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Biomedical subjects

A S Fink

Publications and source records attributed to A S Fink.

At least 19 recordsLinked to original sources
PubMed2000

Recent experience with percutaneous endoscopic gastrostomy/jejunostomy (PEG/J) for enteral nutrition.

BACKGROUND: Enteral feeding is the preferred means of nutritional support in patients unable to eat orally. Jejunal-placed feeding tubes are often considered optimal for this purpose. Successful administration of such tube feedings depends on the method of placement and the size of the tube. Herein we review our experience with endoscopically placed jejunal feeding tubes. METHODS: Thirteen percutaneous endoscopic gastrostomy/jejunostomy (PEG/J) tubes were placed in 13 patients at the Emory University hospital by one surgeon. Indications for jejunal placement included aspiration in five patients and suspicion of increased reflux susceptibility in eight patients. Insertion of an 8.5-Fr nasobiliary tube was attempted in nine patients using the technique described by Coates and MacFadyen. A 12-Fr tube was placed in four patients using a technique that took advantage of previously placed PEG tubes. RESULTS: Initial placement was successful in all but one patient. Nine tube-related complications occurred in seven patients. These included six tube occlusions, one tube site infection, one peristomal leak, and one tube perforation that required replacement. Five of six tube occlusions (83%) occurred in the smaller 8.5-Fr. tubes. There was one non-tube-related death. CONCLUSIONS: PEG/J insertion can be performed successfully and safely in most patients. Long-term tube patency is, however, dependent on the use of tubes with a large diameter; thus, modalities that enable placement of larger-sized tubes are preferable. Further technical developments are needed to facilitate the endoscopic insertion of larger jejunostomy tubes.

Adult↗
PubMed2000

Growth and function of isolated canine pancreatic ductal cells.

These studies investigated the growth characteristics and functional properties of isolated canine pancreatic ductal epithelial cells. Cells were isolated from the accessory pancreatic duct and cultured by using three conditions: on vitrogen-coated petri dishes with fibroblast conditioned medium (nonpolarized); in vitrogen-coated Transwells above a fibroblast feeder layer (polarized); or as organotypic rafts above a fibroblast-embedded collagen layer (polarized). Growth characteristics, transepithelial resistances, and carbonic anhydrase and cyclic adenosine monophosphate (AMP) responses were evaluated. Under polarized conditions, the cells grew as monolayers with columnar epithelial characteristics. The monolayers developed high transepithelial resistance and became impervious to the passage of horseradish peroxidase. Epithelial growth factor (EGF) (2 ng/ml) stimulated ductal cell growth and accelerated the formation of a high-resistance monolayer. Forskolin (10 microM) rapidly decreased transepithelial resistance. Carbonic anhydrase activity, which was lower in nonpolarized compared with polarized conditions, was stimulated by carbachol (175 microM). Secretin, however, did not stimulate carbonic anhydrase activity in these cells. Although secretin stimulated adenylyl cyclase activity in early-passage cells, this response was lost in later-passage cells. Both vasoactive intestinal polypeptide (VIP; 1 microM) and forskolin (10 microM) consistently increased adenylyl cyclase activity. Isolated canine pancreatic ductal epithelial cells proliferate in vitro, develop high-resistance epithelial monolayers, and respond to stimuli that activate adenylyl cyclase. These cells should provide a useful model for regulatory studies of ductal cell functions.

Adenylyl Cyclases↗
PubMed2000

Hyperglycemia alone does not inhibit secretin-induced pancreatic bicarbonate secretion.

