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Duodenal Contents (duodenal + content)
Selected AbstractsThe effect of equicaloric medium-chain and long-chain triglycerides on pancreas enzyme secretionCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2002T. Symersky Summary It has been shown previously that medium chain triglycerides (MCT) do not affect gallbladder emptying and cholecystokinin (CCK) release. The effect of MCT on exocrine pancreas secretion in humans is unknown. We have compared the effect of enteral administration of MCT versus long chain triglycerides (LCT) on exocrine pancreatic secretion. Eight healthy subjects (three female, five male; mean age 22 ± 1·9 years) participated in two experiments, performed in random order. Duodenal contents, obtained by aspiration, were used to calculated the output of pancreatic enzymes and bilirubin. An equicaloric amount of either MCT or LCT (2 kcal min,1) oil was continuously administered in the proximal jejunum for 2 h. Gallbladder volume was measured by ultrasonography and blood samples were drawn for determination of CCK. The experiments consisted of 1 h basal secretion, 2 h of continuous oil administration and 1 h poststimulation. During the LCT feeding the pancreatic enzyme secretion, bilirubin output, gallbladder emptying and CCK release increased significantly (P<0·05) over basal levels. MCT had no effect on pancreatic enzyme secretion nor gallbladder emptying or CCK release. We conclude that enteral administration of MCT in the proximal jejunum does not stimulate exocrine pancreatic secretion nor gallbladder contraction or CCK release, in contrast to an equicaloric amount of LCT. [source] Gastroduodenal reflux induces group IIa secretory phospholipase A2 expression and activity in murine esophagusDISEASES OF THE ESOPHAGUS, Issue 5 2010David Mauchley SUMMARY Exposure of esophageal epithelium to gastric and duodenal contents results in the histologic changes of hyperproliferation and mucosal thickening. We have previously shown that presence of secretory phospholipase A2 (sPLA2) is necessary to produce these histologic changes in a murine model of gastroduodenal reflux. We sought to determine the influence of gastroduodenal reflux (GDR) on sPLA2 protein and mRNA levels as well as enzyme activity in esophageal tissue. BALB/c (sPLA2+/+) mice (n= 28) underwent side-to-side surgical anastomosis of the first portion of the duodenum and GE junction (DGEA) resulting in continuous exposure of esophageal mucosa to mixed gastric and duodenal contents. Sham control mice (n= 14) underwent laparotomy, esophagotomy and closure. Real-time RT PCR was used to quantitate the influence of GDR on group IIa sPLA2 expression. Immunofluorescent staining was quantitated by digital microscopy using a specific antibody to identify and locate sPLA2 protein. A colorimetric assay was used to quantify total sPLA2 activity after standardization of protein levels. Statistical analysis was conducted using Student's t -test. Group IIa sPLA2 mRNA and protein levels were increased at 4 and 8 weeks compared with sham controls. This increase occurred in a time-dependent manner and correlated with esophageal mucosal thickness. Furthermore, sPLA2 enzyme activity was increased significantly at 4 and 8 weeks compared with untreated controls. The expression of group IIa sPLA2 as well as sPLA2 activity is induced by GDR. This novel finding indicates that sPLA2 may play a role in the development of the histologic changes produced by GDR in esophageal mucosa. [source] Exercise-induced cholangitis and pancreatitisHPB, Issue 2 2005JOHN G. TOUZIOS Abstract Background. Cholangitis requires bactibilia and increased biliary pressure. Pancreatitis may be initiated by elevated intraductal pressure. The sphincter of Oddi regulates pancreatobiliary pressures and prevents reflux of duodenal contents. However, following biliary bypass or pancreatoduodenectomy, increased intra-abdominal pressure may be transmitted into the bile ducts and/or pancreas. The aim of this analysis is to document that cholangitis or pancreatitis may be exercise-induced. Methods. The records of patients with one or more episodes of cholangitis or pancreatitis precipitated by exercise and documented to have patent hepatico- or pancreatojejunostomies were reviewed. Cholangitis was defined as fever with or without abdominal pain and transiently abnormal liver tests. Pancreatitis was defined as abdominal pain, with transient elevation of serum amylase and documented by peripancreatic inflammation on computerized tomography. Results. Twelve episodes of cholangitis occurred in