of duodenal motility, which fact permitted reaching a conclusion that it is necessary that cholekinetic be administered just during the second phase when the gallbladder is most ready to evacuate bile directly through a probe during the interdigestive period and one hour after a meal during the digestive period.

Patients with biliary dyskinesia have symptoms consistent with biliary colic and an abnormal gallbladder ejection fraction (GEF) in the absence of cholelithiasis. Cholecystokinin hepatobiliary scan quantifies gallbladder function and may assist in selecting patients with acalculous biliary pain who would benefit from cholecystectomy. Seventy-eight patients with an abnormal GEF (< 35%) on cholecystokinin hepatobiliary scan without cholelithiasis were studied retrospectively. Patients were divided into groups based on diagnosis and treatment. In Group I, the patients who underwent cholecystectomy, 80 per cent (35 of 44) had complete symptomatic resolution whereas the remaining 20 per cent (9 of 44) had symptomatic improvement. Pathology reports demonstrated chronic cholecystitis in 95 per cent of specimens. Group II were patients with symptoms attributable to biliary dyskinesia, but did not undergo cholecystectomy. Persistence of symptoms was noted in 75 per cent (18 of 24) of patients whereas 25 per cent (6 of 24) had symptomatic resolution without any treatment. Group III consisted of patients with an abnormal ejection fraction who had improvement of symptoms after treatment for an alternative diagnosis (n = 10). These findings suggest that an abnormal ejection fraction does not always indicate gallbladder disease. Alternative diagnoses must be investigated and treated. Patients with persistent biliary type symptoms in combination with an abnormal GEF in the absence of other attributable causes can expect a favorable response to cholecystectomy.

This study evaluates the hypothesis that cerulein relaxes the sphincter of Oddi (SO) via nitric oxide (NO). The spontaneous motility and the response to cerulein on the canine SO were recorded using a constant-perfusion technique. N(G)-L-arginine-methyl-ester (L-NAME) increased the spontaneous motility and dose-dependently reduced the cerulein-induced inhibitory response of the SO. After treatment with L-NAME at higher doses, cerulein induced an excitatory response. This effect was reversed by treatment with excess L-arginine. Similar results were obtained using cholecystokinin octapeptide in place of cerulein. In separate studies, cerulein generated increases in intracellular cAMP and cGMP levels in the SO. This indicates that the intracellular mechanism mediating cerulein-induced relaxation involves the production of cAMP and cGMP. On the other hand, treatment with L-NAME absorbed the increase in cAMP and cGMP levels by cerulein. These studies demonstrate that cerulein relaxes the canine SO mainly via NO, increasing intracellular cAMP and cGMP levels.

As many as 163 young male patients with chronic noncalculous cholecystitis were studied for motility of the biliary tract. Normal findings were in 15.9% of cases. Hypocontractility of the gallbladder, hypermyotonia of the Oddi sphincter (with 33.7% and 44.2% respectively), and concurrent presence thereof were the most commonly seen types of dyskinesia. The results obtained suggest that the above abnormalities in motility of the biliary tract may have a part in the origination and/or progression of chronic cholecystitis.

This review is intended to summarize current information on neurohumoral regulation of the gallbladder and sphincter of Oddi motility under both physiological and pathological circumstances with emphasis on Hungarian contributions to today's knowledge. The mechanism of action of neurohumoral agents that interact on these segments of the biliary tract, and the explored details of the stimulation-contraction/relaxation coupling process of these substances, will be discussed. A modified classification of biliary tract motility disorders with new diagnostic and therapeutic approaches will also be provided. This information will aid understanding of the pathogenesis of motor disorders of the gallbladder and sphincter of Oddi, and will indicate possibilities for pharmacological exploitation in the treatment of diseases resulting from biliary tract motility abnormalities.

