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Biomedical subjects

A S Fink

Publications and source records attributed to A S Fink.

At least 55 records · Page 3Linked to original sources

Indolent presentation of pancreatic abscess. Experience with 100 cases.

One hundred cases of pancreatic abscess were identified at five hospitals affiliated with UCLA between 1973 and 1985. Patients were included if a pancreatic mass or phlegmon followed an episode of pancreatitis, if the clinical impression was pancreatic abscess, and if drainage cultures were positive. Less than three Ranson's signs were present on admission in 72% of patients. The admission temperature was less than 38.3 degrees C in 71% of patients, and 27% of patients never had a fever. Abdominal tenderness was absent in 40% of patients. The admission amylase concentrations and white blood cell counts were normal in 36% and 23% of patients, respectively. Extensive débridement, external drainage, and a low threshold for reoperation were the mainstays of surgical therapy. Twenty patients (20%) died, but Ranson's signs did not predict outcome. pancreatic abscess may have an insidious presentation. A high index of suspicion, early computed tomographic scanning, and diagnostic needle aspiration may be necessary to establish this diagnosis.

Abscess↗

Release of secretin along the canine small intestine.

The profile of secretin release along the entire canine small intestine was examined in this study. Four equal loops of the small gut, from the duodenal bulb to the ileocoecal valve, were isolated. In eight anesthetized dogs the four segments were perfused for 40 min each in random order with an acidified (pH 2.5) emulsion of 20 mM oleic acid. In four dogs control experiments were performed using 0.15 M saline. Secretin release in portal venous blood was measured by a sensitive radioimmunoassay. Although secretin was mainly released in the first quarter of the small intestine (310 pM X 40 min), large amounts of secretin, 33% of the total secretin release, were liberated in the second quarter of the small intestine (164 pM X 40 min). Minute amounts of secretin (23 pM X 40 min) were released in the third quarter, whereas perfusion of the last quarter of the small gut failed to release secretin. We conclude that the major portion of secretin is releasable in the first quarter of the small gut. High amounts of secretin can be liberated in the second quarter of intestine, an area that is probably never exposed to pH below 4.5 (the known threshold for secretin release by acid), but is still exposed to fatty acids (other releasers of secretin).

Animals↗

Potential methodologic problems with in vivo immunoneutralization of pancreatic polypeptide.

Dogs with chronic pancreatic fistulae were given 0.5 ml of nonimmune rabbit serum or antibody S5, an antibody raised against the C-terminal pancreatic polypeptide (PP) hexapeptide. A 3-h infusion of secretin (125 ng/kg/h) and CCK8 (50 ng/kg/h) was started 30 min after injecting serum. Exogenous BPP (400 pmol/kg/h) was administered during the middle secretin/CCK hour. In a second protocol, 30 min after injecting nonimmune serum or PP-anti-serum, the animals were fed 15 g/kg cooked ground beef. Pretreatment with S5 enhanced secretin/CCK-induced bicarbonate outputs; protein outputs did not differ. Exogenous BPP inhibited pancreatic secretion, even in S5-treated animals. Meal-induced pancreatic secretion was not altered by S5 pretreatment. Significant increments in PP were measured by radioimmunoassay during administration of secretin/CCK and during BPP infusion. Anti-PP pretreatment abolished the former and significantly decreased, but did not abolish, the latter. The meal evoked significant postprandial increments in PP which were essentially abolished following S5 pretreatment. A physiological role for PP cannot be proved or refuted because antiserum pretreatment failed to block the effects of exogenous hormone. The latter must be established before excluding a peptide's physiological role based on negative in vivo immunoneutralization data.

Animals↗

Percutaneous aspiration of peripancreatic fluid collections: a safe method to detect infection.

During the past 5 years, we have used percutaneous aspiration of peripancreatic fluid collections guided by computed tomography (CT) or ultrasonography (US) to facilitate diagnosis of infection in selected cases. Fifteen of 18 patients undergoing guided needle aspiration had persistent fevers (greater than 38.3 degrees C). The three afebrile patients all had abdominal pain and leukocytosis, and two of the three also had elevated serum amylase levels. Percutaneous aspiration was guided by CT in 14 patients and by US in four. On the basis of aspirate Gram stains and cultures, as well as surgical (15) and percutaneous drainage (1) findings, the final diagnosis was pancreatic abscess in nine patients, infected pseudocyst in four, uninfected pseudocyst in four, and cystadenoma in one. Diagnosis based on percutaneous aspiration was correct in 17 of 18 patients (94%), and no complications could be directly attributed to the procedure. We conclude that CT- or US-guided percutaneous aspiration is a safe and accurate diagnostic procedure for patients with peripancreatic fluid collections in whom secondary infection is suspected.

