Assessment of pancreatic enzyme secretory capacity by a modified Lundh test.

BACKGROUND: The Lundh test is a usual means of estimating the enzyme secretory capacity of the gland. During this procedure, however, a major proportion of the test meal is removed from the duodenum together with the gastric, duodenal, and pancreatic secretions and the bile. This study was undertaken to compare the pancreatic enzyme secretion induced by the Lundh procedure with that resulting from stimulation of the normal digestive process, by reinfusion of the aspirated duodenal juice. METHODS: Nine men (mean age: 46.7, range 42-55 yr) free from pancreatic disease were studied. Pancreatic secretion was measured via a multiple lumen tube by aspiration of the duodenal juice. After a basal period the Lundh test meal was placed in the stomach and the duodenal juice was completely aspirated. On a separate day, the procedure was repeated, but the aspirated duodenal juice was reinfused into the upper jejunum. RESULTS: In the first 30 min of the test period, the enzyme outputs were the same on both test days. In the 30-60-min period, the lipase output, and in the 75-90-min period, the amylase output was significantly lower during the Lundh test compared with the jejunal reinfusion test. The CCK levels were significantly above the basal level at 20 and 40 min, but the increase was significantly lower during the traditional Lundh test. No significant difference in gastrin release was observed during either the Lundh or the reinfusion test. CONCLUSIONS: In the traditional Lundh test, the trypsin secretory capacities of the gland are measured appropriately, but the lipase and amylase secretory capacity and the CCK release are not fully represented compared with the reinfusion test. An association between the lower CCK release and lipase amylase secretion is suggested.

Stimulated gastrointestinal hormone release and gallbladder contraction during continuous jejunal feeding in patients with pancreatic pseudocyst is inhibited by octreotide.

BACKGROUND: Continuous enteral feeding, the old-new therapeutic modality in the treatment of patients with acute pancreatitis and those with complications is considered to bypass the cephalic, the gastric, and (at least in part) the intestinal phase of pancreatic secretion. The aim of this study was to test the GI hormonal changes and gallbladder motility during CJF in patients with pancreatic pseudocysts following acute pancreatitis, with or without octreotide pretreatment. PATIENTS AND METHODS: In 15 patients with pancreatic pseudocysts, an 8-French (8F) nasojejunal catheter was positioned into the jejunum distal to the ligament of Treitz during duodenoscopy. On test d 1, blood samples were taken for CCK, gastrin, insulin-like immunoreactivity (IRI), glucagon, and glucose measurements prior to and at 20, 40, 60, and 120 min following jejunal saline infusion at a rate of 2 mL/min. The gallbladder volumes were determined simultaneously by ultrasonography. On test d 2, CJF (175 kcal/h) was started by the same route and at the same infusion rate. Analogous measurements were performed as indicated above. On test d 3, 100 microg of octreotide was administered subcutaneously and the previous procedure was repeated. The plasma level of CCK and glucagon and the serum levels of IRI and gastrin were determined by bioassay and radioimmunoassay (RIA), respectively. RESULTS: Significant changes in hormone levels were not observed during jejunal saline perfusion. However, the levels of CCK (5.7+/-0.9 pmol), gastrin (10.6+/-1.3 pmol/L), IRI (27.2+/-5.8 microIU/mL), glucagon (322.8+/-32.4 pg/mL), and glucose (5.8+/-1.0 mmol/L) were significantly increased at 20 min during CJF vs the saline controls (2.0+/-0.3 pmol, 6.8+/-1.1 pmol/L, 7.8+/-0.4 microIU/mL, 172.8+/-33.4 pg/mL, and 4.5+/-0.5 mmol/L, respectively) and remained elevated at 40, 60, and 120 min. Octreotide pretreatment eliminated the increases in CCK, gastrin, IRI, and glucagon levels observed during CJF alone. The significant decrease in gallbladder volume during CJF was also prevented by octreotide pretreatment. CONCLUSION: Continuous jejunal feeding (CJF) elicited significant increases in gastrointestinal (GI) regulatory hormone (cholecystokinin [CCK], gastrin, IRI, and glucagon) levels and evoked a consecutive gallbladder contraction. These biological responses are eliminated by octreotide pretreatment. Further clinical studies are needed to assess the eventual therapeutic effect of octreotide during CJF in patients with pancreatic pseudocyst.

