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Biomedical subjects

R Arnold

Publications and source records attributed to R Arnold.

At least 361 records · Page 20Linked to original sources
PubMed1990

Operative findings after percutaneous pulmonary balloon dilatation of the right ventricular outflow tract in tetralogy of Fallot.

Since 1983 percutaneous balloon dilatation of the right ventricular outflow tract has been performed as an alternative to surgical palliation in selected cases of tetralogy of Fallot at the Royal Liverpool Children's Hospital. From 31 December 1984 to 31 December 1988, 27 of these patients underwent subsequent surgical correction. Age at operation ranged from 7 to 58 months (median 2.7 years). The mean interval between balloon dilatation and correction was 15.6 months (range 3-39 months). Two patients had a systemic pulmonary shunt operation performed before dilatation and a further five required one afterwards. Overall 20 (74%) patients had some anatomical alteration as the result of balloon dilatation, while in seven (26%) there was no discernible change in the right ventricular outflow tract. There was no consistent relation between the ratio of balloon size to pulmonary annulus diameter and the morphological findings. Balloon dilatation may obviate the need for systemic-pulmonary shunt at the expense of some structural damage, particularly to the posterior cusp. The present data suggest that dilatation does not bring about growth of the annulus to such an extent that transannular patch is no longer needed at intracardiac repair.

Catheterization↗
PubMed1990

Cholecystokinin release by gastric distension--an atropine-sensitive mechanism.

The effect of gastric distension on plasma cholecystokinin (CCK), pancreatic polypeptide (PP) and gastrin concentrations was investigated in healthy volunteers. Fundic and antral distension was achieved by balloons attached to a gastric tube and inflated with 300 and 600 ml and 100 and 200 ml of air for fundic and antral distension, respectively. Gastric juice was continuously aspirated. Fundic distension was additionally studied during a concomitant intravenous infusion of atropine (5 micrograms/kg/h) or a bolus injection of propranolol (2 mg). Fundic distension with 300 ml caused a significant increase in PP release (+17% above basal). Distension with 600 ml significantly stimulated CCK (+81%), gastrin (+31%) and PP output (+74%) over 30 min. Atropine completely blocked PP release and almost abolished CCK release, whereas gastrin output was enhanced. Propranolol did not prevent CCK release induced by fundic distension, whereas gastrin and PP responses were diminished. Antral distension did not cause any significant changes in hormone response. In conclusion, we demonstrated a gastric phase of CCK release which is atropine sensitive, but not influenced by propranolol.

Adult↗
PubMed1990

Dexamethasone pretreatment of rat insulinoma cells decreases binding of glucagon-like peptide-1(7-36)amide.

The effect of dexamethasone on binding of glucagon-like peptide-1(7-36)amide (GLP-1(7-36)amide) to rat insulinoma-derived cells (RINm5F) was investigated. Preincubation of RINm5F cells with dexamethasone (100 nmol/l) for 24 h resulted in a decrease of GLP-1(7-36)amide binding to 55.0 +/- 8.16% (mean +/- S.E.M.), incubation for 48 h to 39.1 +/- 1.76%, and for 72 h to 15.5 +/- 4.35% of maximal binding. The GLP-1(7-36)amide-induced stimulation of cyclic AMP (cAMP) production was significantly decreased to 61.03 +/- 7.4% of maximum production in cells pretreated with dexamethasone (100 nmol/l) for 48 h. The decreased binding was due to a reduction of the receptor number while the receptor affinity remained unchanged. These inhibitory effects on binding and cAMP formation induced by dexamethasone were completely abolished when the antiglucocorticoid RU 38486 (100 nmol/l) was added during preincubation with dexamethasone. RU 38486 alone had no effects. Our data suggest that the biological action of GLP-1(7-36)amide at the B-cell may be modified by glucocorticoids.

Animals↗
PubMed1990

Myoelectric and manometric patterns of human rectosigmoid colon in irritable bowel syndrome and diverticulosis.