Abscess↗

Gastric processing and emptying of fat.

This study was undertaken to determine whether fat leaves the stomach within or bound to the surface of particles of solid food. We studied gastric emptying of fat in 6 human subjects and in 6 dogs with Roux-en-Y duodenojejunostomies so that chyme leaving the stomach could be collected free of bile and pancreatic enzymes. Humans were studied with a duodenal multilumen tube so that phase-specific, nonabsorbed markers in the meal could be tracked with corresponding, phase-specific markers perfused into the duodenum. In this way, we observed the separate time-courses of gastric emptying of the aqueous and solid phases, as well as the extracellular fat (ECF) and intracellular fat (ICF) phases of the meal. In the dogs, all chyme leaving the stomach was collected from a Roux-en-Y fistula and was analyzed directly for aqueous, solid, ECF, and ICF markers in the meal. In both the humans and the dogs, the aqueous phase emptied promptly, whereas the solid, ECF, and ICF phases emptied together, in parallel, after an initial lag. In humans, 22% of the ECF versus 51% of the ICF (p less than 0.02) emptied on or in the solid food particles. In dogs, 81% of the ECF emptied as an oil, 13% emptied on the solid particles, and only 6% emptied as a stable, aqueous emulsion. Sixty-six percent of the ICF emptied in the solid food particles, 20% as a stable, aqueous emulsion, and 14% as an oil. We conclude that most of the ICF empties within the solid food phase, whereas most of the ECF empties as an oil phase.

Animals↗

Radiologic pitfalls in endoscopic retrograde pancreatography.

Endoscopic pancreatography (ERCP) is currently the least invasive technique for obtaining detailed images of the pancreatic ductal system. Although expert ERCP is now an acceptably safe procedure, interpretation of endoscopic pancreatograms may be difficult, and misdiagnosis is still a risk to the patient. We have been able to divide misinterpretations into three broad categories: technical error, anatomic variation, and unusual images due to disease. Examples of each of these classifications are presented and discussed in hopes of decreasing the incidence of misdiagnosis.

Cholangiopancreatography, Endoscopic Retrograde↗

Regional distribution and release of peptide YY with fatty acids of different chain length.

The present study examines peptide YY responses to regional intestinal perfusion of fatty acids of different chain length--dodecanoate and oleate. Six dogs with chronic gastric, duodenal, and jejunal fistulas were studied. Proximal perfusates were administered into the duodenum and diverted through an intestinal fistula placed 45 cm beyond the duodenal cannula. Distal perfusates were administered into the caudal stoma of this intestinal stoma. Peptide YY responses to proximal, distal, and whole-gut perfusion were compared. Proximal perfusion with oleate or dodecanoate failed to release peptide YY. In contrast, distal and whole-gut perfusion with either fatty acid produced significant increases that were of similar magnitude. Immunocytochemical studies demonstrated that peptide YY cells predominated in the canine ileocolonic mucosa and decreased progressively in an orad direction. We conclude that peptide YY release is not dependent on fatty acid chain length and that the duodenum does not play a dominant role in peptide YY release. As such, peptide YY release differs from that of its cousin pancreatic polypeptide and may result at least in part from direct stimulation of the peptide YY cell in the ileocolonic mucosa.

Animals↗

Hemorrhage into a hepatic adenoma and type Ia glycogen storage disease: a case report and review of the literature.

Older patients with type I glycogen storage disease (GSD) develop hepatic adenomas that may undergo malignant transformation. Despite their similarity to oral contraceptive-related hepatic tumors, only one previous report has even mentioned hemorrhage in GSD-related hepatic tumors. We recently followed a 20-year-old patient with type Ia GSD and a 10 cm focal defect in the left lobe of the liver; angiography suggested that this was a benign adenoma. At 22 years of age, after an acute symptomatic episode, repeat studies (ultrasonography and angiography) revealed a 2 cm increase in diameter of the hepatic mass. Imminent tumor rupture was of grave concern; thus the patient was admitted to the hospital and given 2 weeks of constant glucose administration by central venous line in the hope of improving her metabolic abnormalities. After resolution of the coagulopathy and metabolic disorders, the patient safely underwent surgical enucleation of the tumor. Pathologic examination of the tumor revealed that the patient had indeed hemorrhaged into a typical hepatic adenoma that had focuses of hepatocellular dysplasia. She has done well without evidence of tumor recurrence for 3 years since the operation. We conclude that hemorrhage and malignant transformation are potential complications of GSD-related hepatic adenomas. This conclusion underscores the importance of following these patients closely as they age. Nocturnal nasogastric feeding should be considered in the hope of preventing a tumor or inducing regression. Acute symptomatic attacks should be evaluated promptly for possible tumor hemorrhage.