six patients who had undergone hepaticojejunostomy for biliary stricture (N=3), Type I choledochal cyst (N=2), or pancreatoduodenectomy for renal cell carcinoma metastatic to the pancreas (N=1). Four episodes of pancreatitis occurred in two patients who had undergone pancreatoduodenectomy for ampullary carcinoma or chronic pancreatitis. Workup and subsequent follow-up for a median of 21 months have not documented anastomotic stricture. Each episode of cholangitis and pancreatitis was brought on by heavy exercise and avoidance of this level of exercise has prevented future episodes. Conclusion. Following biliary bypass or pancreatoduodenectomy, significant exercise may increase intra-abdominal pressure and cause cholangitis or pancreatitis. Awareness of this entity and behavior modification will avoid unnecessary procedures in these patients. [source] Effects of ,-glucanase and xylanase supplementation on gastrointestinal digestive enzyme activities of weaned piglets fed a barley-based dietJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 2 2009C. L. Fan Summary The effects of supplementing a barley-based diet for weaned piglets with exogenous ,-glucanase and xylanase on gastrointestinal digestive enzyme activities were investigated. Thirty-six cross-bred weaned piglets were randomly assigned to two groups with three pens based on sex and mass. Each group was fed on the diet based on barley with or without added ,-glucanase and xylanase (0.15%) for a 4-week period. The results showed that enzyme supplementation improved growth performance of piglets significantly (p < 0.05), but had no effect (p = 0.091) on average daily feed intake. The results also showed that supplementation of ,-glucanase and xylanase had no effect on pepsin activity in gastric contents but slightly decreased (p = 0.092) the pepsin activity in gastric mucosa. Meanwhile, no effect of enzyme supplementation on trypsin activity in duodenal contents was observed. However, the activities of amylase and lipase in duodenal contents were significantly (p < 0.05) decreased, whereas the activities of maltase, sucrase and ,-glutamyl transpeptidase (,-GT) in jejunal and ileal mucosa were enhanced significantly (p < 0.05). The improvement of disaccharidase and ,-GT activity may be attributed to the positive impacts of exogenous enzymes on digestion and absorption of the nutrients. In conclusion, the current results indicated that supplementation with enzymes in barley-based diets could improve the growth performance of piglets, decrease the activities of amylase and lipase in duodenal contents and increase the activities of disaccharidase and ,-GT in jejunal and ileal mucosa. [source] Morphine Concentrations in Stomach Contents of Intravenous Opioid Overdose DeathsJOURNAL OF FORENSIC SCIENCES, Issue 5 2009F.R.C.P.A., Johan Duflou M.Med.Path. (Forens.) Abstract:, Death caused by heroin overdose is almost always the result of intravenous injection of the drug in Australia. We briefly describe a case where a heroin overdose was initially thought to be the result of oral ingestion of the drug, primarily as a result of higher concentrations of morphine in stomach contents than in blood. During the subsequent criminal trial and investigation, however, the issue of the entero-hepatic circulation of morphine was raised as a possible reason for the presence of morphine in the stomach contents. In this study, we report on the distribution of opioids in blood, stomach contents, urine, liver, and bile in 29 deaths caused by intravenous heroin overdose. The mean total and free blood morphine concentrations were 0.60 and 0.32 mg/L, respectively, and the mean stomach contents total morphine concentration was 1.16 mg/kg. All cases had detectable morphine in the stomach contents, and 24 of 29 cases (83%) had higher concentrations of total morphine in stomach contents than in blood. The mean total morphine concentration in bile was c. 100 times that in blood, and the liver total morphine concentration averaged twice that of blood levels. We conclude that the entero-hepatic circulation of morphine and subsequent reflux of duodenal contents back into the stomach can result in the deposition of morphine in gastric contents. Consequently, the relative levels of opioids in blood and stomach contents cannot be used to determine the site of administration of the drug. [source] Acute pancreatic damage associated with convulsive status epilepticus: A report of three casesPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 6 2001Katsuhiko Ogawa Abstract Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures. [source] |