The availability of objective and quantitative diagnostic tests in recent years has allowed more precise documentation of biliary dyskinesia. Biliary dyskinesia consists of two disease entities situated at two different anatomical locations: sphincter of Oddi spasm, at the distal end of the common duct, and cystic duct syndrome, in the gallbladder. Both conditions are characterized by a paradoxical response in which the sphincter of Oddi and the cystic duct contract (and impede bile flow) instead of undergoing the normal dilatation, when the physiological dose of cholecystokinin is infused. Quantitative cholescintigraphy can clearly differentiate one disease entity from the other. The therapies of choice are sphincterotomy, sphincteroplasty or antispasmodics for sphincter of Oddi spasm and cholecystectomy for cystic duct syndrome. After quantitative cholescintigraphy, the final impression should identify the disease entity by name to assist the referring physician in making an appropriate therapeutic decision; a mere statement that a test is consistent with biliary dyskinesia is no longer sufficient.

Combined use of tubage with 2% solution of natural agent Shirsal and thermovibromassage of the right hypochondrium area for biliary dyskinesia promotes normalization of biliary system motility. The course of the procedures enhances the positive clinical trend and induces remission which persists for 6-8 months.

Background: The endoscopic measurement of sphincter of Oddi pressure is a technically difficult procedure requiring significant expertise. Intrabiliary pressure is technically easy to measure. Furthermore, since it is believed that the pathogenesis of pain in patients with sphincter of Oddi dysfunction is attributable to increased intrabiliary pressure, its measurement may be more clinically relevant than measurement of sphincter of Oddi pressure., Methods: Intrabiliary pressures were blindly measured in 54 patients who had sphincter of Oddi manometry for abdominal pain., Results: In all patients intrabiliary pressure was significantly higher in patients with sphincter of Oddi dysfunction than those with normal sphincter of Oddi pressure (19.6 +/- 2.2 vs 9.6 +/- 1.2 mm Hg; p < 0.01). These findings were similar when patients were stratified according to presence of intact gallbladder (19.3 +/- 1.6 vs 8.8 +/- 1.4; p < 0.01) and to patients without a gallbladder (20.1 +/- 3.8 vs 12/1 +/- 1.3; p = .034). There was positive correlation between intrabiliary pressure and sphincter of Oddi basal pressure. This correlation was significant both in patients with and without gallbladders., Conclusions: These data suggest that increased intrabiliary pressure may be a useful surrogate marker of sphincter of Oddi dysfunction.

Background: Idiopathic slow-transit constipation may be a pangastrointestinal motility disorder. We have screened patients referred to surgery for constipation for the presence of biliary dyskinesia., Method: Patients had cholecystokinin-augmented trimethyl-3-bromo iminodiacetic acid scans to measure gallbladder ejection fraction., Results: There is a significant difference in gallbladder ejection fraction between patients with idiopathic slow-transit constipation (median value, 28.5) compared with patients with other causes of constipation (median value, 71; Mann-Whitney, P = 0.0025)., Conclusion: Idiopathic slow-transit constipation may be a pangastrointestinal motility disorder.

Background: Technical improvement in endoscopic and manometric technique has allowed direct manometry of the human sphincter of Oddi (SO). The aim of the present review is to describe the present status of physiologic and clinical knowledge of the SO, with emphasis on contributions from Danish Gastroenterology., Results: The SO is a zone with an elevated basal pressure with superimposed phasic contractions. It acts mainly as a resistor in the regulation of bile flow. Neurohormonal regulation influences the motility pattern. The contractions are under the control of slow waves. Clinical subgroups show abnormalcy in SO manometric pattern especially in patients with biliary or pancreatic pain without demonstrable organic substrate. Evidence suggests that endoscopic sphincterotomy may be of benefit in these patients.

The paper presents the results obtained upon examination of inpatients with various types of biliary dyskinesia. The examination included: fraction chromatic duodenal intubation, stepwise manometry, cholecystography, ultrasound investigation of the liver, gall bladder, biochemical tests of the bile. Fraction duodenal intubation discovered gall bladder dysfunction. The manometry was necessary for diagnosis of duodenal hypertension. X-ray revealed primary defects in gall bladder motility. It is concluded that the diagnosis of functional disorders implies combined clinical and instrumental modalities.