Effect of a liquid meal given as a bolus into the jejunum on human pancreatic secretion.

Major features of pancreatic secretion stimulated by a meal depend on intestinal phase mechanisms. However, an intrajejunal (i.j.) meal infusion is widely used for the treatment of inflammatory pancreatic diseases when the resting of the gland is desired. This study was undertaken to compare the effects of an intragastric (i.g.) and an i.j. complete fluid (Lundh) test meal on pancreatic enzyme secretion. Eight men (mean age, 43 years; range, 31-48) free from pancreatic disease were studied. Pancreatic secretion was measured via a multiple-lumen tube by aspiration of the duodenal juice. After a fasting period, the Lundh test meal was placed in the stomach or the upper jejunum. After the i.g. administration of the test meal, the aspirated duodenal juice was reinfused into the jejunum. The effect of atropine infusion (0.5 microg/kg/h) on the pancreatic enzyme secretion was studied. The pancreatic amylase, trypsin, and lipase outputs were determined. The plasma levels of cholecystokinin (CCK) and of gastrin were measured by bioassay and radioimmunoassay, respectively. The trypsin, amylase, and lipase secretions increased significantly after either an i.g. or an i.j. test meal intake. The trypsin, amylase, and lipase outputs were significantly decreased during the i.j. perfusion as compared with i.g. administration. The gastrin levels increased significantly after i.g., but remained unchanged after i.j. administration. The CCK release attained its maximum 40 and 60 min after the i.g. and i.j. test meal, respectively. However, the CCK release was significantly lower during the i.j. administration as compared with i.g. perfusion. An atropine infusion significantly reduced the i.g. and i.j. test meal-stimulated enzyme outputs. An i.j.-administered meal stimulates the pancreatic enzyme secretion, but this effect is significantly lower than that which occurs on i.g. administration. The i.j. meal-stimulated secretion of pancreatic enzymes is subject to both cholinergic and peptidergic regulation. The deficiency of gastrin and the delayed and decreased CCK release are believed to account for the reduced enzyme output.

[Comparative analysis of diagnoses by the referring family physician and the hospital admission committee in ambulatory patients at an internal medicine department]. / A háziorvosi beutalókban és a klinikai véleményekben szerepló diagnózisok összehasonlító elemzése nagy forgalmú belgyógyászati ambulancia beteganyagában.

The objectives of the present study were, as follows: 1. To what rate do the primary care doctors refer their patients to the regional internal medicine emergency department? 2. What sort of problems are the reasons of the referring? 3. To what extent are the opinions of the referring doctors confirmed or reviewed by the specialists? 4. What rate of the referred patients are admitted or discharged after the urgent consultations and-or interventions. 5. What kind of additional tests were used by the institutional caregivers in order to make accurate diagnoses? 6. What was the fate of the unaccepted patients? Data were collected in the patient document archive of the First Dept. of Medicine of the Albert Szent-Györgyi Medical University, Szeged, Hungary. Each patients' referring notes and inpatient charts between September 15th, 1995 and January 15th, 1996 were studied in a retrospective way. Upon the results of the study, it was concluded, as follows: The primary care doctors referred their patients with right orientation diagnosis to the emergency department in 70% of the cases. 45.8% of the referred pts. were admitted to the internal inpatient ward. The agreement of the referring and discharge diagnoses was greater (85.7%) among the admitted patients as compared to the unaccepted ones (56.8%). 14% of the referred pts. were referred to other specialists by the internists. On the basis of the results the actual messages of the study for an under- and postgraduate medical teaching group, and for the health care politicians are discussed in the paper.

Beneficial effect of lovastatin on sphincter of Oddi dyskinesia in hypercholesterolemia and hypertriglyceridemia.

