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At least 19 recordsLinked to original sources
PubMed1997

Sincalide: a cholecystokinin agonist as an aid in endoscopic retrograde cholangiopancreatography--a prospective assessment.

Although several approaches to overcome difficult bile duct cannulation and gain free biliary access have been popularized, the use of gastrointestinal peptide hormonal agents such as sincalide, a cholecystokinin agonist, as an alternative method has not been evaluated. I have carried out a prospective, nonrandomized assessment of the use of sincalide for diagnostic and therapeutic endoscopic retrograde cholangiopancreatography (ERCP). Overall, sincalide was used in 23% (32/136) of ERCPs in 26.6% (29/109) patients. Sincalide was successfully used to (a) obtain a cholangiogram after initial failure using only a standard catheter in 12 of 19 patients; (b) precisely locate the papilla and bile duct orifice in five of five patients; (c) locate the bile duct opening to obtain a cholangiogram and free cannulation during needle-knife papillotomy or weeks later in five of seven and three of three patients, respectively; and (d) gain free access (deep cannulation) to the bile duct after a cholangiogram in 5 of 10 patients. The selected use of sincalide appears to enhance the success of diagnostic and therapeutic ERCP; however, perseverance alone may account for some of this success. Controlled, randomized trials comparing sincalide or nothing, sincalide or a sphincterotome, or sincalide or glide or guide wire in patients in whom initial attempts to obtain a cholangiogram are unsuccessful are warranted.

Biliary Tract Diseases↗
PubMed1981

Comparison of intravenous and intramuscular sincalide (C-terminal octapeptide of cholecystokinin) on gallbladder contraction in man.

The effects of intramuscular and intravenous sincalide on gallbladder contraction and visualization of the bile ducts were compared in a group of 37 subjects referred for oral cholecystography. The maximum reduction in gallbladder size observed after sincalide 400 ng/kg intramuscular, 54.7 +/- 7.2% (mean +/- SEM), occurred 25 min after injection and was significantly greater than that observed after sincalide 20 ng/kg intravenous, 26.5 +/- 8.2%. Maximum reduction after sincalide 100 ng/kg intramuscular was 47.3 +/- 8.2%. The common bile duct was visualized in 60 and 45% of subjects after intramuscular and intravenous sincalide, respectively. The use of intramuscular sincalide 400 ng/kg intramuscular is an effective and convenient adjunct to oral cholecystography when significant gallbladder contraction and visualization of the common bile duct is desired.

Adolescent↗
PubMed1983

Studies of gallbladder contraction using intramuscular sincalide.

Intramuscular sincalide (the carboxy terminal octapeptide of cholecystokinin) was evaluated as an agent for producing gallbladder contraction. Following oral cholecystography 35 patients received intramuscular sincalide in one of two dosages, 18 patients received intravenous sincalide, and six patients were given intramuscular placebo. Generalized symptoms, often similar to those noted clinically, were more common following intravenous injection of sincalide; gallbladder contraction was greater following intramuscular injection. Both of these findings may be related to lower but more sustained blood levels of sincalide following intramuscular administration. Intramuscular sincalide may be useful for further studies of the value of cholecystokinin cholecystography.

Cholecystography↗
PubMed1994

Protein c-fos induction in rat brain and spinal dorsal horn by sincalide and opioids in vitro.

Sincalide (CCK-8) is an antiopioid substance. In this study, we investigated the effects of sincalide and opioids on c-fos expression and their interaction in brain and spinal dorsal horn in vitro. Immunoprecipitation was used for detection of c-fos protein. The results indicated that 0.1 mumol.L-1 sincalide induced c-fos expression markedly in both brain (a 3.8-fold increase in c-fos protein level) and in spinal dorsal horn (a 3.6-fold increase). NDAP (a kappa receptor agonist) 0.1 mumol.L-1 showed some activating effects on c-fos expression, the c-fos protein level increased 2.7 and 2.6 times respectively in brain and spinal dorsal horn. Ohmefentanyl (Ohm, a mu receptor agonist) 0.1 mumol.L-1 also exhibited an inducing effect on c-fos protein production. Sincalide and NDAP exerted some additive effects on c-fos protein production in spinal cord. In contrast, the effect of sincalide on c-fos protein production is antagonistic to that of Ohm. The results suggested that there were changing patterns of interaction on c-fos expression between sincalide and opioids.