The time course of biliary secretion of prostaglandins (PG)E1 and F2 alpha was studied in 20 patients with primary dysfunctions in the cholepoietic system. The studies indicated that baseline high PGE1 levels and slow increases in PGF2 alpha during vesical reflex might be one of the factors predisposing to biliary hypokinesia. In patients with Oddi's sphincter spasms, the period of active PGE1 synthesis coincides with that of sphincter spasm. It is suggest that the latter is due to PGE1-induced muscle spasm of the duodenum whose fibers are an integral part of the intricate muscle system of Oddi's sphincter. In Oddi's sphincter spasm concurrent with biliary dyskinesia, the curve of PGF2 alpha virtually little differs from that in Oddi's sphincter spasm alone. PGE1 increases at the closed sphincter stage in the same way as that elevates in isolated sphincter spasm, but in patients with biliary hypokinesia contaminant with Oddi's sphincter spasm PGE1 shows its concentration in the vesical reflex phase, which appears to result in biliary hypokinesia. PGE1 and PGF2 alpha imbalance is one of the links in the pathogenesis of biliary dyskinesia.

Objectives: to evaluate the treatment possibilities in different forms of sphincter of Oddi dysfunction (SOD), in particularly that of the hypertonic sphincter of Oddi dyskinesia (HOD, biliary type group III). In the first part of retrospective evaluation the higher complication rate of endoscopic sphincterotomy (EST) and its probable causes were analysed., Material and Methods: The frequency and reasons of post-EST complications were retrospectively evaluated in a three-year (1990-1992) EST material of two gastroenterological departments using identical treatment principles and methods. Endoscopic sphincterotomies performed for bile duct stone extraction or treatment of HOD in cholecystectomized patients were included only. The data of 308 patients were analysed regarding two areas: 1. EST was performed for HOD treatment in 20 patients, and in 288 patients for stone removal, 2. the diameter of common bile duct was found non-dilated in 40 patients, and dilated in 268 patients, respectively., Results: 1. The frequency of complications in the group of patients with EST for HOD treatment was significantly higher: 8/20 (40%) vs. 17/288 (5.9%) (p < 0.01). 2. There was also a significant difference in the percentage of total complications between the patients of nondilated bile ducts and those patients with dilated bile ducts: 8/268 (3.3%) vs. 17/40 (42.50%) (p < 0.01), detailed: bleeding: 4/268 vs. 6/40, pancreatitis: 4/268 vs. 10/40, and perforation: 0 vs. 1/40., Conclusions: Therapeutic endoscopic sphincterotomy is more hazardous in patients with non-dilated bile ducts, thus evidently also in patients suffering from the biliary III. type (hypertonic Oddi-sphincter dyskinesia) of sphincter of Oddi dysfunctions.

Fifty two diabetic patients and 15 healthy control subjects were prospectively studied for their gall bladder function by ultrasound examination. The fasting gall bladder volume (FGBV) was calculated by using ellipse formula from the dimension of gall bladder shadow seen on ultrasound screen in two different cuts. The contractility of gall bladder was measured by calculating post prandial ejection fraction (EF) of the gall bladder. The mean FGBV and EF in 52 diabetic patients was found to be 20.7 +/- 10.7 cc and 47.5 +/- 20.1%, which was not significantly different from that in normal controls. Age, sex, obesity, diabetic control and presence of dyspeptic symptoms had no impact in FGBV and EF. Diabetic symptoms had no impact in FGBV and EF. However, diabetics with longer duration of disease had poorer gall bladder contractility (p < 0.05). Patients with autonomic neuropathy (AN) had significantly larger FGBV but normal contractility. Our results suggest that (a) long standing diabetics may have poor gall bladder emptying predisposing to gall stone formation (b) patients with autonomic neuropathy have reduced tone of fasting gall bladder but normal contractility.