Rectosigmoid electric control activity and intraluminal pressure were measured in the fasting state and after a standard 3040-kJ meal in irritable bowel syndrome (IBS) patients (n = 41), diverticulosis patients (n = 15), and healthy controls (n = 13). Analysis of myoelectric and motor patterns was performed computer-based with home-made software. Spectral analysis (fast Fourier transform) and computer recognition of slow waves emulating visual scoring showed very similar slow-wave frequency patterns in all three groups. Calculation of contractile indices displayed a widely scattered variable of motility in all three groups without significant differences. IBS subgroups with different bowel patterns showed very similar frequencies of basic myoelectric rhythm and a considerable overlap of contractile activity without significant differences among the subgroups and compared with controls. Slow-wave rhythm seems unlikely to be the basis of disturbed motility in IBS and diverticular disease. A specific pattern of contractile activity was not detectable in either condition.

Adult↗
PubMed1990

Effect of glucagon-like peptide-1 on gastric somatostatin and gastrin secretion in the rat.

The effect of glucagon-like peptide-1 (GLP-1) amide on gastric somatostatin and gastrin secretion was investigated in the isolated, vascularly perfused rat stomach preparation. GLP-1 (7-36) amide, 10(-12) to 10(-7)M, dose-dependently increased gastric somatostatin release, achieving maximal stimulation (314 +/- 15% above basal) at the highest dose. The somatostatin response to 10(-8)M GLP-1 (7-36) amide was not affected by concomitant perfusion with tetrodotoxin. GLP-1 (1-36) amide did not affect somatostatin release. Both basal and acetylcholine-stimulated gastrin were inhibited by GLP-1 (7-36) amide but were not influenced by GLP-1 (1-36) amide. In is concluded that GLP-1 (7-36) amide is the biologically effective peptide that stimulates gastric somatostatin and inhibits gastrin secretion, probably via non-neural pathways. GLP-1 (7-36) amide-induced inhibition of gastric acid secretion may, at least in part, be due to enhanced somatostatin and/or decreased gastrin release.

Animals↗
PubMed1990

Graft failure after T cell-depleted bone marrow transplantation: clinical and immunological characteristics and response to immunosuppressive therapy.

We have investigated the clinical and immunological features of 10 cases of graft failure after T cell-depleted marrow transplantation. In addition, the hypothesis that the process of graft failure can be reversed by immunosuppressive therapy with cyclosporin + steroids +/- monoclonal antibodies was tested in seven patients. Early graft failures (before day 50) presented a uniform clinical syndrome with a host T lymphocytosis preceding the loss of the graft. In the majority of cases of late graft failure (after day 50) a syndrome comprising delayed granulopoietic regeneration, fever of unknown origin and abdominal symptoms was observed. Surface marker analysis of peripheral blood and bone marrow lymphocytes implicated a population of CD3+, CD8+, DR+ host T lymphocytes with a frequent co-expression of the Leu7+ antigen in the pathogenesis of graft failure. Immunosuppressive therapy reversed graft failure in the three cases of incomplete graft failure (i.e. with residual reticulocytes) and failed in the four cases of complete graft failure (i.e. no residual reticulocytes).

Antibodies, Monoclonal↗
PubMed1990

Effect of peptide YY on gastric acid secretion, gastrin and somatostatin release in the rat.

The influence of PYY on stimulated gastric acid secretion and the possible role of gastric somatostatin was measured in rats. PYY, infused intravenously at a dose of 800 pmol/kg/h, reduced pentagastrin (20.8 nmol/kg/h) stimulated gastric acid secretion by 34 +/- 3%, whereas in controls acid secretion remained constant throughout the 90 min observation period. In a second series the effect of PYY on the endogenous gastric somatostatin-like immunoreactivity and gastrin-release was tested in the isolated, vascularly perfused rat stomach. PYY perfused at concentrations of 10 pM to 100 nM did not change either somatostatin or gastrin secretion from the rat stomach in vitro. The study shows that PYY suppressed acid secretion in the rat. Endogenous somatostatin or gastrin is unlikely to mediate the inhibitory effect of PYY on acid production.

Animals↗
PubMed1990

Effect of omeprazole on serum gastrin levels: influence of age and sex.

