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Biomedical subjects

H A Reber

Publications and source records attributed to H A Reber.

At least 109 records · Page 6Linked to original sources
PubMed1990

Pancreatic cystic endocrine neoplasms.

A rare case of cystic pancreatic endocrine tumor is presented, and the literature is reviewed. The patient was initially misdiagnosed as having a pancreatic pseudocyst, and that condition was managed accordingly. Persistence of the cystic lesion and reoperation led to the correct diagnosis and management. The neoplasm stained positive for glucagon and pancreatic polypeptide, but there were no clinical abnormalities that suggested hyperfunction. All cystic lesions of the pancreas should undergo biopsy at operation, to avoid an erroneous diagnosis of benign pseudocyst. Neoplastic lesions should be resected, not internally drained.

Adenoma, Islet Cell↗
PubMed1990

Treatment of acute alcoholic pancreatitis in cats.

We created acute pancreatitis in cats by instilling ethanol (20 ml of a 40% solution) into the stomach and then perfusing activated pancreatic enzymes through the main pancreatic duct. Edematous pancreatitis developed within 24 h as the enzymes leaked out of the duct into the surrounding pancreatic parenchyma. We tested the effects of a number of agents on the amelioration of the severity of the pancreatic inflammation. Cimetidine (an H2 receptor blocker) and Benadryl (an H1 receptor blocker) given in combination decreased the incidence of pancreatic hemorrhage but not the overall degree of inflammation. Indomethacin (a cyclooxygenase inhibitor) had a similar effect. Terbutaline (a beta-agonist) given alone decreased the overall degree of inflammation, including the incidence of hemorrhage. All of the drugs given together were no more effective than terbutaline alone. The combination was effective even when given up to 12 h after the onset of pancreatitis.

Acute Disease↗
PubMed1990

The cause and management of the pain of chronic pancreatitis.

The cause of pain in chronic pancreatitis appears to be related to ductal and parenchymal hypertension and possibly to pancreatic ischemia. The management of pain needs a multidisciplinary approach. Medical measures such as abstinence from alcohol and therapy with mild analgesics are useful. Surgery should be considered when the pain begins to interfere with the patient's quality of life. Ductal drainage operations may be indicated when the duct is dilatated. The alternative is pancreatic resection, which, although safe and effective, creates diabetes when much of the pancreas is removed. Newer operations that relieve pain while preserving function are being devised.

Abdominal Pain↗
PubMed1989

Pancreatic duct pressure, duct permeability and acute pancreatitis.

The relationship between pancreatic duct pressure, duct permeability to macromolecules and the development of acute pancreatitis was studied in a cat model. Perfusion of the pancreatic duct with 15 mM glycodeoxycholic acid, ethanol administration, or secretagogue-stimulated pancreatic secretion against greater than 50 per cent duct obstruction resulted in an increase in peak pancreatic duct pressure in all animals. Duct permeability to 20,000 molecular weight dextran molecules was increased in 22 of 29 experimental animals compared with two of 22 control animals (P less than 0.01). Perfusion of the pancreatic duct with activated pancreatic enzymes resulted in acute pancreatitis in 24 of 29 experimental animals compared with three of 22 control animals (P less than 0.01). These results suggest that pancreatic ductal hypertension, resulting in increased ductal permeability to large molecules, may be a common early event in gallstone and alcoholic pancreatitis.

Acute Disease↗
PubMed1989

Surgical palliation for pancreatic cancer.