This report describes an impaired sphincter of Oddi relaxation function in relation to hypercholesterolemia and hypertriglyceridemia. As indicated by repetitive amyl nitrite-augmented quantitative hepatobiliary scintgraphy, normalization of serum lipids by means of diet and a 3-month treatment period with 20 mg of lovastatin per day resulted in an improvement of sphincter of Oddi relaxation.

Calculation of dose, dose equivalent, and relative biological effectiveness for high charge and energy ion beams.

The Green's function for the transport of ions of high charge and energy is utilized with a nuclear fragmentation database to evaluate dose, dose equivalent, and RBE for C3H10T1/2 cell survival and neoplastic transformation as a function of depth in soft tissue. Such evaluations are useful to estimates of biological risk for high altitude aircraft, space operations, accelerator operations, and biomedical applications.

[Direct dissolution therapy of biliary tract calculi]. / Az epeúti kövesség direkt oldószeres kezelése.

The aim of this study was to evaluate the effect of a recently developed biphasic multicomponent solvent in 39 patients with biliary duct stones that are too large (15-35 mm) to be removed after endoscopic sphincterotomy. From November 1991 to October 1993, 37 patients with common bile duct stones were papillotomized during endoscopic retrograde cholangiography and a nasobiliary catheter was positioned above the stone. In 2 patients, the residual stones were dissolved via the T-tube inserted during cholecystectomy. Solvent mixtures (solvent 1:26 mM ethylene diamine tetraacetic acid, 40 mM sodium deoxycholate and 30% dimethyl sulfoxide in an aqueous buffer solution glycine-NaOH, pH: 9.2; solvent 2: a 70: 30 mixture of dimethyl sulfoxide and methyl-tert-butyl-ether) were infused continuously and alternatively for 2 h at a rate of 0.3-0.5 ml/kg b.w./h. In order to diminish the absorption of the solvent from the duodenum, charcoal was given orally periodically. Fluoroscopy indicated that the common bile duct stones disappeared during 13-24 h of infusion in 10 of 39 patients. In 25 patients, the size of the stones diminished sufficiently for them to be removed by basket extraction. In 4 patients, the size of the stone did not change and surgery (1 pt) or endoscopic stenting (3 pts) was required. Only mild toxic side-effects were observed, including laboratory abnormalities and moderate duodenitis (34/39). Transient abdominal pain and/or cramp (21/39), nausea and vomiting (34/39) and diarrhoea (19/39) were the most common complaints during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Pancreatic trophism in experimental liver cirrhosis.

Pancreatic trophism and pancreatic enzyme composition, and plasma levels of cholecystokinin, insulin, glucagon, and glucose in liver cirrhosis induced by chronic thioacetamide administration (0.02% in the drinking water for 12 mo) were studied in rats. Advanced liver cirrhosis was evident in all thioacetamide-treated rats. The weight of the pancreas and its contents of DNA, protein, trypsinogen, chymotrypsinogen, proelastase, secretory trypsin inhibitor, and amylase were significantly increased as compared to the controls. The pancreatic secretory enzyme content changes showed a nonparallelism, characteristic of a cholecystokinin effect. Light and electron microscopy revealed a normal pancreatic architecture. Bioassayed plasma cholecystokinin levels in both fed and 24-h-fasted cirrhotic rats were significantly higher than in the corresponding controls. The plasma glucose, insulin, and glucagon levels demonstrated hypoglycemic tendencies with a glucagon predominance. These findings indicate that advanced liver cirrhosis in the rat is accompanied by pancreatic hypertrophy and hyperplasia, which might be attributed, at least in part, to elevated circulating cholecystokinin levels.

Influence of gastrointestinal (GI) hormones on suckling, gastric emptying and pancreatic trypsin content in the developing rat.

