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Biomedical subjects

R Arnold

Publications and source records attributed to R Arnold.

At least 415 records · Page 23Linked to original sources
PubMed1988

Influence of experimental hyperthyroidism on blood and myocardial serotonin in rats.

Recent reports suggest a role for serotonin in the pathogenesis of primary hypertension and left ventricular (LV) hypertrophy. In this study, we have induced LV hypertrophy by oral feeding of thyroxine at increasing dosages (150-450 micrograms/kg b.wt.) over a 5-week period. The effects of hyperthyroidism on cardiovascular parameters, blood and myocardial serotonin concentrations were assessed. Water-fed rats and formerly hyperthyroid recovered animals served as controls. Thyroxine caused a significant LV hypertrophy: hyperthyroid rats 2.19 +/- 0.16*; controls 1.65 +/- 0.13 g/kg b.wt. (mean +/- SD; *P less than 0.05). An almost complete regression of LV hypertrophy occurred in the recovery group (1.66 +/- 0.20 g/kg b.wt.) 3 weeks after cessation of thyroid hormone application. Thyroxine-treated animals showed a significant increase of serotonin blood levels (thyroxine rats: 2108 +/- 781*, recovery: 1132 +/- 726, controls: 705 +/- 480 ng/ml; *P less than 0.05). The concentrations of serotonin in left ventricular myocardium were increased after thyroid hormone application, whereas the highest levels were found in the recovery group (thyroxine rats: 139.1 +/- 30.4, recovery: 167.2 +/- 43.1, controls: 68.9 +/- 27.9 mg/ml homogenate). Serotonin-containing cells in the left ventricular myocardium were stained immunohistochemically. They were localized perivascularly and were assumed to represent tissue mast cells. In experimental hyperthyroidism the serotonin levels in blood and heart are increased possibly indicating an interaction of both hormones in thyroxine-induced cardiomyopathy.

Administration, Oral↗
PubMed1988

Morphometric analysis of the endocrine pancreas in streptozotocin-diabetic rats kept on different dietary regimens.

The effects of different diets on the endocrine pancreas of streptozotocin-diabetic rats were investigated by morphometry. Three dietary regimens were used over a period of 43 weeks: standard diet (SD), low carbohydrate-high protein diet (LC-HP), and low carbohydrate-high fat diet (LC-HF). Nondiabetic controls received standard diet. Volume density of the total endocrine tissue was significantly reduced in streptozotocin-diabetic rats kept on standard diet as compared to control rats. This reduction of endocrine tissue was significantly less in rats kept on LC-HP diet, whereas diabetic rats kept on LC-HF did not differ from diabetic rats on standard diet. In streptozotocin-diabetic rats volume density of B cells was drastically reduced, whereas volume densities of A, D and PP cells did not differ from nondiabetic controls. This decrease of B cells was partially prevented by LC-HP diet, but not by LC-HF diet. In nondiabetic control rats as in diabetic rats on standard diet most of the islets of Langerhans sized 500-6000 microns2. In contrast, diabetic rats on LC-HP diet revealed more endocrine tissue sized from 50 to 560 microns2 consisting of two to four endocrine cells, single cells, and small islets. The results suggest that LC-HP diet may initiate reparation processes in the endocrine pancreas of streptozotocin-diabetic rats.

Animals↗
PubMed1988

Somatostatin-gastrin interactions in the rat stomach.

Low concentrations of somatostatin and gastrin within or slightly above the range of physiologically circulating levels were perfused in the isolated, vascularly perfused rat stomach preparation. Somatostatin at 10 and 50 pg/ml significantly inhibited acetylcholine-stimulated gastrin secretion by 26% and 45%, respectively, whereas perfusion of 50 and 500 pg/ml exogenous gastrin did not modify gastric somatostatin secretion. Perfusion of somatostatin-antiserum significantly increased gastrin release by 235%. It is concluded that (1) somatostatin is a powerful inhibitor of the gastrin cell under in vitro conditions; the data are in accordance with a concept that endogenous somatostatin could act as a true hormone; (2) the secretory activity of the somatostatin cell is not significantly affected by circulating gastrin.