The effectiveness of surgical palliation for pancreatic cancer has been reviewed. Jaundice should be relieved early as this eliminates distressing pruritus, improves the quality of life, and avoids the sequelae of prolonged extrahepatic obstruction. The procedure may prolong survival, but this has not been proved. Biliary obstruction is managed best by a simple loop cholecystojejunostomy. If the gallbladder is unavailable, a choledochojejunostomy is equally effective. Nonsurgical techniques such as percutaneous or endoscopically placed biliary stents may be appropriate in patients who are not candidates for surgery. A gastrojejunostomy should be done in all patients who have gastroduodenal obstruction by tumor. Most patients who undergo surgical biliary bypass also should have a gastrojejunostomy, even if gastroduodenal obstruction has not yet developed. Otherwise, more than 20 per cent of patients may need a second operation if gastroduodenal obstruction develops later. Pain, a problem in more than half of patients, is best relieved by an intraoperative celiac ganglion block with 50 per cent ethanol. Laparotomy is desirable in most of these patients with pancreatic cancer, because it provides tissue for diagnosis, allows a definite assessment of resectability, and produces effective palliation.

Anastomosis, Roux-en-Y↗
PubMed1988

Possible mechanisms of acute pancreatitis induced by ethanol.

We investigated the effect of intravenous and intragastric ethanol on pancreatic duct pressure, duct permeability to dextran molecules (20,000 molecular weight), and on the development of acute pancreatitis in an experimental model of the disease. Intragastric ethanol caused a small increase in pancreatic duct pressure (6 to 7 mm Hg) and an increase in duct permeability to dextran. Intravenous ethanol with exclusion of the sphincter of Oddi did not increase pancreatic duct pressure or permeability. Intravenous ethanol and intragastric normal saline solution altered neither pressure nor permeability. Artificial elevation of pancreatic duct pressure alone with no ethanol had no effect on duct permeability. However, when intravenous ethanol was given to produce similar systemic concentrations as achieved in the intragastric experiments (250 mg/dl) and duct pressure was artificially raised, duct permeability was increased. Ethanol concentrations similar to those found in peripheral blood were detected in secretin-stimulated pancreatic juice. Perfusion of the pancreatic duct with activated pancreatic enzymes after intragastric but not intravenous ethanol (that is, only in animals with increased duct permeability) caused acute edematous pancreatitis. Our results confirmed that increased duct permeability was necessary to produce acute pancreatitis in this model, and that this increase in permeability resulted from both a small increase in duct pressure and probably from the toxic metabolic effects of ethanol.

Acute Disease↗
PubMed1988

Acute hypercalcemia, pancreatic duct permeability, and pancreatitis in cats.

We investigated the effects of hypercalcemia on pancreatic duct permeability and pancreatitis in cats. Acute hypercalcemia was maintained by an infusion of calcium gluconate; controls received saline solution. Chronic hypercalcemia was maintained by diet and by vitamin D and dihydrotachysterol injections. Portal venous blood was analyzed for large dextran molecules that had been perfused through the pancreatic duct. In a separate group of hypercalcemic animals, we perfused the duct with activated pancreatic enzymes to induce acute pancreatitis. After 24 hours of hypercalcemia, dextrans were detected in the portal venous blood of 6 of 11 hypercalcemic and none of the 6 control animals (p less than 0.05). After 12 hours of hypercalcemia, dextrans were detected in all 7 hypercalcemic and 1 of 7 control animals (p less than 0.001). The degree of pancreatic inflammation was greater in the 12-hour animals than in the controls (p less than 0.001). After 14 days of hypercalcemia, however, there were no differences in dextran permeability or pancreatitis in experimental or control animals. Our results indicate that acute hypercalcemia increases the permeability of the pancreatic duct to molecules the size of pancreatic enzymes. This could be important in the pathogenesis of acute pancreatitis associated with hypercalcemic states.

Acute Disease↗
PubMed1987

Vasoactive drugs, microvascular permeability, and hemorrhagic pancreatitis in cats.