UNLABELLED: Aim of this study was to investigate how gastrointestinal hormones such as exogenous s.c. caerulein (6 micrograms/kg body weight), secretin (100 U/kg body weight), bombesin (20 micrograms/kg body weight, s.c.), CCK-8 (10 micrograms/kg body weight, i.p.), the CCK-A receptor antagonist L 364,718 (100 micrograms/kg body weight, i.p.), camostate (400 mg/kg body weight per os) which releases endogenous CCK and the coadministration of camostate with atropin (250 micrograms/kg body weight, s.c) or L 364,718 (1 mg/kg) influence milk intake from nipples, gastric emptying, and discharge of pancreatic trypsin content in 10-day-old rat pups. Saline-treated pups served as controls. The non-fasting Wistar rat pups of both sexes were used in littermate order. The suckling lasted for 30 and 45 min, respectively. One pup was used only once. After suckling the pups were decapitated, their stomach and pancreas were removed and weighed. The gastric food content was regarded as intake of milk and expressed as difference between the filled minus empty stomach. Pancreatic trypsin and protein content, plasma CCK level were measured. The exogenous agents did not influence gastric content. The investigated peptides decreased, L 364,718, however, increased the pancreatic trypsin/protein ratio. Camostate increased gastric content by 60% and decreased pancreatic trypsin/protein ratio vs saline by 90%. The gastric and pancreatic effects of camostate were not reversed by atropine or L 364,718. CONCLUSION: Exogenous and endogenous CCK seem not to influence milk intake while decrease pancreatic trypsin/protein ratio. However, endogenous CCK inhibit gastric emptying. The plasma CCK level was elevated due to the applied CCK-8 and camostate during the observed suckling period.

Gallbladder dysfunction in diabetes mellitus.

To further elucidate the mechanism of impaired gallbladder emptying in diabetics with and without neuropathy, gallbladder function was assessed by ultrasonography following a medium-chain triglyceride (lipomul, 1.5 mg/kg) infusion into the duodenum and compared to that during intravenous infusion of cholecystokinin in diabetic women. Results were compared with five healthy control women. Mean (+/- SD) maximal percent gallbladder volume in diabetics following lipomul was reduced to 49 +/- 8% and after intravenous cholecystokinin to 47 +/- 9%, which was less than those in controls, 21 +/- 9% and 24 +/- 6%, respectively, but not significantly different. Further analysis of gallbladder emptying to lipomul differentiated two subgroups of diabetics: one subgroup (N = 5) had emptying comparable to controls (responders), while the other (N = 5) had very modest emptying (nonresponders). Two of the patients in the latter group had normal gallbladder emptying during exogenous cholecystokinin and their response would be compatible with visceral neuropathy. Blood levels of cholecystokinin, measured by bioassay, following lipomul and exogenous cholecystokinin were similar in controls and diabetics. Presence of diabetic neuropathy did not correlate with impaired gallbladder emptying. Follow up at 6 and 12 months of the three nonresponder diabetics revealed that no gallstones had developed and that two of them became responders to exogenous cholecystokinin.(ABSTRACT TRUNCATED AT 250 WORDS)

Pancreatic secretion in chronic alcoholics. Effects of acute alcohol or wine on response to a meal.

To gain further insight on the effects of alcohol on human pancreatic enzyme secretion, we tested the effects of a 12% (v/v) alcohol solution, wine, and a glucose solution added to a meal on trypsin output in duodenal aspirate of nonalcoholic volunteers and compared the results to those of chronic alcoholics. Plasma concentrations of gastrin, cholecystokinin, and pancreatic polypeptide were monitored pre- and postprandially. Similar blood alcohol concentrations were determined in nonalcoholics and alcoholics following wine and the alcohol solution. Nonstimulated trypsin output (basal) was higher in alcoholics but not significantly so when compared to nonalcoholics. However postprandial trypsin output, 2014 +/- 301 mg/5 hr was significantly greater in alcoholics (P < 0.05) compared to nonalcoholics 1271 +/- 118 mg/5 hr. Alcohol and wine when added to the meal significantly (P < 0.05) inhibited trypsin output in both groups. Basal and postprandial levels of gastrin and cholecystokinin were similar in nonalcoholics and alcoholics. Basal plasma pancreatic polypeptide levels were similar in both groups, but the postprandial increments in pancreatic polypeptide levels observed in nonalcoholics were not observed in alcoholics. We conclude that chronic alcoholics have increased postprandial pancreatic enzyme secretion, and that this secretion, as that of nonalcoholics, can be affected by alcohol or wine. The postprandial hypersecretion of enzymes in alcoholics is not related to increased plasma levels of cholecystokinin or gastrin. It is possible that the impaired release of pancreatic polypeptide may participate in the mechanism for increased pancreatic enzyme secretion in chronic alcoholics.