Adenoma↗

Canine intestinal transit and digestion of radiolabeled liver particles.

Using conscious dogs with chronic gastrointestinal fistulas, we studied the intestinal transit of radiolabeled liver particles relative to the transit of a liquid phase marker, polyethylene glycol. All studies were performed during a "fed" intestinal motility pattern induced by feeding or by intestinal perfusion with a fat-containing solution. Median transit times were determined from duodenum to fistulas at the midintestine, or at the terminal ileum, by recovery of polyethylene glycol and radiolabel in effluent from the fistulas. We also sized recovered particles of liver to determine the extent of digestion or fragmentation, or both, in transit. After a steak meal, when liquid flows were very low, the liquid marker and small (0.5-0.7 mm) and large (2-3 mm) particles moved through the proximal intestine together at a slow rate. When intestinal liquid flows were progressively increased from 2 to 24 ml/min by intestinal perfusion, transit was progressively accelerated; but 2-mm particles moved at 25%-20% of the rate of polyethylene glycol or 0.5-mm particles. Increasing transit with increasing flows was associated with decreasing digestion or fragmentation of liver particles. Under most conditions, 2-mm particles were well digested or fragmented than 0.5-mm particles. We conclude that fluid flows have a major effect on transit and digestion of food particles in the small intestine.

Animals↗

Pancreatic bicarbonate response to food-bound hydrogen ion along the gut.

Recent reports suggest most solid food enters the duodenum as small particles. Our studies showed that small particles of liver were capable of binding hydrogen ions (H+), but there was slow equilibration of H+ between particulate and aqueous phases. We wondered whether titratable acid as H+ bound to meat particles could effectively stimulate pancreatic bicarbonate secretion despite slow diffusion. We studied mongrel dogs with chronic pancreatic fistulas; the intestinal lumen was washed free of endogenous pancreatic enzymes. Pancreatic bicarbonate and protein responses were measured during duodenal perfusion with pH 2 or pH 3 gels that delivered 1, 2, or 4 mEq/15 min of titratable acid (endpoint pH 4.5). Gels consisted of acidified, 0.1-0.7-mm particles of beef liver or bovine serum albumin or lactic acid suspended with 2% starch in 0.15 M NaCl. The liver, bovine serum albumin, and lactate had similar titration curves. At pH 2 or pH 3, liver particles were about as effective as bovine serum albumin in stimulating pancreatic bicarbonate secretion. Likewise, pH 3 liver particles were equipotent with pH 3 lactate on pancreatic bicarbonate secretion when both perfusates were allowed access to the whole intestine. However, when confined to the first 45 cm of proximal intestine, much less H+ was dissipated from the liver versus the lactate; and, correspondingly, there was a much greater decrement in pancreatic bicarbonate secretion from whole gut responses with liver versus lactate. We conclude that titratable acid bound to solid food particles is a potent stimulus of pancreatic bicarbonate secretion despite its slow diffusion. Our studies suggest that H+ slowly diffusing from particles excites pancreatic bicarbonate secretion by triggering H+ receptors along more distal intestine.

Animals↗

Pancreatic polypeptide release by intraluminal fatty acids.

The question of whether the response of pancreatic polypeptide to intestinal fatty acids is influenced by the site of intestinal perfusion or the chain length of the fatty acid was investigated. Six dogs with chronic gastric, pancreatic, and intestinal fistulas were studied. Proximal perfusates were administered at the pylorus and diverted via a Foley catheter in the orad stoma of an intestinal fistula placed 45 cm beyond the pancreatic cannula. Distal perfusates were administered into the caudal stoma of the intestinal cannula. Three experimental protocols were used: proximal fatty acid perfusion (20, 40, or 80 mmol/L) combined with distal saline perfusion; distal fatty acid perfusion (20, 40, or 80 mmol/l) combined with proximal saline perfusion; or distal fatty acid perfusion combined with proximal fatty acid perfusion of 80 mmol/L. Each dose of fatty acid was given in random order and the two fatty acids (dodecanoate and oleate) were tested on different days. Blood samples were drawn for pancreatic polypeptide radioimmunoassay, and pancreatic secretion was collected for determination of bicarbonate and protein outputs. Pancreatic polypeptide responses to perfusion of both proximal and distal segments with oleate exceeded (P less than 0.05) those evoked by dodecanoate. The responses of pancreatic polypeptide to dodecanoate administration into either the proximal segment or the distal intestine were not significantly different. In contrast, perfusion of the proximal intestinal segment with oleate release significantly (P less than 0.05) less pancreatic polypeptide than did distal intestinal perfusion with oleate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Regionally perfused fatty acids augment acid-induced canine pancreatic secretion.