We investigated the mechanisms by which 16,16-dimethyl prostaglandin E2 and histamine induced pancreatic hemorrhage in an experimental model of acute pancreatitis in cats. In normal animals, when large molecular weight dextran molecules were infused into the systematic circulation, they were recovered in secretin-stimulated pancreatic juice in low concentrations. Both 16,16-dimethyl prostaglandin E2 (in a dose that increased splenic artery blood flow and microvascular permeability) and histamine (in a dose that increased permeability only) increased the amount of dextran recovered in pancreatic juice. Isoproterenol, in a dose that produced the same increase in blood flow as 16,16-dimethyl prostaglandin E2 but which did not increase microvascular permeability, did not alter the amount of dextran recovered. This suggested that the increase in dextran output after 16,16-dimethyl prostaglandin E2 was primarily due to the increase in microvascular permeability caused by the drug. In other experiments, a combination of H1- and H2-receptor antagonists (mepyramine and cimetidine) protected against the development of pancreatic hemorrhage in both the prostaglandin- and histamine-treated animals. Indomethacin (a cyclooxygenase inhibitor) protected against the development of hemorrhage in the histamine-treated animals. Our results support the hypothesis that changes in microvascular permeability may be important in the pathogenesis of parenchymal hemorrhage in this model.

Animals↗
PubMed1987

Treatment of acute pancreatitis with beta-adrenergic agonist drugs.

An increase in microvascular permeability may be important in the pathogenesis of acute pancreatitis. beta-adrenergic receptor agonist drugs are known to inhibit the increase in microvascular permeability induced by histamine and related vasoactive substances. These inflammatory mediators have been shown to be released during the course of experimental and human pancreatitis. We investigated the effect of isoproterenol and terbutaline sulfate on the development of acute edematous (AEP) and acute hemorrhagic (AHP) pancreatitis in a feline model of biliary pancreatitis. When given at the time of pancreatic insult, isoproterenol prevented the development of both AEP and AHP. Both isoproterenol and terbutaline sulfate reduced the severity of pancreatic inflammation, even when given up to 12 hours after the onset of AEP. Although neither drug was effective in treating established AHP, our findings suggest that, if given early in the course of the disease, they may be useful in preventing the progression of AEP to AHP.

Acute Disease↗
PubMed1986

Effects of oral agents on pancreatic duct permeability. A model of acute alcoholic pancreatitis.

The main pancreatic duct can be made permeable to molecules of up to 20,000 daltons by oral pretreatment with aspirin and ethanol. Because pancreatic enzymes have similar molecular weights, we hypothesized that activated pancreatic enzymes would leak from a permeable duct and produce pancreatitis. Four groups of cats were pretreated with either milk, aspirin, ethanol, or aspirin and ethanol for 48 hr. Then pancreatic juice (either activated by enterokinase or nonactivated) was perfused along the duct from tail to duodenum. Twenty-four hours later the animals were examined. Animals pretreated with aspirin, ethanol, or both, and in which ducts were perfused with activated juice, developed acute edematous pancreatitis. Animals that had perfusion with nonactivated enzymes had pancreases indistinguishable from control animals. Morphological studies on ductal permeability in animals pretreated with ethanol and aspirin showed electron-dense material (believed to be dextran) between the basal plasma membrane and basal lamina, and in the basal intercellular space.

Acute Disease↗
PubMed1986

A model of hemorrhagic pancreatitis in cats--role of 16,16-dimethyl prostaglandin E2.

Acute edematous pancreatitis was induced in cats by perfusing activated pancreatic enzymes through their pancreatic ducts. The ducts had been made permeable to large molecules by one of two techniques. The cats either received ethanol (2 ml/kg every 8 h) and aspirin (25 mg/kg every 8 h) orally for 48 h or had their pancreatic ducts perfused for 1 h with 7.5 mM glycodeoxycholate. When the same procedure was followed, but using 16,16-dimethyl prostaglandin E2 (dmPGE2) (2 micrograms/kg X h infused intravenously for 1 h before and during ductal perfusion with activated enzymes), hemorrhagic pancreatitis developed instead. To investigate whether an increase in pancreatic blood flow or microvascular permeability (both caused by dmPGE2) was important in this phenomenon, we tested the effects of isoproterenol (which increased blood flow) and histamine (which increased microvascular permeability) in the model. Thus in similar experiments, either isoproterenol (0.3 micrograms/kg . min) or histamine phosphate (2 micrograms/kg . min) was infused instead of dmPGE2. The animals that received histamine also developed hemorrhagic pancreatitis. Those that received isoproterenol did not. These observations suggested that an increase in microvascular permeability in the pancreas converted edematous pancreatitis to hemorrhagic pancreatitis. These findings suggest also that clinical studies using prostaglandins to treat patients with pancreatitis should be approached with caution.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Pancreatic duct and microvascular permeability to macromolecules. The relation to acute pancreatitis.