The main aim of our study was the investigation of gallbladder motility prior to gallstone formation in vivo in guinea pigs fed a lithogenic diet. In a first experiment guinea pigs were fed a lithogenic diet for 5, 15, 30 and 45 days. First gallstones (pigment calculi) appeared after 30 days diet application. The in vitro contractility after lithogenic diet remained unchanged. In a second experimental part the in vivo gallbladder contractility was measured in two experimental animal groups (control group and 21 days lithogenic fed guinea pigs). The isovolumetric pressure rise inside the gallbladder following the intravenous injection of 10(-9) mol/kg body weight ceruletid was the essential contractility parameter (intraluminal basal pressure 5 mm hg). Due to lithogenic feeding of 21 days--that means prior to gallstone formation--the isovolumetric pressure rise was significantly elevated (p < 0.01). Moreover we observed passive distensibility changes of gallbladder muscle due to muscular hyperplasia. The main result of this investigation is the fact that gallbladder muscle in guinea pigs fed a lithogenic diet response to ceruletid application with hypercontractility prior to provable pigment gallstone formation. However gallbladder hypomotility--believed to be a causal factor in cholelithogenesis--was not observed in our experimental conditions.

Standard biliary manometry, including cholecystokinin (CCK) provocation, was performed on 42 consecutive patients (36 F, 6 M, median age 45 years) with postcholecystectomy syndrome (PCS) who had no evidence of organic disease but who had objective clinical features suggesting sphincter of Oddi dysfunction (SOD) (classes I and II). Patients were subdivided into those with (N = 14) and without (N = 28) irritable bowel syndrome (IBS) using a validated symptom questionnaire based on the modified Rome criteria. Resting sphincter of Oddi (SO) motor parameters (basal pressure, contractile amplitude and frequency, and proportion of retrograde contractions), the presence of abnormal manometry, and the presence of an abnormal response to CCK were compared in the two groups. No significant differences in resting parameters of SO motor activity between patients with and without IBS were observed, and abnormal biliary manometry as a whole was not more prevalent in either group (8/13 and 18/27, respectively). An abnormal response to CCK (failure of complete inhibition of phasic contractions), however, was demonstrated in five of 12 patients with IBS compared with only one of 23 patients without IBS (P = 0.01). In patients with postcholecystectomy SOD, an abnormal response of the SO to CCK thus appears to be an important feature of the subset of patients with concomitant IBS.

The ampulla of Vater is strategically located at the confluence of the terminal end of the bile duct and the pancreatic duct. It is entwined by smooth muscle fibers often referred to as the sphincter of Oddi. As a result, the ampulla demonstrates dynamic motor activity. A variety of structural and functional abnormalities can involve the ampulla and the periampullary region. Disorders involving the ampulla often produce remarkably similar clinical features, such as acute pancreatitis, biliary colic, or jaundice. Therefore, it is important that patients with periampullary disorders are systematically studied using endoscopic retrograde cholangiopancreatography, sphincter of Oddi manometry, and endoscopic ultrasonography. Common disorders involving the periampullary region and state-of-the-art techniques for diagnosis and treatment of these disorders are discussed.

Endoscopic manometry and quantitative cholescintigraphy are the diagnostic cornerstones for the detection of suspected sphincter of Oddi dysfunction. In patients with recurrent biliary pain after cholecystectomy, endoscopic manometry proves an elevated sphincter of Oddi baseline pressure as the most common finding. The probability for the detection of an elevated baseline pressure in these patients is significantly correlated with the presence of certain clinical features (i.e. biliary pain and/or cholestasis and/or dilated bile duct and/or delayed drainage of contrast material after ERCP). Therefore, these features enable a clinical classification of patients with suspected sphincter of Oddi dysfunction. Isolated baseline pressure elevations in the pancreatic portion of the sphincter of Oddi were reported in patients with recurrent, idiopathic, acute pancreatitis. In patients with biliary sphincter dysfunction, therapeutic relief can be expected from pharmacological therapy, but controlled studies are lacking. However, the clinical value of endoscopic sphincterotomy could be established in this field. Despite endoscopic manometry is not a prerequisite for the performance fo endoscopic sphincterotomy in every case of suspected sphincter of Oddi dysfunction, in most patients endoscopic manometry allows the only definitive diagnosis of sphincter dysfunction. Further on, the clinical value of semi-invasive methods as alternative treatment strategies (i.e. botulinum-toxin, transcutaneous electric nerve stimulation, balloon dilation) for sphincter of Oddi dysfunction has to be evaluated in the future.

