Noninfectious ascitic fluid leukocytosis associated with penetrating duodenal ulcer.
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Ascitic Fluid↗
Biomedical subjects
R F Harty
Publications and source records attributed to R F Harty.
Sclerosing peritonitis and propranolol.
Sclerosing peritonitis developed in a 43-year-old man with angina pectoris who had been receiving the beta-adrenergic receptor antagonist, propranolol. The patient had abdominal and back pain, weight loss, a midabdominal fullness, ascites, and evidence of partial small bowel obstruction. At surgery, the small bowel was distended and encased by dense fibrous tissue. Infectious and neoplastic causes of fibrosing peritoneal inflammation were excluded. The patient described in this report illustrates several features commonly experienced by individuals who developed sclerosing peritonitis associated with beta-adrenergic receptor blockade therapy. To my knowledge, the development of ascites and considerable ascitic fluid leukocytosis have not been described previously with this disorder.
Adult↗
Severe hyperchloremic acidosis complicating jejunoileal bypass.
In summary, severe hyperchloremic acidosis developed in two patients as a late complication after jejunoileal bypass for morbid obesity. This acidosis was associated with episodes of dizziness, ataxia, headache, weakness, confusion and transient loss of consciousness. Recognition of this symptom complex in the patient with a jejunoileal bypass should suggest metabolic acidosis as a complication of this surgical procedure. Bicarbonate replacement provided prompt, but temporary, improvement in the symptoms and the acidosis. Revision of the intestinal bypass was required for correction. Special studies to rule out renal tubular acidosis were performed and definitely excluded the kidney as a source of the acidosis.
Acidosis↗
Stimulation of gastrin secretion and synthesis in antral organ culture.
The purpose of the present study was to examine stimulation of gastrin release and the synthesis of gastrin directly by measurement of incorporation of [(3)H]tryptophan into gastrin in rat antral mucosal explants maintained in organ culture. Gastrin synthesis and secretion were assessed simultaneously at intervals over the 24-h duration of explant culture. Antral mucosal explants from fed female Wistar rats (4-5 wk, 100-150 g) were cultured at 37 degrees C (95% O(2)/5% CO(2)) in medium containing 70% Trowell-T8 and 10% NCTC-135 without unlabeled tryptophan, 10% dialyzed fetal calf serum and [(3)H]tryptophan (100 muCi/ml). Antral tissue was harvested at regular intervals during 24-h culture periods. Incorporation of [(3)H]tryptophan into immunoreactive gastrin was determined by techniques utilizing double-antibody immunoprecipitation. Antral tissue protein synthesis was assessed by measurements of incorporation of [(3)H]tryptophan into tissue protein of cultured antral explants. In paired experiments, gastrin synthesis and secretion in the presence of dibutyryl cAMP (DBCAMP) were compared to those observed under control conditions. Gastrin and protein specific activity progressively increased with time. Gastrin specific activity at 30 min increased from 3.3+/-0.5 (SEM) to 55.2+/-10.6 fmol [(3)H]tryptophan/pmol gastrin (or from 1.57+/-0.48 to 26.28+/-5.05 pmol [(3)H]tryptophan/mug gastrin) at 24 h: specific activity of antral tissue protein at 30 min increased from 33.6+/-8.4 to 1,660+/-236 fmol [(3)H]tryptophan/mug protein at 16 h. Culturing of explants for 4 h in the presence of cycloheximide (100 mug/ml) inhibited both gastrin synthesis and protein synthesis by greater than 90 and 95%, respectively. DBCAMP (10 mM) significantly increased both the synthesis and secretion of antral gastrin when compared with control cultured explants. Results of these experiments provide direct demonstration of gastrin synthesis by rat antral mucosal explants in organ culture, indicate that both gastrin and total antral protein synthesis are inhibited by cycloheximide, and demonstrate DBCAMP-induced stimulation of both gastrin synthesis and secretion, suggesting the potentially important role of cyclic AMP in gastrin cell function.
Animals↗
Stimulation of hepatic bile secretion by dopamine.