To study interactions between hydrochloric acid and fatty acids on pancreatic secretion, six dogs with chronic gastric, pancreatic, and small intestinal cannulas received various combinations of the following intestinal perfusates: 20, 40, and 80 mM hydrochloric acid, oleate, dodecanoate, or 0.15 M saline. Regional intestinal perfusion (a proximal segment measuring 45 cm from the pancreatic duct versus the remaining small bowel) was utilized to separate the aqueous acid and lipid solutions. Both oleate and dodecanoate augmented the bicarbonate output induced by intraluminal acidification. In other experiments, intraluminal oleate, when combined with exogeneous intravenous secretin (12.5-900 ng . kg-1 . h-1), potentiated the secretin-induced bicarbonate output at low secretin doses. Dodecanoate also increased secretin-induced bicarbonate output. In all of these studies, protein outputs were increased by intestinal fatty acids. It is concluded that intestinal fatty acids can enhanced acid-induced canine pancreatic secretion.

Animals↗

Intraduodenal emulsions of oleic acid augment acid-induced canine pancreatic secretion.

To study interactions between intraduodenal acid and emulsified oleic acid, dogs with chronic gastric and pancreatic fistulas received two sets of intestinal perfusates. The first set contained HCl plus bovine serum albumin (BSA) with or without 20 mM oleic acid. The BSA and HCl were varied so that each 50 ml contained 1, 2, or 4 meq of acid titratable from an initial pH of 2.0 or 3.5 to an end-point pH of 4.5. Oleic acid significantly enhanced pancreatic bicarbonate and protein outputs induced by acidified BSA. In additional studies, a less soluble protein solution, a 1:1 mixture of bovine hemoglobin and ovalbumin (HB-OV), was utilized. Fixed amounts of HCl (1, 2, or 4 meq/50 ml) were added to native or pepsin-digested HB-OV solution with or without 20 mM oleic acid. In these studies, initial pH and titratable acid (to end-point pH 4.5) varied with the nature of the HB-OV (undigested or digested), as well as with the amount of HCl added. Under these conditions, digested HB-OV and oleic acid potentiated acid-induced bicarbonate output, but only in those solutions with the greatest amount of added HCl. Acid-induced bicarbonate or protein outputs were not further augmented upon combination of HB-OV digests with oleic acid. We conclude that acid-induced pancreatic bicarbonate secretion is potentiated by intraduodenal protein digests and emulsified fatty acids.

Animals↗

Digests of protein augment acid-induced canine pancreatic secretion.

To study interactions between intraluminal acid and protein digests, six dogs with chronic gastric and pancreatic fistulas received three sets of intestinal perfusates. The first set contained HCl (1, 2, or 4 mmol/50 ml) and 64 mM D- or L-phenylalanine. The second set contained HCl plus either intact or pepsin-digested bovine serum albumin (BSA); the BSA and HCl were varied so that each 50 ml contained 1, 2, or 4 meq of acid titratable from an initial pH of 2.0 to an end-point pH of 4.5. The third set was identical to the second set except for an initial pH of 3.5. All perfusates were adjusted to 300 mosM and randomly infused at 200 ml/h. L-Phenylalanine enhanced acid-induced bicarbonate and protein outputs, as did pH 2.0 BSA digests. At pH 3.5, only acid-induced protein output was augmented by BSA digests. In additional studies, undigested or digested BSA at pH 7.0 was infused with secretin (82 pmol.kg-1.h-1). Only digested BSA enhanced secretin-induced pancreatic secretion. We conclude that there is an important, albeit complex, interaction between the intestinal acid stimulus and the protein digest stimulus on pancreatic secretion.

Animals↗

Release of human pancreatic polypeptide and gastrin in response to intraduodenal stimuli: a case report.

A recent clinical case afforded an opportunity to study the effects of duodenal stimulation on plasma human pancreatic polypeptide and gastrin concentrations, independent of gastric stimulation. A distension stimulus was provided by rapid injection of 100 ml of water and saline via a T-tube into an isolated duodenal afferent limb. In a third experiment, the saline contained 200 pg/ml of heptadecapeptide human gastrin. Within 2 min after each injection, a rapid rise in circulating human pancreatic polypeptide levels appeared that fell promptly towards basal thereafter. Injections of 100 ml of Flexical, a supplemental tube feeding, resulted in a biphasic human pancreatic polypeptide response, the initial peak comparable to that seen following distension with water, saline, or saline containing gastrin, and a second peak of much greater magnitude and duration followed the initial peak. Plasma gastrin concentrations were not influenced following any of the stimuli. Duodenal distension alone may induce an early transient increase in plasma human pancreatic polypeptide concentrations, while intraduodenal nutrients per se may induce a later increment of greater magnitude and duration.

Aged↗