Administration of exogenous insulin (INS) inhibits secretin-stimulated pancreatic bicarbonate (HCO3) output via a dose-dependent, neurally mediated mechanism. To determine whether this effect was due to systemic hyperinsulinemia or to reduced endogenous insulin production, we examined the effect of hyperglycemia on secretin-stimulated pancreatic secretion. Chronic pancreatic fistulae were created in six dogs. After 30 minutes of equilibration, a computer-assisted hyperglycemic clamp protocol was used to maintain glucose (GLU) levels 100 or 150 mg/dL above basal in clamp animals; control animals received volume- and rate-matched infusions of 0.9% saline. One hour after beginning the clamp period, intravenous secretin dose-response (16-125 ng/kg/h) was begun, doubling the dose every half hour. Unstimulated (0-30 minutes) HCO3, GLU, and INS levels did not differ between groups. INS and GLU levels in clamp animals were significantly elevated during clamp (30-90 minutes) and stimulated (90-210 minutes) periods. For the same periods, HCO3 secretion was not significantly changed despite profound hyperinsulinemia. We conclude that systemic hyperinsulinemia alone does not inhibit secretin-stimulated HCO3 output. Since exogenous INS exerts feedback regulation on the pancreas, we propose that suppression of endogenous INS secretion mediates the previously reported inhibitory response.

Animals↗
PubMed1999

Experience with percutaneous transhepatic cholangioscopy (PTCS) in the management of biliary tract disease.

BACKGROUND: Biliary tract disorders often present significant management difficulties, particularly in patients who are poor surgical candidates. Percutaneous transhepatic cholangioscopy (PTCS) is an infrequently utilized alternative that might offer significant therapeutic benefit. We reviewed our experience with the use of this modality as a definitive therapy for biliary tract disorders. METHODS: Patient records at the Atlanta VAMC and Emory University hospitals were reviewed. We identified 17 patients who had undergone 25 PTCS interventions between August 1994 and December 1998. The indications for PTCS included dilatation of biliary-enteric anastomoses in four patients, biliary stone removal (with or without lithotripsy) in eight patients, stricturoplasty in four patients, biopsy of suspected biliary neoplasms in seven patients, and removal of obstructing clot in one patient. Most procedures (n = 17) were performed through percutaneous transhepatic tracts (12-18 Fr) that were <1 week old. All tracts were dilated to operating size on the day of the procedure. All patients received periprocedural antibiotics. RESULTS: The interventions were successful in seven of eight stone removals, four of five stricturoplasties, three of four anastomotic dilatations, seven of seven biopsies, and the single clot removal. The only complication involved one episode of hemobilia, requiring angio-embolization of a small branch of the right hepatic artery. CONCLUSIONS: PTCS is a safe, useful, and well-tolerated adjunct to the more common endoscopic and surgical techniques for managing complicated biliary tract disorders. Our experience suggests that PTCS can be performed early, without prolonged sequential dilatation of the percutaneous transhepatic tract, and may allow avoidance of operation in high-risk surgical candidates.

Adult↗
PubMed1999

Current management of endoscopic feeding tube dysfunction.

Surgically placed gastrostomy and jejunostomy feeding tubes allow administration of enteral nutrition for patients who are unable to swallow safely. Several endoscopic techniques have been used for tube placement. Endoscopically placed feeding tubes provide access to the gastrointestinal tract, but only when patent. Use of the approaches presented permits optimal feeding tube care and prolongs tube patency. Table 1 summarizes the recommendations for preventing and restoring patency to feeding tubes.

Adult↗
PubMed1998

Management of pancreatic pseudocysts.