Mucous barrier resistance was studied in 232 duodenal ulcer patients with signs of exacerbation as shown by PAS-positive substances and acid mucopolysaccharides in antral mucosa of the stomach and duodenum as well as by gastric juice levels of gastromucoproteins, fucose and sialic acids. In addition, measurements were performed of biliary motility. The tests indicated that half of the ulcer patients developed biliary dyskinesia manifesting as hyperkinesia or hypokinesia. The resultant decrease in gastric mucins requires individual correction.

Sphincter of Oddi activity partly regulates bile flow into the small intestine. This regulation is mainly controlled by phasic contractions and basal tone of the sphincter, together with gallbladder contraction. Manometric studies of the sphincter have permitted a better understanding of its physiological role and implication in biliary dyskinesia symptoms. Motility abnormalities of Oddi's sphincter present classically as bouts of recurrent pain and/or idiopathic pancreatitis, that can be successfully cured by endoscopic sphincterotomy.

He-Ne laser irradiation of biologically active points and infrared laser irradiation of the liver were employed to improve gallbladder and sphincter functions, bile production and biochemistry, respectively, in a total of 57 patients with biliary dyskinesia presenting as hypokinetic dyskinesia of the gallbladder, hyperkinetic dyskinesia of the sphincter of Oddi or the combination of the two affections. Simultaneous use of the two kinds of laser irradiation appreciably shortens treatment duration, abolishes biliferous dysfunction, reestablishes physiological balance of bile components in case of its initial lithogenic potential.

Endoscopic manometry of sphincter of Oddi (SO) and serum levels of gastrin, glucagon, and somatostatin were measured in patients with postcholecystectomy syndrome (n = 12), asymptomatic cholecystectomy patients (n = 6), and controlled subjects (n = 14). Pentagastrin-stimulated gastric acid secretion test was also performed in part of patients who had symptoms or no symptoms after the removal of gallbladder. The results showed that the patients of symptomatic group had hypertonic dyskinesia of SO as shown by deep and wide waves superimposed on high basal pressure plateau of SO. The symptomatic group also had a higher serum level of gastrin and a greater BAO than those of other two groups. No difference of serum levels of glucagon and somatostatin was found among these three groups. The hypertonic dyskinesia of SO and hypergastrinemia are possibly important factors in the pathogenesis of postcholecystectomy syndrome.

Vasoactive intestinal polypeptide (VIP) has been postulated as a neuropeptide with inhibitory neurotransmitter activity in nonadrenergic noncholinergic pathways. Transcutaneous electric nerve stimulation (TENS) relaxes the lower esophageal sphincter in patients with achalasia. Such response is accompanied by a 30% increase in VIP concentrations in the systemic circulation. Since the sphincter of Oddi (SO) receives a very dense VIP nerve supply, we evaluate the effect of TENS on SO motor activity and on VIP plasma concentrations in patients with biliary dyskinesia and in healthy volunteers. TENS was performed with a pocket stimulator for 45 min. SO pressure and VIP levels were obtained before and after 45 min of TENS. In patients with SO dyskinesia, TENS produced a significant decrease in SO pressure from 80.1 +/- 11.9 mm Hg to 58.3 +/- 9.7 mm Hg p less than 0.01); this was accompanied by a significant increase in VIP plasma levels from 21.1 +/- 0.5 pg/ml to 32.6 +/- 1.5 pg/ml (p less than 0.01). In healthy volunteers, TENS did not produce significant changes in SO pressure. However, a significant increase in VIP plasma values was observed (p less than 0.01). No significant changes in amplitude, duration and frequency of SO phasic contractions were observed in either of the two groups evaluated. We conclude that, in patients with SO dyskinesia, TENS decreases SO basal pressure, possibly by a direct action of the released VIP in the systemic circulation. In healthy volunteers, TENS increases VIP plasma values without significant effect on SO basal pressure. These findings suggest that the response to TENS may be mediated by VIP. It is also possible that the alterations seen in patients with biliary dyskinesia may be due to impairment of the VIP nerve supply at the level of the SO.