Animals↗
PubMed1999

Devazepide reversed effect of sincalide against morphine on rat jejunal activities.

AIM: To study the antagonism of sincalide to the effect of morphine and its mechanism. METHODS: The electrophysiologic and mechanic activities of rat jejunum in vitro were recorded. RESULTS: Acetylcholine (ACh, 150 nmol.L-1) increased the spike potential amplitude (SPA) and the number (SPN) of rat jejunum in vitro, followed by an increase of jejunal contraction amplitudes (CA), showing a positive correlation. Morphine 330 nmol.L-1 inhibited the potentiation of ACh, showing a negative correlation. Sincalide 0.7 nmol.L-1 antagonized the effects of morphine, i.e., the SPA and SPN were increased again, followed by an increase of CA. CCK-A receptor antagonist devazepide (10 nmol.L-1) reversed the antagonism of sincalide to the effect of morphine. CONCLUSION: Sincalide antagonized the effect of morphine which inhibited the potentiation of ACh on jejunal activities in vitro. The antagonistic effect of sincalide on morphine was mainly mediated by CCK-A receptor.

Action Potentials↗
PubMed1985

Practical hepatobiliary imaging using pretreatment with sincalide in 139 hepatobiliary studies.

Hepatobiliary studies were performed over a three-year period on 139 patients suspected of having cystic duct obstruction. Each patient was infused intravenously with sincalide, a C-terminal octapeptide of CCK, 15 minutes prior to the administration of the hepatobiliary imaging agent Tc-99m paraisopropyl iminodiacetic acid (PIPIDA). Analysis of the results demonstrated significant advantages in pretreating patients with sincalide in hepatobiliary studies in a small facility with a relatively large patient load. Most of our studies were completed within 2 hours without jeopardizing the sensitivity (97%) or accuracy (96%) of the test. The specificity (88%) was comparable to percentages reported by others. Most investigators have reported that chronic cholecystitis contributed to the majority of false-positive cases. In addition, inconsistency in the documentation of criteria for the determination of acute cholecystitis (surgical, radiologic, or histologic also could be a cause for such a discrepancy. Knowledge of some important variables may help improve the specificity of the test: an awareness of the following factors during scan interpretation: 1) the effectiveness of the sincalide pretreatment dose, 2) the patient's pretest status (fasting or nonfasting, postanalgesic medication or no analgesics), and 3) time limit for gallbladder visualization. With these variables in mind, the hepatobiliary imaging using pretreatment with sincalide is proven to be a practical procedure protocol with good sensitivity and accuracy as well as specificity.

Bile Duct Diseases↗
PubMed1998

Can sincalide cholescintigraphy fulfil the role of a gall-bladder stress test for patients with gall-bladder stones?

BACKGROUND: Patients referred to general surgeons for the treatment of gall-bladder stones were studied to evaluate the role of sincalide cholescintigraphy as a gall-bladder stress test in an effort to identify a group of patients whose pain was non-biliary in origin and who would not be improved by cholecystectomy. METHODS: Ten asymptomatic controls and 57 patients with gallstones and abdominal symptoms were studied. All patients were interviewed by an independent assessor who identified a group of patients in whom the role of gallstones in their presentation was uncertain (clinically possibly biliary group). All patients and controls underwent sincalide cholescintigraphy. The surgeons remained blinded to the study results throughout the study period. All patients were re-evaluated 6-12 months later to establish the ultimate diagnosis based on their therapeutic response. RESULTS: Several parameters of gall-bladder function were studied from analysis of the sincalide cholescintigram. Lag time, ejection period, ejection rate and ejection fraction did not differ significantly among controls, patients proven to have non-biliary disease and patients proven to have biliary disease. There were significant differences in mean gall-bladder filling fraction between proven biliary and proven non-biliary groups. However, the group of patients with clinically possibly biliary symptoms could not accurately be separated into those who benefited from cholecystectomy and those who improved without surgery on the basis of this parameter. CONCLUSIONS: Significant differences in gall-bladder filling fraction between symptomatic and asymptomatic gallstone patients were identified suggesting reduced gall-bladder compliance in symptomatic patients. However, the sincalide cholescintigram failed to emerge as a useful gall-bladder stress test. Even in the 1990s, assessment by an experienced surgeon appears to be the most appropriate way to select patients for cholecystectomy.