BACKGROUND: Operative internal drainage has been standard treatment for chronic unresolved pancreatic pseudocysts (PPs). Recently, percutaneous external drainage (PED) has become the primary mode of treatment at many medical centers. STUDY DESIGN: A retrospective chart review was performed of 96 patients with PPs who were managed between 1987 and 1996. Longterm followup information was obtained by telephone and mail questionnaire. RESULTS: Twenty-seven patients underwent computed tomographic (CT)-guided PED. PP resolution occurred in 17 patients. Clinical deterioration or secondary infection mandated urgent pancreatic debridement in 7 (26%) patients and cystgastrostomy in 2 (7%) patients. There was one hospital death in this group. Thirty-two patients underwent cystgastrostomy or cystjejunostomy (n = 21), distal pancreatectomy (n = 8), pancreatic debridement and external drainage (n = 2), or cystectomy (n = 1). Two (6%) patients required postoperative pancreatic debridement for failure of resolution and peritonitis and two patients underwent PED of abscess. There was one hospital death in the expectantly managed group of 37 patients. Median followup of 3 years (range, 0.5-9.3 years) in 66 patients revealed that 6, 3, and 4 patients of PED, surgery, and expectantly managed groups, respectively, had radiologic evidence of recurrent PPs. CONCLUSIONS: Operative management for PPs appears to be superior to CT-guided PED. Although the later was often successful, it required major salvage procedures in one third of the patients. An expectant management protocol may be suitable for selected patients.

Abscess↗
PubMed1998

Alternative methods for management of the complicated gallbladder.

Laparoscopic cholecystectomy is the procedure of choice for symptomatic cholelithiasis. However, in the presence of acute cholecystitis, 10% to 15% of patients face conversion to laparotomy. Alternatives to conventional therapy may therefore help to improve the clinical outcome of patients with complicated gallbladder disease. In selecting patients for alternative therapies, preoperative and intraoperative factors must be considered. Preoperative factors include the severity of biliary disease and preexisting medical risk factors; whereas intraoperative factors include conditions at the time of surgery that make dissection difficult or unsafe. Alternative therapies provide the least invasive management to safely temporize or definitively treat the acute condition. These alternatives include percutaneous cholecystostomy alone or followed by laparoscopic cholecystectomy, laparoscopic cholecystostomy followed by laparoscopic cholecystectomy, laparoscopic subtotal cholecystectomy, endoscopic retrograde cannulation of the gallbladder, and extracorporeal shockwave lithotripsy. By appropriate selection of the initial therapeutic approach, the surgeon may ultimately improve the clinical outcome in these complicated patients.

Catheterization↗
PubMed1996

The effect of pancreatic denervation and atropine on the cholecystokinin-induced pancreatic exocrine response.

To study the influence of extrapancreatic neural and cholinergic activity on the pancreatic response to cholecystokinin (CCK), six dogs underwent creation of Herrera pancreatic fistulas, placement of Thomas gastric cannulas, and distal pancreatectomies (innervated; INN). Six additional dogs were prepared similarly, with the addition of total extrinsic pancreatic denervation (denervated; DEN). The pancreatic protein and bicarbonate response to graded 12.5 to 200 ng/kg/h CCK doses was determined for INN and DEN animals both alone and with 10 micrograms/kg/h atropine infusion. The influence of extra-pancreatic neural and cholinergic activity on secretin's potentiation of the CCK-induced pancreatic response was then determined by repeating the studies with a 125 ng/kg/h secretin infusion. The latter results were compared to those predicted by summating the responses seen during separate 12.5-200 ng/kg/h CCK dose-response and 125 ng/kg/h secretin studies. Unstimulated protein output was diminished by atropine in INN animals (78 +/- 21 vs. 39 +/- 9 mg/15 min; p < 0.05) but not in DEN animals. Unstimulated bicarbonate outputs, integrated bicarbonate and protein outputs, and bicarbonate and protein dose-response curves were unaffected by denervation or atropine. Potentiation of CCK-induced bicarbonate output by secretin was also unaffected by atropine and denervation. We conclude that cholinergic elements are involved in unstimulated, but not CCK-induced, enzyme secretion. Further, potentiation of CCK-induced bicarbonate output by secretin does not depend on extrinsic neural or cholinergic elements.

Animals↗
PubMed1996

Exogenous insulin does not influence CCK- and meal-stimulated pancreatic secretion.