Serum gastrin levels were determined in 120 consecutive patients (43 females, 77 males) with peptic disease 24 h post dose after 4 weeks continuous omeprazole (40 mg daily) treatment. Serum gastrin levels were elevated in 33 (28%) but exceeded the twice normal range in only 6 patients (5%). Age and sex did not influence the magnitude of gastrin levels. Gastrin increments induced by omeprazole compared to pretreatment with H2-blockers in 60 cases were similar in both males (42 +/- 10 pg/ml) and females (44 +/- 9 pg/ml). It is concluded that the magnitude of gastrin increases observed during omeprazole therapy are small and independent of age and sex.

Adolescent↗
PubMed1990

Pravadoline: profile in isolated tissue preparations.

Pravadoline is a novel cyclooxygenase-inhibiting analgesic with a preclinical profile of activity in vivo clearly distinct from that of other cyclooxygenase inhibitors. The purpose of the present study was to assess the possibility that pravadoline possesses pharmacologic actions in addition to inhibition of cyclooxygenase. The data demonstrate that pravadoline inhibits neuronally stimulated contractions of the guinea pig ileum and mouse vas deferens preparations. These actions of pravadoline are not shared by known cyclooxygenase inhibitors, but are mimicked by close structural analogs of pravadoline devoid of the ability to inhibit prostaglandin formation. Some structural analogs were inhibitory also in the rat vas deferens preparation. The inhibitory effects of pravadoline and a representative noncyclooxygenase-inhibiting analog in isolated tissue preparations are not mediated by an interaction with muscarinic cholinergic, adrenergic (alpha-1 or alpha-2), serotonin (5-hydroxytryptamine2 or 5-hydroxytryptamine3), opioid (mu, kappa or delta), purinergic (P1), neurokinin-1, bradykinin (B2) or prostaglandin (E2) receptors. It is concluded that pravadoline and aminoalkylinodole analogs are inhibitory in several bioassay systems via a presynaptic mechanism which does not involve inhibition of cyclooxygenase, or the activation or inhibition of several known receptors. The relevance of this mechanism to aminoalkyindole actions in vivo is the subject of future studies.

Animals↗
PubMed1990

[Ultrastructural diagnosis of neuroendocrine tumors using fine needle biopsy].

Ultrasonic-guided fine-needle-biopsies of primary pancreatic tumours or liver metastasis were performed in 13 patients with neuroendocrine tumours of the gastrointestinal tract (5 carcinoids, 3 gastrinoma, 1 PPoma, 1 calcitoninoma, 1 insulinoma, and 2 non-functional tumours). Specimens obtained were examined on the light- and electronmicroscopic level. In all cases ultrastructural examination sufficiently revealed the correct diagnosis, due to the presence of cytoplasmic neuroendocrine granules within the tumour cells. Additionally performed immunocytochemical investigations at the ultrastructural level enabled the discrimination of gastrinomas, insulinomas, and PPomas. In contrast, light-microscopic examination was less sensitive for tumour classification. It is concluded that ultrastructural investigation of fine needle biopsies represents a valuable method to sufficiently discriminate neuroendocrine neoplasms.

Adenoma, Islet Cell↗
PubMed1990

Carbachol priming increases glucose- and glucagon-like peptide-1 (7-36)amide-, but not arginine-induced insulin secretion from the isolated perfused rat pancreas.

The priming effect of carbachol on glucose-, arginine- and glucose plus GLP-1 (7-36)amide induced insulin secretion was investigated. The isolated rat pancreas was perfused in vitro during a basal period of 10 min with Krebs-Ringer-bicarbonate buffer containing 2.8 mmol/l glucose. This medium was then supplemented with carbachol (10,1.0.1 mumol/l, respectively). After an additional 10 min period at 2.8 mmol/l glucose insulin secretion was stimulated for 44 min with 10 mmol/l glucose, or glucose plus GLP-1 (7-36)amide (0.5 nmol/l), or arginine (10 mmol/l). Pretreatment with carbachol resulted in a concentration dependent sensitization of B-cells to a consecutive glucose load (10 mmol/l). Both phases of the biphasic insulin secretory response were significantly enhanced. Priming experiments followed by a subsequent combined glucose / GLP-1 (7-36)amide or arginine stimulation were performed with 10 mumol/l carbachol. Prior exposure of the pancrease to carbachol enhanced the glucose / GLP-1 (7-36)amide induced insulin release, but left the arginine stimulated secretion unaltered. Our data suggest that in the regulation of postprandial insulin release cholinergic sensitizing effects might be involved which are mediated by muscarinic receptors.