Abdominal Pain↗
PubMed1990

Sincalide-augmented quantitative hepatobiliary scintigraphy (QHBS): definition of normal parameters and preliminary relationship between QHBS and sphincter of Oddi (SO) manometry in patients suspected of having SO dysfunction.

Sphincter of Oddi (SO) dysfunction presents with vague abdominal pain and/or abnormal liver function tests, and is presumably due to SO stenosis or spasm. Clinical, laboratory, and imaging methods of diagnosis have been less than ideal. Initially, we determined normal quantitative hepatobiliary scintigraphy (QHBS) parameters both pre- and post-sincalide administration. Thirty-one "normals" were analyzed, and post-sincalide common bile duct (CBD) dynamics could be satisfactorily determined in 29 (94%) subjects. Normal values at sincalide-augmented QHBS are reported. Next, 10 patients suspected of having SO dysfunction were studied prospectively using SO manometry and QHBS. The two tests were in agreement in seven cases (4: normal CBD dynamics, 3: abnormal). In one case of advanced SO stenosis, QHBS was abnormal, but SO manometry could not be performed. In the two remaining cases, SO manometry and QHBS gave discordant results. Of greatest importance, no significant correlation existed between the quantitative parameters of these two tests. Sincalide-augmented QHBS is possible and may, in the future, be of value in the diagnosis of SO dysfunction and/or partial CBD obstruction.

Adult↗
PubMed1985

The role of sincalide cholescintigraphy in the evaluation of patients with acalculus gallbladder disease.

Thirty-six patients with biliary colic and normal oral cholecystograms, upper gastrointestinal tract roentgenograms, and results of gallbladder ultrasonography underwent sincalide-stimulated biliary excretion scanning. Nineteen of these patients subsequently underwent cholecystectomies. Gallbladder ejection fractions (EFs) ranged from 0% to 88% (mean, 38%) and nine of 19 patients had exact pain reproduction with sincalide. All patients except one (EF, 35%) were cured of their symptoms. However, five patients were also cured who had a normal EF (greater than 50%). Histologically, 11 gallbladders showed chronic cholecystitis and eight were normal. We conclude that the sincalide biliary excretion scan is a useful test to study this group of patients. In patients with a decreased EF, cholecystectomy can be recommended with a high probability of symptom relief. In patients with normal EFs, clinical judgment is required, as some of these patients (five of five in this series) may still benefit from operation.

Adult↗
PubMedDate not supplied

Sincalide-aided ultrasonography of the common bile duct as a predictor of biliary obstruction determined by ERCP and biliary manometry.

Sonographically observed changes in common bile duct caliber following intravenous sincalide injection were correlated with distal common duct pathology as defined by endoscopic retrograde cholangiopancreatography and biliary manometry. Thirty-two patients, 17 with prior cholecystectomies, were studied. In post-cholecystectomy patients, a 1-mm or greater diminution of duct caliber within 5 min represented a normal response. When gallbladder contraction occurred in normal patients with an intact gallbladder, no change or a diminution in duct caliber was observed. When gallbladder contraction was not observed, a normal response was considered to be the same as that in post-cholecystectomy patients with a diminution in duct caliber occurring. By using these criteria two false negatives, both with hypertensive sphincters of Oddi that responded normally to sincalide injection, were encountered. This technique was valuable in defining non-obstructed post-cholecystectomy dilated bile ducts which demonstrated a prompt diminution in caliber following sincalide injection.

Adult↗
PubMed1991

Kinevac (sincalide for injection)/Squibb Diagnostics.