Acetylcholine↗
PubMed1988

Influence of a small molecular weight proteinase inhibitor, gabexate mesilate (FOY), on insulin receptor function in vitro.

The effects of the low molecular weight serine proteinase inhibitor FOY (gabexate mesilate) upon insulin action was studied in three different experimental systems. Placenta membranes containing insulin receptors preincubated with FOY (10 microM) showed a reduction of insulin-stimulated tyrosine kinase activity (p less than 0.01). However, FOY (0.1-100 microM) did not affect the insulin-stimulated tyrosine kinase activity in a preparation of solubilized and partially purified insulin receptors from placental membranes. Isolated adipocytes were used to study the effect of FOY on intact cells. FOY neither altered the insulin induced inhibition of the catecholamine-stimulated lipolysis nor (at the low concentration of 0.1 mM) the stimulation of glucose transport by the hormone. High concentrations (0.5 mM) of FOY decreased the effect of insulin on the hexose transport.

Adipose Tissue↗
PubMed1988

Identification of rat pancreatic secretory proteins after separation by high-performance liquid chromatography.

In the present study an improved method of reversed-phase high-performance liquid chromatography (HPLC) for separation of rat pancreatic juice proteins is introduced. Aliquots of pancreatic juice were saved from conscious rats during basal secretion. The secretory proteins were separated on a wide-pore silica column by use of a multistep acetonitrile/water gradient. Up to 14 individual peaks could be separated by one run. Molecular weight analysis by sodium dodecyl sulfate (SDS)-gels allowed identification of peaks representing amylase, lipase, procarboxypeptidases, proelastase, chymotrypsinogen, and trypsinogen. Injection of pure rat amylase increased one specific peak which was assumed to represent amylase in the juice profile. Small amounts of residual enzymatic activities were measured for amylase, trypsin, and chymotrypsin in material of certain peaks. Activities of lipase, ribonuclease, and carboxypeptidases were not found, which reflected degradation of these enzymes by the separation procedure. High activities of phospholipase A2 were detected in one specific, early-eluting peak. Reversed-phase HPLC offers precise, reproducible, and rapid separation of the major proteins of rat pancreatic juice.

Animals↗
PubMed1988

Increased CCK-response to proteinase inhibitor feeding after induction of pancreatic hypertrophy in rats.

Repeated intragastric instillation of a trypsin inhibitor (camostate) to rats resulted in pancreatic growth. This was ascribed to the trophic effect of endogenously released cholecystokinin (CCK). We evaluated the CCK-releasing potency of different doses of camostate (50-400 mg/kg body weight administered perorally) during the course of experimentally induced pancreatic growth. Significant increments of pancreatic weight and protein and trypsin content of the pancreata were observed after 5 days of camostate treatment; changes were further pronounced after 10 days. Juice flow and protein and trypsin output from the hypertrophied pancreata were enhanced after 5 days. These effects were diminished after 10 days of camostate treatment. The direct increase in plasma CCK in response to camostate after pretreatments by daily oral doses of 200 mg/kg camostate over 5 or 10 days was more pronounced in rats with pancreatic hypertrophy compared with untreated controls. These findings mirror possible adaptation of CCK-releasing cells to "desensitisation" of acinar cells after pancreatic hypertrophy.

Animals↗
PubMed1988

Effect of cholestyramine on plasma cholecystokinin and pancreatic polypeptide levels, and exocrine pancreatic secretion.

The effect of acute and long-term administration of cholestyramine, a non-absorbable bile salt binding resin, on exocrine pancreatic secretion, plasma-cholecystokinin (CCK) and plasma-pancreatic polypeptide (PP) was investigated in 10 healthy volunteers. Oral ingestion of 12 g cholestyramine augmented the stimulatory effect of a liquid test meal on plasma-CCK (3.5-fold) and plasma-PP (2-fold). During prolonged treatment with 3 x 12 g cholestyramine daily for 4 weeks, the most pronounced increase in basal hormone levels was observed after 1 day, but progressively decreased during treatment and had normalized after 4 weeks. However, the stimulated plasma-CCK output was still significantly elevated after cessation of treatment, compared with pretreatment values. After acute and chronic cholestyramine administration only stimulated lipase secretion was elevated, whereas trypsin and amylase remained unchanged. It is suggested that removal of bile salts enhances CCK and thereby PP release and pancreatic lipase secretion.