Although previous reports suggest interactions between the endocrine and the exocrine pancreas, insulin's effect on pancreatic exocrine function remains unclear. Chronic pancreatic fistulae were created in five dogs; these animals were studied using the euglycemic, hyperinsulinemic clamp technique. After a 30-min unstimulated period, both groups received a 60-min, 1.5 mU/kg/min insulin (clamp) or vehicle (control) infusion. Cholecystokinin (CCK) or meal stimulation was then begun. Intravenous CCK was initiated at 12.5 ng/kg/h; the CCK dose was doubled every 30 min until 100 ng/kg/h was achieved. The intraduodenal liquid test meal (1.5 kcal/ml; 15% protein, 32% fat, 53% carbohydrate) was administered at 100 ml/h. Unstimulated (0- to 30-min) serum glucose and insulin levels and pancreatic bicarbonate and protein outputs did not differ between groups. Clamp (30- to 90-min) and stimulated (90- to 210-min) insulins were significantly elevated in clamp groups (p < 0.001); glucose and bicarbonate were unchanged. Exocrine outputs during clamp periods were unaffected by insulin. Neither CCK- nor meal-stimulated pancreatic secretion (90-210 min) was influenced by insulin administration. These data suggest that hyperinsulinemia does not alter pancreatic acinar cell secretion in the intact animal.

Animals↗
PubMed1996

Insulin inhibits secretin-stimulated pancreatic bicarbonate output by a dose-dependent neurally mediated mechanism.

Although previous reports suggest interactions between endocrine and exocrine pancreas, insulin's effect on pancreatic exocrine function remains unclear. Chronic pancreatic fistulas were created in six dogs with innervated INN and five dogs with denervated (DEN) pancreata; these animals were studied using the euglycemic, hyperinsulinemic clamp technique. After a 30-min unstimulated period, both groups received a 60-min 1.5 mU.kg-1.min-1 insulin (clamp) or vehicle (control) infusion. Intravenous secretin was then initiated at 16 ng.kg-1.h-1; the secretin dose was doubled every 30 min until 125 ng.kg-1.h-1 was achieved. These studies were then repeated in INN animals during infusion of a 10 micrograms.kg-1.h-1 atropine background. Finally, INN animals underwent a similar unstimulated period followed by a 1.25 mU.kg-1.min-1 insulin (clamp) or vehicle (control) infusion. after 60 min, a 64 ng.kg-1.h-1 secretin infusion was initiated. Insulin infusion was then increased by 0.25 mU.kg-1.min-1 at 30-min intervals until 2.0 mU.kg-1.min-1 was reached. Unstimulated (0-30 min) serum glucose and insulin levels and pancreatic bicarbonate and protein outputs did not differ between groups. Clamp (30-90 min) and stimulated (90-210 min) insulin were each significantly elevate in clamp groups (81.9 +/- 2.4 vs. 7.0 +/- 0.3 microU/ml, P < 0.001); glucose and bicarbonate were unchanged. Protein outputs during clamp (64 +/- 9 vs. 24 +/- 6 mg/10 min; P < 0.05) and secretin-stimulated (52 +/- 9 vs. 29 +/- 3 mg/10 min; P < 0.05) periods were diminished by atropine but were unaffected by insulin. Secretin-stimulated (90-210 min) bicarbonate output was diminished by insulin (0.03 +/- 0.01 vs. 0.31 +/- 0.05 meq/10 min; P < 0.003) in INN but not DEN animals; this effect was partially reversed by atropine. Dose-response studies demonstrated a threshold for insulin's inhibitory actions between 1.5 and 1.75 mU.kg-1.min-1. These data provide further evidence for exocrine-endocrine regulatory interactions and suggest that insulin may influence secretin's stimulation of ductal cell secretion by a mechanism that is at least partially cholinergic in character.

Animals↗
PubMed1995

Adrenergic pathways do not mediate peptide YY-induced inhibition of pancreatic exocrine secretion.