Sincalide is a rapid-acting, synthetic analog of cholecystokinin for intravenous use in postevacuation cholecystography. Serious reactions to sincalide have not been reported. The intravenous administration of sincalide causes a prompt contraction of the gallbladder as compared to the stimulus of a fatty meal which causes progressive contraction that becomes maximal in about 40 minutes. The use of Kinevac to accelerate the transit time through the small bowel decreases the time and extent of radiation associated with fluoroscopy and length of the x-ray examination of the intestinal tract. Duodenal aspiration obtained after the administration of Kinevac provides a sample of concentrated bile for analysis of cholesterol, bile salts, phospholipids and crystals. When used in conjunction with secretin to stimulate pancreatic secretion, an aspirate is readily obtained for analysis of enzyme activity, composition and cytology. As the development of endoscopic manometry affords a modality to measure and record sphincter of Oddi pressures, the paradoxical responses noted to the intravenous administration of CCK during manometric evaluation supports the diagnostic value of Kinevac used as a provocative agent in the evaluation of biliary dyskinesia.

Cholecystography↗
PubMed1996

Should the presence of other diseases exclude subjects as controls in studies of gallbladder response to cholecystokinin octapeptide (sincalide)? Scintigraphic results in patients with malignancies but no known gallbladder disease.

Findings of hepatobiliary scintigraphy with intravenous cholecystokinin octapeptide (sincalide) were examined in 26 asymptomatic patients with various malignancies but no known pre-existing gallbladder disease, and normal hepatobiliary and gallbladder morphology on sonography. The maximum gallbladder ejection fraction (GBEF) following a 30 min infusion of 0.04 of micrograms kg-1 sincalide ranged from 2 to 100%, with a mean of 68%, a median of 78% and GBEF < 35% in five patients (19%), findings similar to those reported in 'normal' subjects. There was no correlation between decreased GBEF and the previous chemotherapy agents received, as well as with gallbladder wall thickness, volume, and whether the gallbladder or small bowel was seen first on scintigraphy. These results suggest that despite the presence of other diseases and histories which include extensive chemotherapy, asymptomatic patients with normal hepatobiliary sonography can serve as controls in studies of gallbladder contractility using sincalide.

Adult↗
PubMed1982

Treatment of vincristine-induced ileus with sincalide, a cholecystokinin analog.

Sincalide, a synthetic analog of cholecystokinin capable of stimulating bowel motility, has been administered to 12 patients with symptoms and signs of vincristine-induced ileus. Patients were given intravenous infusions of sincalide 0.01 microgram/kg/h over 2-24 h (mean, 8 h) for 1-12 days (mean, 5 days), usually until all evidence of ileus had resolved. Improvement was noted within 48 h of initiation of therapy in eight patients (75%), whereas marginal or no responses were observed in four patients. The mean duration of ileus was 3.6 days in responders and 7.7 days in nonresponders. Toxicity was minimal and consisted of diarrhea in two patients, in whom symptoms promptly resolved with discontinuation of the drug. Further explorations of this promising agent in the treatment of vincristine-induced ileus appears warranted.

Cholecystokinin↗
PubMed1999

Effect of atropine and sincalide on the intestinal uptake of F-18 fluorodeoxyglucose.

PURPOSE: Variable diffuse intestinal uptake of F-18 fluorodeoxyglucose (FDG) is commonly seen in patients undergoing positron emission tomography (PET) imaging. Diffuse high uptake can obscure a lesion, whereas occasional high focal uptake can mimic a lesion. The cause of intestinal FDG uptake and the parameters that influence the level of uptake are unknown. METHODS: We hypothesized that intestinal FDG uptake may result from smooth muscle peristalsis. We tested our hypothesis by comparing FDG uptake at baseline and after administration of two drugs (atropine and sincalide) that are known to affect intestinal motility. We performed FDG PET scans in random order in five healthy male volunteers without medication, after intramuscular administration of atropine, and after intravenous administration of sincalide. RESULTS: Qualitative comparison of the images before and after both medications did not show any significant difference in the level of intestinal FDG uptake. CONCLUSIONS: We conclude that intestinal FDG uptake is probably not caused by peristalsis. Mucosal uptake may be an alternative explanation.

Adult↗
PubMed2001

Normal values for sincalide cholescintigraphy: comparison of two methods.