Stopping power and the concept of effective ion charge at low energies.

A new formalism for the calculation of the ion-matter interaction phenomenon was developed by incorporating the atomic electron shell structure. This formalism allows for discrimination among the electrons of the target atoms according to their average positions with respect to the shell structure of the projectile ion. By doing so, we are able to show a strong dependence of the ion energy loss on its electron shell distribution. Thus a detailed quantum mechanical description of the moving ion is necessary to predict its precise trajectory and energy loss inside matter. The concept of an "effective charge" in the context of the electron stopping power formalism is emphasized and extended.

Biological effectiveness of high-energy protons: target fragmentation.

High-energy protons traversing tissue produce local sources of high-linear-energy-transfer (LET) ions through nuclear fragmentation. We examine the contribution of these target fragments to the biological effectiveness of high-energy protons using the cellular track model. The effects of secondary ions are treated in terms of the production collision density using energy-dependent parameters from a high-energy fragmentation model. Calculations for mammalian cell cultures show that at high dose, at which intertrack effects become important, protons deliver damage similar to that produced by gamma rays, and with fragmentation the relative biological effectiveness (RBE) of protons increases moderately from unity. At low dose, where sublethal damage is unimportant, the contribution from target fragments dominates, causing the proton effectiveness to be very different from that of gamma rays with a strongly fluence-dependent RBE. At high energies, the nuclear fragmentation cross sections become independent of energy. This leads to a plateau in the proton single-particle-action cross section, below 1 keV/micron, since the target fragments dominate.

Essential role of cholecystokinin in pancreatic regeneration after 60% distal resection in rats.

The essential role of cholecystokinin (CCK) in pancreatic regeneration after pancreatitis or resection has been supposed, but not yet clearly demonstrated. In rats, 6-8 weeks after 60% distal resection of the pancreas a gradual increase in pancreatic weight and contents of DNA, protein, trypsin, chymotrypsin and amylase, occurred (there was no increase in lipase); Pancreatic regeneration stopped thereafter. Nonparallel increases in enzyme values were similar to those seen after CCK administration. Indeed, basal CCK levels increased significantly by the 6th week and declined thereafter. A one month s.c. administration of CCK-octapeptide (CCK-8) (3 x 300 ng/kg/d) accelerated regeneration in the first month, but it had almost no effect during the second or third postoperative months. A two week s.c. administration of a specific CCK antagonist, CR 1409 (3 x 4 mg/kg/d) totally prevented regeneration by the fifth and sixth weeks, but did not diminish pancreatic weight or DNA and protein contents during the first two weeks. Alcohol administration (12 g/kg/d) reduced CCK release and prevented pancreatic regeneration during the three-month experimental period. These data indicate that CCK has an essential role in pancreatic regeneration and that the deleterious effect of alcohol on regeneration involves inhibition of CCK release.

Analytical relationships of nuclear field and microdosimetric quantities for target fragmentation in tissue systems.

A simple analytic formula for the nuclear fields formed by target fragmentation in tissue systems is derived using the continuous slowing down approximation (CSDA). The energy fluctuations in sensitive localized sites within the tissue system caused by these nuclear events are defined by microdosimetry. In that CSDA is used, the energy fluctuations exclude the role of secondary electrons. The relations also relate to the response of microdosimetric devices to nuclear fragmentation fields.

Energy deposition at the bone-tissue interface from nuclear fragments produced by high-energy nucleons.