The influence of extrapancreatic nerves and intrapancreatic adrenergic activity on the inhibition of pancreatic exocrine secretion by peptide YY (PYY) was studied in conscious dogs. Chronic pancreatic fistulae were created in five mongrel dogs while a second group of five dogs also underwent complete pancreatic denervation. After recovery, a continuous infusion of secretin (62 ng/kg/h) and cholecystokinin (CCK; 50 ng/kg/h) was administered over 2 h. An infusion of PYY (400 pmol/kg/h) was then given randomly, during either the first or second experimental hour. The experiments were then replicated after establishing adrenergic blockade with continuous background infusions of either phentolamine (0.2 mg/kg/h), propranolol (0.5 mg/kg bolus) or a combination of phentolamine and propranolol. The secretin/cholecystokinin-induced bicarbonate and protein outputs were significantly inhibited by PYY in both the innervated and denervated animals. Adrenergic blockade failed to eliminate the inhibitory effects of PYY. We conclude that extrapancreatic neural pathways, including adrenergic mechanisms, do not mediate the inhibitory effects of PYY. The results suggest that PYY inhibits secretin/cholecystokinin-induced pancreatic response by an indirect nonadrenergic mechanism.

Adrenergic Antagonists↗
PubMed1995

Somatostatin inhibits cholecystokinin-induced pancreatic protein secretion via cholinergic pathways.

Although somatostatin is a potent inhibitor of pancreatic exocrine secretion in vivo, its mechanism of action remains unclear. The influence of extrapancreatic nerves and intrapancreatic cholinergic activity on somatostatin-induced inhibition of pancreatic exocrine secretion was studied in conscious dogs. Chronic pancreatic fistulae were created in six mongrel dogs, and a second group of six dogs also underwent complete pancreatic denervation. The pancreatic responses to graded doses of cholecystokinin (12.5-200 ng/kg/h) and bethanechol (57-916 micrograms/kg/h), both alone and during background infusion of somatostatin-14 (800 pm/kg/h), were determined in all dogs. The cholecystokinin dose-response with a somatostatin-14 background was then repeated with the addition of atropine (10 micrograms/kg/h). In both groups of animals, cholecystokinin elicited a dose-dependent increase in pancreatic protein secretion that was inhibited significantly by somatostatin-14. Regardless of the status of extrapancreatic nerves, atropine further inhibited cholecystokinin-induced protein secretion beyond that evoked by somatostatin-14. In both innervated and denervated animals, cholinergic stimulation with bethanechol elicited a dose-dependent increase in pancreatic protein secretion that was unaffected by somatostatin-14. We conclude that extrapancreatic nerves do not mediate the inhibitory effects of somatostatin-14. Somatostatin-14 appears to inhibit cholecystokinin-induced pancreatic secretion by an intrapancreatic cholinergic mechanism.

Animals↗
PubMed1994

Extrapancreatic cholinergic nerves mediate cholecystokinin-stimulated pancreatic polypeptide release.

Although vagal cholinergic stimulation is the predominant regulatory mechanism governing the release of pancreatic polypeptide (PP), recent studies suggest that cholecystokinin (CCK) is also an important mediator. The present study examined the role of cholinergic neural pathways in the PP response to exogenous CCK-8 using a selectively denervated canine pancreas model. Chronic denervated pancreatic preparations were created in five dogs, while five dogs underwent sham laparotomy as controls. On study days, the fasted animals were infused intravenous CCK-8 (40 or 400 pmole/kg/hr) for 60 min both with and without atropine (20 micrograms/kg/hr). Plasma was collected at 20-min intervals and PP levels were determined by radioimmunoassay. CCK-8 elicited a dose-dependent increase in circulating PP in dogs with a neurally intact pancreas. Atropine and pancreatic denervation eliminated the PP response to CCK-8 at 40 pmole/kg/hr (P < 0.01) and inhibited the PP response to CCK-8 at 400 pmole/kg/hr (P < 0.05). The high dose of CCK-8 still elicited a small PP response in the denervated dogs (P < 0.05), which was subsequently abolished by the addition of atropine. These findings suggest that extrapancreatic cholinergic nerves are essential components of CCK-stimulated PP release, and that intrapancreatic cholinergic activity may play a limited role.

