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Biomedical subjects

J H Landor

Publications and source records attributed to J H Landor.

At least 19 recordsLinked to original sources
PubMed1995

Colonic histiocytic neoplasm mimicking malignant histiocytosis and presenting as intussusception.

It is now apparent that distinction between the so-called malignant histiocytosis and lymphoma can be made using panels of established immunohistochemical markers and/or genotypic analysis. Many, if not all, of the previously diagnosed cases of malignant histiocytosis have been shown to be of lymphoid, rather than histiocytic, lineage. We report a rare case of colonic histiocytic neoplasm accompanied by a lymphoreticular dissemination that mimicked that of malignant histiocytosis. In addition, barium studies and computed axial tomography confirmed an intussusception that subsequently developed. The histiocytic nature of the neoplastic cells was supported by immunohistochemical, ultrastructural, and cytochemical studies. To our knowledge our case may represent the fifth documented case of a histiocytic malignancy reported in the literature. The relationship among the various cases will be discussed as well as the significance of the focal S-100 immunoreactivity observed in the present case.

Colonic Diseases↗
PubMed1984

Control of the Zollinger-Ellison syndrome by excision of primary and metastatic tumor.

In a patient with Zollinger-Ellison syndrome, control of the peptic ulcer diathesis was attempted by excision of a small duodenal gastrinoma and removal of three lymph nodes containing metastases. The patient has been asymptomatic for 2.5 years with basal achlorhydria, a normal serum gastrin level and a negative gastrin response to secretin. Our experience with this patient emphasizes the fact that the presence of metastatic disease does not preclude the possibility of long-term control of hypergastrinemia by resection of the tumor. Attempts to cure the Zollinger-Ellison syndrome by tumor resection alone, however, should only be made in patients whose hypersecretion is adequately controlled by antisecretory drugs.

Antacids↗
PubMed1984

Mechanisms of protein activation of the intestinal phase of gastric secretion.

To determine if the secretory response to protein in the gut is due to direct effects of absorbed amino acids on the parietal cells, to hormonal effects, or to a combination of both, Heidenhain pouch secretion and plasma amino nitrogen levels were measured during enteral infusions of casein or liver extract, as well as during intravenous infusions of amino acids, in three dogs with and three dogs without portacaval transposition. In the dogs without portacaval transposition, gastric secretory responses were slight and did not differ significantly; secretory responses were seen only during infusions in which elevations of plasma amino nitrogen values occurred. In dogs with portacaval transposition, secretory responses to both casein and liver extract were significantly higher (P less than 0.02) than was the response to intravenous amino acids, while plasma amino nitrogen levels rose to virtually identical levels during all three kinds of infusion. These data support the hypothesis that absorbed amino acids contribute to the intestinal phase of gastric secretion. The finding that casein and liver extract in the gut evoked greater gastric secretion responses than did intravenous amino acids, even though increases in plasma amino nitrogen levels were similar, suggests that the intestinal phase results form the combined effects of absorbed amino acids and hormonal influences rather than from the effects of amino acids alone.

Amino Acids↗
PubMed1981

Results of surgical management in 92 consecutive patients with Zollinger-Ellison syndrome.

Hospital records and follow-up information on 92 patients with surgically proven Zollinger-Ellison syndrome have been reviewed, and data relating to symptomatology, age and sex incidence, pathologic findings, and early and late results of surgical procedures have been summarized. The postoperative mortality rate was 15%, and was adversely affected by previous peptic ulcer surgery, by the necessity of urgent operation for complications of peptic ulcer, and by employment of a procedure that failed to control acid secretion. Thirteen patients were found to have primary gastrinomas of the duodenum and an additional 13 patients had islet cell hyperplasia without evidence of frank neoplasm; prognosis in these two groups appears to be particularly favorable. Despite the current availability of effective nonoperative measures for control of gastric hypersecretion, surgical exploration is warranted in all patients to determine location and extent of tumor and to attempt to control the ulcer diathesis by resection of tumor. Long-term therapy with H2 receptor antagonists is advised for patients whose hypersecretory state has not been alleviated by tumor resection or whose gastrinoma cannot be removed. Total gastrectomy is still indicated in patients whose tumors are not amenable to resection and who are resistant to, or cannot follow, a rigid medical regimen.