In a model of acute pancreatitis which requires that pancreatic enzymes leak from a permeable duct, we studied the role of intravenous enterokinase (195,000 daltons) in pancreatic enzyme activation. Anesthetized cats were given intravenous 16,16-dimethyl prostaglandin E2 to increase pancreatic blood flow and microvascular permeability. In some animals the permeability of the pancreatic duct was increased by perfusion of the duct with glycodeoxycholic acid (7.5 mM). Endogenous enzyme secretion was stimulated by IV CCK and secretin. Some cats also received enterokinase intravenously. Those animals that received PGE2, glycodeoxycholate, and enterokinase all developed pancreatitis. When any of these agents were not given the pancreases appeared normal. These findings were consistent with the hypothesis that intravenous enterokinase leaked from small pancreatic blood vessels into the pancreatic parenchyma and/or ducts where activation of pancreatic enzymes occurred. The development of pancreatitis appeared to require an increase in both microvascular and ductal permeability.

16,16-Dimethylprostaglandin E2↗
PubMed1984

Effects of bile salts on permeability and morphology of main pancreatic duct in cats.

We studied the changes in permeability and morphology in the main pancreatic duct of cats after exposure of the duct to specific bile salts. Cats were anesthetized and the main pancreatic duct was cannulated in the tail and head of the pancreas. The duct was perfused with sodium cholate (1, 1.5, 2, 15 mM) or sodium glycodeoxycholate (1, 2, 15 mM) for 60 min at pressures which never exceeded 20 cm water. Then the duct was perfused with fluorescein-tagged dextran molecules of specific size (3000, 20,000, or 40,000 daltons). Recovery of the dextran from portal venous blood indicated that the duct was permeable to that particular dextran. Normally the ducts were impermeable to even the 3000-dalton dextran, and perfusion with either 1 mM cholate or glycodeoxycholate did not change this. However, perfusion with either bile salt at concentrations above 1 mM progressively increased duct permeability. At this highest bile salt concentrations used, the ducts became permeable to molecules as large as 20,000 daltons. Morphologic changes paralleled the changes in permeability. Control animals had pancreatic ducts whose ultrastructure was indistinguishable from normal. Perfusion of the ducts with low concentrations of bile salt for up to 60 min resulted only in a loss of microvilli from the cell surface and an increase in cytoplasmic phagolysosomes. Perfusion with higher concentrations of bile salt for 5-60 min induced progressively severe alterations. These included disruption of the tight junctions and the swelling of intercellular spaces between the duct cells, flattening of the duct epithelium, and eventual cell loss which left a break in the epithelial lining of the duct. These studies indicate that the pancreatic duct in cats, exposed to specific bile salts at physiological concentrations and pressures, undergoes marked structural alterations. The duct becomes permeable to molecules at least as large as 20,000 daltons, whereas it is normally impermeable to molecules as small as 3000 daltons.

Animals↗
PubMed1984

Delayed gastric emptying after operation for obstructing peptic ulcer disease: the influence of cimetidine.