The transport of nuclear fragmentation recoils produced by high-energy nucleons in the region of the bone-tissue interface is considered. Results for the differential flux and absorbed dose for recoils produced by 1-GeV protons are presented in a bidirectional transport model. The energy deposition in marrow cavities is seen to be enhanced by recoils produced in bone. Approximate analytic formulae for absorbed dose near the interface region are also presented for a simplified range-energy model.

Effect of alcohol and alcoholic beverages on meal-stimulated pancreatic secretion in humans.

Alcohol and alcoholic beverages may have different effects on pancreatic secretion and hormone release in humans. To test this hypothesis we studied the effects of an alcohol solution and a glucose solution and compared them with those of alcoholic beverages on postprandial pancreatic secretion and release of gastrin, trypsin, and cholecystokinin in 6 healthy nonalcoholic male volunteers. Pancreatic enzyme secretion was measured in duodenal aspirate, plasma trypsin, and gastrin by radioimmunoassay and cholecystokinin by bioassay. The meal plus glucose significantly stimulated pancreatic enzyme secretion, release of gastrin and cholecystokinin, and caused no changes in plasma trypsin. The alcohol solution and all beverages added to the meal caused similar increases in alcohol blood levels and significantly less pancreatic enzyme secretion compared with the meal plus glucose. Plasma trypsin levels remained unchanged. Compared with the meal plus glucose, wine and beer caused a significantly higher release of gastrin, and beer also released significantly more cholecystokinin. Inhibition of pancreatic enzyme secretion stimulated by a meal in nonalcoholics is a common effect of alcohol and alcoholic beverages despite some differences on release of gastrointestinal peptides. This effect may have some implications in the pathogenesis of alcoholic pancreatitis.

Mechanisms of action of alcohol administration on the trophic effect of soybean trypsin inhibitor and cholecystokinin octapeptide in rat.

Influence of alcohol administration on the trophic effect of cholecystokinin-octapeptide and soybean trypsin inhibitor administration was examined in male Wistar rats. Two x 4 mL of 20% alcohol given intragastrically during 2 wk did not significantly influence pancreatic weight, DNA, protein, trypsin, chymotrypsin, amylase, lipase, or trypsin inhibitor contents of the pancreas. It diminished the hypertrophy but not the hyperplasia seen after CCK-8 treatment, and eliminated the hyperplasia, as well as the hypertrophy provoked by SBTI administration. Secretory studies and CCK measurements demonstrated decreased CCK release in response to SBTI stimulation after 3-d alcohol administration. The results indicate that alcohol inhibits the enzyme synthesis of the CCK stimulated dividing and/or newly formed acinar cells and the endogenous CCK release.

Effect of alcohol and alcoholic beverages on nonstimulated pancreatic secretion in humans.

The effects of alcoholic beverages on pancreatic secretion, blood trypsin levels, the release of gastrin and cholecystokinin were studied and compared with those of an alcohol and a glucose solution. Studies were done on six healthy male volunteers. The trypsin level was measured in the duodenal aspirate, while blood trypsin and gastrin levels were measured by radioimmunoassay and the cholecystokinin level was measured by bioassay. Studies were done on 5 different days, and on each day, the effects of either a glucose solution; an alcohol solution; or wine, beer, and gin solutions infused into the stomach were compared. The glucose solution stimulated trypsin secretion (a threefold increase above the basal measure) and the release of cholecystokinin without changes in the blood trypsin level. Blood alcohol levels, after the alcohol solution and all alcoholic beverages, were similar, and subjects showed mild symptoms of intoxication. Pancreatic enzyme secretion and trypsin blood levels were not significantly affected by either alcohol or the alcoholic beverages. Wine and beer caused significant release of gastrin and cholecystokinin. Under the conditions of this study, which reproduce those of excessive alcohol drinking, alcohol and alcoholic beverages did not stimulate pancreatic enzyme secretion, although wine and beer increased the release of gastrin and cholecystokinin. We conclude that alcohol and alcoholic beverages do not affect nonstimulated pancreatic enzyme secretion.