Adolescent↗
PubMed1980

Effect of an intravenous fat preparation on canine gastric secretion.

The effect of intravenous administration of a fat emulsion on canine gastric secretion stimulated by intravenous infusion of amino acids, pentagastrin or insulin was studied. The fat preparation was given at a rate of 30 ml/hour for 2 hours, and its effects were compared with those of a comparable amount of saline solution, each given on three separate occasions in each dog. Fat did not alter the Heidenhain pouch secretion stimulated by intravenous amino acids (1.10 versus 1.11 mmol of hydrogen ion, p greater than 0.9) or the gastrostomy secretion stimulated by intravenous insulin (9.22 versus 9.54 mmol of hydrogen ion, p greater than 0.7) but had a modest inhibitory effect on Heidenhain pouch secretion stimulated by pentagastrin (2.75 versus 3.54 mmol of hydrogen ion, p less than 0.05). These data provide indirect support for the contention that the inhibition of gastric secretion by fat in the gut is mediated by the release of an enterogastrone rather than by a direct effect of absorbed fat. Because gastric stimulation by intravenous fat was not observed in the dog, it seems likely that intravenous fat emulsion can be given to seriously ill patients without fear of an increased likelihood of peptic ulceration due to induced gastric hypersecretion.

Amino Acids↗
PubMed1980

Relationship between amino acid dose and gastric secretory response.

Gastric secretory dose-response studies, using an 8.5% mixed L-amino acid solution as the agonist, were carried out in three dogs with Heidenhain pouches and gastric fistulae. Secretory responses of the Heidenhain pouches were measured during two hour infusions of amino acids given at rates of 0, 0.05, 0.1, 0.2, 0.4, 0.8, and 1.6 g/kg/h and plasma amino nitrogen was measured before and during the infusion. Three separate studies at each dose level were made in each dog. The maximum secretory response occurred at the dose of 0.4 g/kg/h and amounted to approximately 20% of the maximal histamine response. Larger doses produced no additional increase in secretion or an actual decrease in secretory rate. It is concluded that the solution of amino acids used acts as a modest gastric agonist and that increases in plasma amino nitrogen such as may be observed after a protein meal are capable of eliciting a slight, but definite, gastric secretory response.

Amino Acids↗
PubMed1980

Amino acids as possible mediators of the intestinal phase of gastric secretion.

In a group of six dogs with Heidenhain pouches, the infusion of a solution of L-amino acids caused identical increases in gastric secretion when given into the jejunum as when administered directly into the portal venous system. Elevations in plasma amino nitrogen were also similar in the two circumstances. In four dogs with Heidenhain pouches and portacaval transposition, a similar infusion caused an identical increase in gastric secretion when given into the jejunum as when given into the peripheral venous system; plasma amino nitrogen levels were almost as high with the jejunal administration as with venous infusion. It is concluded that all, or almost all, of the gastric secretion evoked by amino acids in the canine intestine can be accounted for by the direct effect of absorbed amino acids on parietal cell secretion, with little or no contribution from release of an intestinal hormone.

Amino Acids↗
PubMed1978

Gastric secretory response to intravenous amino acids in eviscerated dogs.

Eight dogs, four with intact vagi and four with vagotomy, were studied to see if the gastric secretory effect of intravenously administered L-amino acids is mediated by a gastrointestinal (GI) hormone or hormones. Intravenous infusion of amino acids produced a significant secretory response in denervated and in innervated stomachs. When the known sites of formation of GI hormones were removed by resection of antrum, duodenum, pancreas, jejunum, ileum, and colon, the gastric stimulatory effect of amino acids was not changed significantly in denervated stomachs but was greatly increased in innervated stomachs. We conclude that amino acids have a direct effect on parietal cell secretion that is not dependent on the intermediary release of a stimulatory hormone, and that evisceration enhances this effect in dogs with intact vagi.

Amino Acids↗
PubMed1978

Some properties shared by amino acids and entero-oxyntin.