We studied the factors related to delayed gastric emptying after operation for obstructing peptic ulcer disease. The records of 76 consecutive patients who underwent operation for obstructing peptic ulcer were examined retrospectively. Delayed gastric emptying (unable to tolerate solid food for at least 2 weeks after operation) occurred in 11 of 76 patients (14.5%). It was not related to the type of operation performed, including procedures that employed truncal vagotomy. It did not correlate with the preoperative severity of obstruction, duration of preoperative nasogastric decompression, or the nutritional status of the patient. Delayed emptying occurred in four of six patients (66.7%) with insulin-dependent diabetes mellitus but only 10 of 70 patients (14%) without insulin-dependent diabetes (p less than 0.001). It was seen in six of 16 patients (37.5%) receiving long-term cimetidine therapy (more than 3 months) but only five of 60 patients (8.3%) not receiving long-term cimetidine therapy (p less than 0.01). Patients receiving long-term cimetidine therapy had an average number of 2.3 prior hospitalizations for ulcer disease while those not receiving long-term cimetidine therapy had an average of 1.4 prior admissions (p less than 0.01). Thus we advise against the long-term use of cimetidine in chronic peptic ulcer disease complicated by obstruction. Patients with diabetes mellitus who require insulin appear to be at particular risk for delayed gastric emptying after operation for obstructing peptic ulcer.

Cimetidine↗
PubMed1983

Effect of acid secretory capacity and chronic endogenous hypergastrinemia on pancreatic secretion and intestinal morphology in the rat.

To study the trophic effects of gastrin on the gastrointestinal tract, chronic endogenous hypergastrinemia was produced in rats by implantation of the gastric antrum into the colon. Rats were sham-operated (normal gastrin, normal acid) or were prepared with BII gastrojejunostomy and antral resection (low gastrin, low acid), or BII gastrojejunostomy and antral implantation into colon (high gastrin, acid present). To separate effects of hypergastrinemia from those of acid hypersecretion, two additional groups were prepared with total gastrectomy and either resection of the antrum (low gastrin, no acid) or antral implantation into colon (high gastrin, no acid). After 12 weeks, the pancreatic secretory response to secretin was measured. The animals were then sacrificed, and liver, pancreas, small intestine, and colon were weighed. In separate groups of animals villous height and width and crypt depth of small intestine and transverse colon were measured. Serum gastrin concentrations increased three- to fivefold in fasting and fed antral implant animals. Serum gastrin levels in the fed state were lower in antrectomy rats compared to controls but did not differ in the fasting rats. Pancreas and colon were heavier in all hypergastrinemic rats. Liver weights did not differ between hypergastrinemic animals and controls. Stimulated pancreatic bicarbonate secretion following secretin infusion was elevated only in hypergastrinemic, hyperacidic rats. Hypertrophy of the small bowel was seen in antral implant rats only when the gastric remnant was preserved (ie, when acid was present). Colonic mucosal thickness was increased in antral implant rats with or without gastrectomy. No significant increases in small-bowel villous height or crypt depth were found in antral implant rats. Thus, chronic endogenous hypergastrinemia caused pancreatic and colonic hypertrophy independent of acid secretion. In addition to hypergastrinemia, gastric hyperacidity was also needed for enlargement of small bowel or increase in secretin-stimulated pancreatic bicarbonate secretion.

Animals↗
PubMed1983

Modification of pancreatic carcinogenesis in the hamster model. XII. Dose-related effect of ethanol.

Ethanol (E) was given to outbred Syrian golden hamsters in drinking water at a 5% (wt/vol) concentration for life beginning either before or after a single dose of N-nitrosobis(2-oxopropyl)amine (BOP). No effects on tumor induction were seen in the pancreas or in other BOP target tissues (e.g., the common duct and gallbladder), whether E was given immediately after or 4 weeks before and immediately after BOP. These results sharply conflicted with our previous findings in which a higher concentration of E (25% wt/vol) inhibited BOP-induced pancreatic lesions, and they indicated a dose-related action of E on pancreatic carcinogenesis. Development of a few acinar cell foci in hamsters treated with BOP and E, but not in those treated with E alone or BOP alone, indicated that E in this concentration alters pancreatic functions without modifying carcinogenesis.

Animals↗