The authors analyze data obtained in a complex clinico-instrumental study of the functional activity of the liver, portal and hepatic blood flow in 77 patients with different forms of dyskinesias of the biliary tract. Obtained data evidence in these patients development (against the background of cholestasis) functional insufficiency of the liver and involvement of its parenchyma associated with a moderate pressure increase in the portal vein, reduction of the hepatic blood flow intensity, increase of its lability that may be a proof of development (in patients with functional bile secretion disorders) of chronic diffuse inflammatory process in the liver with subsequent appearance of clinically clear portal hypertension.

The sphincter of Oddi is a small sphincter which is strategically placed at the junction of the bile duct and pancreatic duct with the duodenum. It regulates the flow of bile and pancreatic juice into the duodenum and prevents reflux of duodenal contents into the ducts. The structure of the sphincter of Oddi differs from species to species and consequently its physiological action varies in different species. Anatomical and immunohistochemical investigations have demonstrated that the sphincter of Oddi is richly innervated by cholinergic, adrenergic and peptidergic neurons. In addition, neural connections exist between the sphincter, gallbladder and proximal gastrointestinal tract. These nerves in addition to hormones are important in the control of sphincter of Oddi motility and function. The normal human sphincter of Oddi is characterized by prominent phasic contractions which are superimposed on a modest basal pressure. These contractions are present throughout the interdigestive period. The contractions and basal pressure are inhibited by ingestion of a meal or infusion of cholecystokinin octapeptide, thus enhancing the flow of bile and pancreatic juice into the duodenum. Sphincter of Oddi dysfunction has been described in patients who present with recurrent biliary type pain and no evidence of a structural cause for the pain. Motility disorders characterized as an elevated basal pressure, rapid contraction frequency, paradoxical response to cholecystokinin octapeptide or excess of retrograde contractions have been identified. A number of pharmacologically active substances have been used in an attempt to treat these patients. Such pharmaceuticals include nitrites, Ca2+ channel blockers and smooth muscle relaxants. Their effect is transient and side effects relating to cardiovascular actions preclude their longterm use. Division of the sphincter either endoscopically or by open operation has been demonstrated by prospective clinical trials to be the most efficacious treatment for patients with a stenosed sphincter manometrically demonstrated by a high basal pressure. Improved understanding of the controlling mechanisms of sphincter of Oddi motility and the pathophysiology of sphincter of Oddi dysfunction should assist in the development of effective pharmacotherapy for these disorders.

In up to 30% of cases of the so-called postcholecystectomy syndrome functional disturbances of the sphincter of Oddi are responsible for the clinical picture. These pathological changes in pressure and motility at the sphincter can be identified by means of endoscopic manometry. We found dysfunction of the sphincter of Oddi in 4 out of 10 patients with so-called postcholecystectomy syndrome. In 2 patients in whom the basal pressure was higher than 40 mmHg endoscopic papillotomy was performed, after which the patients remained symptom-free. In one case tachyoddi was diagnosed and in another case the proportion of retrograde sphincter contractions exceeded 50%. Endoscopic manometry at the sphincter of Oddi enables many of the as yet unclarified postcholecystectomy symptoms to be identified.

Secretion of prostaglandins (Pg) E and F2 alpha in bile in basic condition (without stimulation) and under stimulation with cholecystokinin (CCK) ("Boots", England, 1 unit/kg) in patients with fatty liver with normal (15) and hypokinetic (20) function of gallbladder by radioimmunoassay method was investigated. The mediator role of Pg F2 alpha in the realization of effect of CCK on the contractile function of gallbladder was found. It was concluded, that the disturbance of mediator effect of Pg F2 alpha in the hormone regulation of bile excretion may play an important role in the pathogenesis of biliary dyskinesia. This disturbance of mediator effect of Pg was connected with the reducing of concentration and debit Pg F2 alpha in bile, as well as with the slowing of maximal Pg excretion under stimulation with CCK.