Animals↗
PubMed1989

[Stomach tolerance of acetylsalicylic acid by addition of calcium carbonate. A study of a 2-treatment/3-period cross-over design].

18 male volunteers (age 24 +/- 4 years; Broca index 0.94 +/- 0.08; mean +/- SD) underwent six upper endoscopies (three control and three test investigations) in a single blind two treatments-crossover designed study which evaluated the effect of buffering on aspirin-induced (one single oral dose of 0.5 g aspirin to fasted subjects) gastroduodenal mucosal injury. All subjects had a normal endoscopy prior to applications of 0.5 g plain aspirin (group A; swallowed) or 0.5 g aspirin + 0.3 g calcium carbonate (group B; chewed before swallowing). The sequence groups were A-B-B (n = 9) or B-A-A (n = 9). In advance fo the performed tests a washout period of six days was chosen. Endoscopies were performed two hours after ingestion of the respective tablets. The appearance of corpus, antrum, and duodenum was scored. Biopsies were taken for histological examinations. 15 volunteers experienced no gastrointestinal side effects. Three complained short-lasting gastric burning (two of group A, one of group B). In both treatment groups no significant lesions of the duodenum were found. Buffering significantly (p less than 0.0005) reduced mucosal injuries which occurred mainly as submucosal hemorrhage but without histological alterations of the mucosal architecture after aspirin ingestion. These findings suggest that oral administration of calcium carbonate buffered, chewable aspirin tablets is less harmful to the gastric mucosa than plain aspirin.

Adult↗
PubMed1989

Synergistic stimulatory effect of glucagon-like peptide-1 (7-36) amide and glucose-dependent insulin-releasing polypeptide on the endocrine rat pancreas.

The interaction of glucagon-like peptide-1 (7-36)amide (GLP-1) and glucose-dependent insulin-releasing polypeptide (GIP) on insulin release from the perfused rat pancreas was studied. The GLP-1 stimulated (0.5 nmol/l), glucose-induced (6.7 mmol/l) insulin secretory answer was enhanced by GIP (0.1, 1.0 and 10.0 nmol/l) to the arterial perfusate. This effect was maximal at 1 nmol/l GIP and smaller but still significant at 0.1 nmol/l GIP. The high GIP concentration of 10 nmol/l GIP did not further increase insulin secretion compared to the stimulation by 1 nmol/l GIP. Our data demonstrate an additive synergistic effect of GLP-1 and GIP on the glucose-induced insulin release. This supports the concept of an action "in concert' of gastrointestinal incretin hormones postprandially released on the endocrine pancreas to guarantee adequate insulin answers after meals.

Animals↗
PubMed1989

[Nizatidine versus ranitidine in the treatment of acute duodenal ulcer. Comparison of 300 mg nizatidine and 300 mg ranitidine in a single evening dose].

In a double-blind, endoscopically controlled study on 367 duodenal ulcer patients, we compared the clinical efficacy of 300 mg ranitidine nocte with that of 300 mg nizatidine nocte, which is known to reliably provide selective inhibition of nocturnal acid secretion. Nizatidine was administered to 183, ranitidine to 184 patients. Endoscopy was performed at the start of the study, as well as at 2, 4 and 8 weeks. The presence of ulcer was defined as a benign lesion of the gastric mucosa measuring at least 5 mm in diameter; healing was characterized as complete reepithelialization. In the nizatidine group, as many as 76% of our patients were free from night pain at 2 weeks, and 88% at 4 weeks. Identical values were obtained in the group treated with 300 mg ranitidine nocte. The healing rates at 2, 4 and 8 weeks were comparable in the nizatidine and ranitidine groups (nizatidine: 57%, 87%, 92%, respectively; ranitidine: 63%, 90%, 96%, respectively). Clinically significant adverse effects were seen in neither of the two treatment groups. These results demonstrate that selective inhibition of nocturnal acid secretion achieves healing of duodenal ulcer and freedom from pain as rapidly and effectively as protracted inhibition of acid secretion provided by the administration of 300 mg ranitidine nocte.

Adolescent↗