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Animals↗
Comparison of adrenergic and cholinergic receptor-mediated stimulation of gastrin release from rat antral fragments.
Rat antral mucosal fragments were maintained in short-term culture to examine the relative potencies and receptor specificity of the cholinergic agonist, carbachol, and adrenergic agents, norepinephrine, isoproterenol, clonidine and phenylephrine in stimulating gastrin release. Results of these studies indicate that norepinephrine and carbachol evoke pharmacologically and temporally distinctive patterns of antral gastrin release. Dose-response experiments indicate that norepinephrine is approximately 10,000 times more potent on a molar basis than carbachol in stimulating antral gastrin release. Adrenergic (norepinephrine, isoproterenol) stimulation of antral gastrin release was prevented by propranolol, and cholinergic- (carbachol) mediated peptide release was blocked by both atropine and pirenzepine. Phenylephrine and clonidine did not alter basal gastrin release. The pattern of peptide release as a function of time was quite different for each agent: norepinephrine exerted its stimulatory effect acutely during the initial 30 minutes of incubation, while carbachol exhibited a sustained stimulatory action throughout the 2-hour culture period. In conclusion, data from these studies suggests that there are marked differences between norepinephrine and carbachol in their pharmacological potency and time-dependent activation of the G cell.
Animals↗
GABA affects the release of gastrin and somatostatin from rat antral mucosa.
gamma-Aminobutyric acid (GABA) is regarded as the major inhibitory neurotransmitter in the central nervous system of vertebrates. GABA exerts its inhibitory actions by interacting with specific receptors on pre- and postsynaptic membranes and has been shown to inhibit somatostatin release from hypothalamic neurones in vitro. Concepts of innervation of the gastrointestinal tract have been expanded by recent studies which suggest that GABAergic neurones are not confined solely to the central nervous system but may also exist in the vertebrate peripheral autonomic nervous system. Jessen and coworkers have demonstrated the presence, synthesis and uptake of GABA by the myenteric plexus of the guinea pig taenia coli, and have documented the presence of glutamic acid decarboxylase (GAD) in isolated myenteric plexus. This enzyme is responsible for the conversion of glutamic acid to GABA in GABAergic neurones. The possibility that GABA may have a role in neurotransmission or neuromodulation in the enteric nervous system of the vertebrate gut has been suggested by several investigators. Furthermore, GABA receptors have been demonstrated on elements of the enteric nervous system. The effects of GABA on gastrointestinal endocrine cell function have not been examined. We report here the effects of GABA on gastrin and somatostatin release from isolated rat antral mucosa in short-term in vitro incubations.
Animals↗
Postresection hypergastrinemia correlates with malabsorption but not adaptation.
Massive intestinal resection is associated with transient hypergastrinemia and gastric hypersecretion. Gastric hypersecretion impairs intestinal absorption, but gastrin may be trophic during intestinal adaptation. Our aim was to determine if postresection hypergastrinemia correlates with malabsorption or adaptation. Ten dogs (13 to 19 kg) underwent 75% proximal intestinal resection. Intestinal remnant length and villus height was assessed at 12 weeks (n = 5) and 40 weeks (n = 5). Body weight and serum albumin, as well as stool fat, moisture, and weight, were measured preoperatively and at 4-week intervals for 40 weeks. Fasting serum gastrin values were measured by radioimmunoassay at similar intervals. Significant hypergastrinemia occurred between 4 and 28 weeks postresection. Hypergastrinemia did not correlate with increased intestinal remnant length (r = -.486, p = .407) or villus height (r = -.410, p = .584). Duration of hypergastrinemia (> 100 pg/ml) correlated with percentage of fecal fat at 12 weeks (r = .807, p = .015) and stool weight at 40 weeks (r = .881, p = .046). Thus, postresection hypergastrinemia correlates with early fat malabsorption and increased stool weight, but there is no correlation between hypergastrinemia and adaptation. These findings suggest that gastric hypersecretion, not hypergastrinemia, may be the more important pathophysiologic event after intestinal resection.
Adaptation, Physiological↗