Animals↗
PubMed1994

Metastatic implantation of an oral squamous-cell carcinoma at a percutaneous endoscopic gastrostomy site.

Percutaneous endoscopic gastrostomy (PEG) has become an important adjunct in the care of the head-and-neck cancer patient. When resection will likely affect swallowing, PEG can be performed just prior to cancer resection. However, it is unclear whether PEG should be the procedure of choice for establishing enteral access in head-and-neck cancer patients. In this report we describe a man with advanced oral squamous cell carcinoma who had a One-Step PEG button inserted immediately prior to his cancer resection. Six months later, the patient developed metastatic squamous-cell carcinoma at the PEG site. Although the mechanism of spread cannot be confirmed, direct seeding from passage through the cancer-filled oral cavity seems likely. Methods of establishing enteral access which avoid tumor-contaminated fields, such as use of an overtube during conventional PEG, open gastrostomy, or laparoscopic gastrostomy, may be more appropriate in head-and-neck cancer patients.

Abdominal Muscles↗
PubMed1994

Thermal injury of the posterior duodenum during laparoscopic cholecystectomy.

While complications of laparoscopic cholecystectomy occur in 3-7% of cases, bowel injuries are uncommonly reported. Bowel injuries appear to be of two types: penetrating bowel injury from either the Veress needle or trocar, and thermal bowel injury from either contact or conductive burn. The duodenum is usually spared from Veress needle or trocar injury because of its posterior location. However, during dissection in the triangle of Calot, the duodenum is at risk for direct contact burn or energy conduction burn. In this report we describe a presumed conductive burn injury of the posterior second portion of the duodenum which followed laparoscopic cholecystectomy. This unrecognized injury resulted in full-thickness necrosis of the duodenal wall with delayed perforation. This injury was successfully managed with pyloric exclusion. The diagnosis and management of this previously unreported injury are described.

Aged↗
PubMed1994

Potentiation of canine pancreatic bicarbonate output by oleic acid is not neurally dependent.

To study neural involvement in potentiation of acid-induced pancreatic bicarbonate output, six dogs underwent extrapancreatic denervation and pancreatic fistula creation. Pancreatic responses to secretin (16 and 32 ng/kg/h) and cholecystokinin (50 ng/kg/h) were then assessed. The duodenum was then perfused with three sets of perfusates. The first set contained hydrochloric acid with either D- or L-phenylalanine. The second set contained bovine serum albumin and hydrochloric acid with or without oleic acid; the albumin and acid were varied so that each 50 ml contained 1, 2, or 4 meq titratable acid (pH 2.0-4.5). The third set was identical to the second except for initial pH of 3.5. Pancreatic responses predicted upon addition of cholecystokinin to secretin, L-phenylalanine to hydrochloric acid, or oleic acid to bovine serum albumin were compared with observed responses. At both doses, secretin-induced bicarbonate output was increased by cholecystokinin (16 ng/kg/h: 0.88 +/- 0.29 meq/15 min; 32 ng/kg/h: 1.01 +/- 0.23 meq/15 min). The latter significantly exceeded predicted output (16 ng/kg/h: 0.38 +/- 0.10 meq/15 min; 32 ng/kg/h: 0.58 +/- 0.15 meq/15 min), verifying potentiation. L-phenylalanine failed to potentiate bicarbonate output evoked by acidified D-phenylalanine. In contrast, addition of oleic acid to pH 2.0 or 3.5 bovine serum albumin potentiated bicarbonate output. These data suggest that enteropancreatic reflexes mediate potentiation of acid-induced pancreatic bicarbonate output by amino acids, but not by fatty acids.

Animals↗