PURPOSE: To establish normal gallbladder ejection fraction (GBEF) values for two sincalide (cholecystokinin [CCK]) infusion dose rates, 0.01 microg per kilogram of body weight infused for 3 minutes and 0.01 microg/kg infused for 60 minutes. MATERIALS AND METHODS: Twenty healthy subjects were examined. GBEFs were calculated for the 3-minute infusion and for each 15-minute interval for the 60-minute infusion. Normal values were determined by using the mean +/- 2 SDs and a more rigorous statistical analysis. RESULTS: With the 3-minute infusion, GBEFs were significantly more variable than with the 45- and 60-minute values for the 60-minute infusion (P < .01, .002). With intervals including 95% of the population, the GBEF lower normal range was 16.8% for the 3-minute infusion but 31% and 41% for the 45- and 60-minute values, respectively. GBEFs of less than 35% were noted in six (30%) of 20 healthy subjects with the 3-minute infusion but in only one with the 60-minute infusion. Hepatobiliary ultrasonography was performed in six of seven subjects with GBEF of 36% or less, and US findings in all six were normal. CONCLUSION: A 3-minute infusion of sincalide, 0.01 microg/kg, produces too variable a GBEF response to establish a clinically useful normal range. With 0.01 microg/kg infused for 60 minutes, clinically useful normal values were established at 45 and 60 minutes.

Adult↗
PubMed1982

The effect of intravenously administered sincalide on the human gallbladder during oral cholecystography.

Sincalide, the C-terminal octapeptide fragment of the cholecystokinin, was used to contract the gallbladder during routine oral cholecystography in 18 patients. In 14 patients clinically important contraction occurred. The average reduction in gallbladder size for these patients was 32.7% of the preinjection size (range 15.1%-67.9%). Within 8-12 minutes cystic duct visualisation occurred in 8 and common bile duct visualisation in 3 patients. Spasm of the gallbladder neck was found in 2 cases. The blood pressure and heart rate did not change significantly during the study. Six patients felt slight nausea for 1-4 minutes and two vomited. We conclude that sincalide may be useful in biliary tract function studies in special clinical conditions (i.e. upper abdominal pain with unknown aetiology).

Adult↗
PubMed1976

Cholecystokinetic cholecystography: efficacy and tolerance study of sincalide.

The intravenous administration of sincalide, the C-terminal octapeptide fragment of cholecystokinin, affords safe and effective means for gallbladder contraction with resultant cystic and common bile duct visualization. Intravenous sincalide circumvents the problem of unpredictability of response of the gallbladder to a fatty meal and variability in the rate of release of endogenous cholecystokinin. Peak gallbladder contraction occurs earlier than with a fatty meal.

Adult↗
PubMedDate not supplied

Pharmacological manipulation of sincalide (CCK-8)-induced suppression of feeding.

The current study involves an investigation of the possible neurotransmitter systems involved in the ability of exogenously administered sincalide (cholecystokinin octapeptide, CCK-8) to suppress feeding. Male rats previously trained to obtain food either during a daily 3-hr session, or conditioned to obtain food pellets on a fixed-ratio or fixed-interval schedule of reinforcement, were treated IP with CCK-8, following pretreatment with representative drugs of several pharmacological classes. Pretreatment with phenoxybenzamine, tolazoline, yohimbine, morphine, haloperidol or picrotoxin reduced the efficacy of CCK-8. However, pretreatment with naloxone or clonidine potentiated the suppressant action of CCK-8 on feeding. Propranolol, diphenhydramine, cimetidine, atropine, d-amphetamine, fenfluramine or diazepam pretreatment either had no effect or no consistent action in altering the activity of CCK-8. The ability of CCK-8 to suppress feeding was not altered by subacute treatment with the anorectics, d-amphetamine or fenfluramine, using a regimen known to induce tolerance. These data indicate that CCK-8 exerts a different mechanism of action than that of fenfluramine or d-amphetamine, and furthermore, that noradrenergic, dopaminergic, GABAergic or endogenous opioid systems either mediate or can modify the effect of CCK-8 on feeding.

Animals↗