The intestinal phase of gastric secretion has been thought to be due to the release of a hormone from the gut mucosa, and several properties have been attributed to this as-yet unidentified hormone. An amino acid solution, known to stimulate gastric secretion, was tested to see if it possesses several of these properties, i.e., inactivation by the liver, and the ability to augment the maximum responses to pentagastrin and histamine. In six dogs with Heidenhain pouches the gastric secretory responses to peripheral and portal intravenous administration of a solution of mixed L-amino acids were measured. The mean peak response of three such separate peripheral infusions in each dog was 370 microEq/30 minutes while the peak response to intraportal infusion was only 45 microEq/30 minutes (p < .05). In three dogs with Heidenhain pouches the intravenous administration of amino acids together with pentagastrin resulted in significant augmentation of the peak response to pentagastrin alone (p < .025). Similarly, administration of amino acids with histamine resulted in augmentation of the peak response to histamine alone (p < .05). Because amino acids mimic the actions of the "intestinal phase hormone" in these respects it is suggested that they may account, at least in part, for the intestinal phase of gastric secretion. In addition, amino acids absorbed during protein digestion may contribute to the gastric hypersecretion which is regularly seen with portosystemic shunts.

Amino Acids↗
PubMed1977

Bile-fat relationships in gastric secretory inhibition and bile flow stimulation.

The effect of intraduodenal infusion of olive oil, bile, or a mixture of olive oil and bile on pentagastrin-stimulated gastric secretion, bile flow, and serum immunoreactive secretin levels was studied in dogs. Bile alone had no effect on gastric secretion, but the mixture of bile and olive oil induced prompt, statistically significant gastric secretory inhibition. Bile had the early choleretic effect that would be expected to result from the absorption of bile salts, whereas the bile--olive oil mixture brought about a delayed amd much greater increase in bile flow rates. None of the agents given intraduodenally produced a significant change in the serum secretin level. Intravenous pentagastrin infusion caused a significant increase in rate of bile flow.

Animals↗
PubMed1977

Gastric secretory effect of amino acids given enterally and parenterally in dogs.

To investigate the possible role of absorbed amino acids in the "intestinal phase" of gastric secretion, experiments were carried out in 5 mongrel dogs with Heidenhain pouches, gastrostomies, and Roux en-Y jejunostomises. A 3% solution of mixed amino acids was infused at a constant rate of 120 ml per hr throughout a 2-hr period either intravenously or intrajejunally, and the secretory response of the pouches was compared to that obtained during similar infusions of 0.9% NaCl. Intravenous administration of saline did not stimulate gastric secretion. The mean secretory responses (muEq per 2 hr) were: intrajejunal saline 37, intravenous amino acids 330, and intrajejunal amino acids 301. These results suggest that amino acids, absorbed from the gut, may play a role in the stimulation of gastric secretion which occurs when food passes through the intestine.

Amino Acids↗
PubMed1976

Effect of nicotine on serum secretin and exocrine pancreatic secretion.

The effect of nicotine (100 mug/kg hr-1) on serum secretin and pancreatic secretions was studied in dogs with chronic pancreatic fistulas. Release of immunoreactive secretin (IRS) was stimulated by intraduodenal infusion of HCl (9.6 mEq/30 min). Pancreatic flow rate and bicarbonate and protein secretions were stimulated either by intestinal acidification or infusion of exogenous secretin (1.0 IU/kg hr-1). It was found that nicotine delayed the appearance of peak IRS concentrations in response to intraduodenal HCl by about 20 min. However, nicotine had no effect on the total amount of IRS released nor was this delay accompanied by a similar delay in the appearance of peak bicarbonate output. Furthermore, nicotine did not affect pancreatic secretory function stimulated by either HCl or exogenous secretin. These data do not support the thesis that nicotine plays an important role in the pathogenesis of duodenal ulcers in smokers by inhibiting the pancreatic secretion of bicarbonate.

Animals↗
PubMed1975

Somatostatin suppresses secretin and pancreatic exocrine secretion.

Somatostatin, a hypothalamic peptide, suppresses hydrochloric acid-stimulated release of secretin, pancreatic flow rate, and bicarbonate and protein secretion in fasted, conscious dogs. It also reduces nonstimulated pancreatic exocrine secretion but does not affect basal secretin concentrations. Suppression of HCl-stimulated secretin release is complete, whereas pancreatic flow rate and bicarbonate and protein secretions are only partially inhibited. The action of somatostatin is rapid in onset and quickly reversible.

Animals↗