Adult↗
PubMed1988

Stimulation of pancreatic secretion in man by a protease inhibitor (camostate).

Pancreatic secretion and plasma cholecystokinin (CCK) and secretin levels were measured in 10 healthy volunteers after application of a serine protease inhibitor (camostate) to study the mechanism of feedback regulation. Camostate produced a strong inhibition of trypsin and chymotrypsin activity in duodenal juice for 1 h. This was accompanied by an increase in duodenal aspirate volume and pancreatic enzyme secretion under both basal and secretin-stimulated conditions. Due to inhibition of tryptic activity, survival of lipase activity in duodenal juice was prolonged. In control experiments we ruled out that the volume and the pH of the solution were responsible for stimulation of pancreatic secretion. The protease inhibitor did not alter pancreatic secretion, which was stimulated by a test meal. Plasma levels of CCK and secretin were not changed after duodenal perfusion of camostate. These observations suggest that trypsin and chymotrypsin are involved in feedback regulation of pancreatic secretion in man which is, however, not mediated by CCK or secretin.

Cholecystokinin↗
PubMed1988

T-cell depletion versus methotrexate as GvHD-prophylaxis in allogeneic bone marrow transplantation for leukaemia.

Graft-versus-host disease (GvHD) prophylaxis using methotrexate (23 patients) and T-cell depletion of the graft (40 patients) was compared in 63 allogeneic bone marrow transplantations (BMT) for leukaemia. T-cell depletion significantly reduced (p = 0.001) the incidence of GvHD from 68% to 11% and the GvHD-associated mortality from 79% to 5%. Actuarial disease-free survival for low-risk patients (57% with T-cell depletion and 47% with MTX) was not significantly improved, due to graft failure and possibly due to a higher leukaemic relapse rate after T-cell depletion. Prevention of graft failure after T cell-depleted BMT is essential and could also reduce the risk of leukaemic relapse by improved engraftment.

Acute Disease↗
PubMed1988

Balloon dilatation of the pulmonary valve in the first year of life in patients with tetralogy of Fallot: a preliminary study.

Fifteen infants with tetralogy of Fallot, who would otherwise have required a palliative operation, underwent balloon dilatation of the right ventricular outflow tract. The mean period of palliation was 8.5 months (range 0-26 months). The procedure was performed without serious complications on 88% of occasions. This preliminary study suggests that balloon dilatation may be useful in the management of tetralogy of Fallot.

Catheterization↗
PubMed1988

Effect of atropine on intestinal phase of pancreatic secretion in man.

The effect of atropine on prestimulatory and Lundh-meal-stimulated pancreatic secretion and on plasma cholecystokinin (CCK) levels has been studied in 20 human volunteers. Prestimulatory secretion was lowered by infusion of atropine. From 10 to 30 min after ingestion of the Lundh meal, atropine had no effect on secretion. From 30 to 120 min, the stimulated enzyme secretion was reduced by 90% during infusion of atropine. Plasma CCK levels were not altered by atropine. Similar results were obtained when the test meal was instilled into the duodenum to exclude a delay of gastric emptying caused by atropine. These data show that cholinergic blockade does not interfere with CCK-mediated stimulation of pancreatic secretion during the first 30 min after ingestion of a meal, and that afterwards the intestinal phase is mainly under cholinergic control.

Adult↗
PubMed1988

Comparison of the effect of single and repeated administrations of a protease inhibitor (Camostate) on pancreatic secretion in man.

In the present study pancreatic secretion and plasma cholecystokinin (CCK) levels were analyzed in eight volunteers after daily ingestion of the serine protease inhibitor camostate for 5 days. This was compared with the effect of a single intraduodenal dose of camostate. Prolonged administration of camostate for 5 days had no effect on basal and stimulated pancreatic secretion and plasma CCK. A single dose of camostate completely inhibited enzymatic activity of trypsin and chymotrypsin and stimulated volume, amylase, and lipase secretion but induced an only slight and insignificant increase in plasma CCK. After the ingestion of a test meal, camostate did not influence stimulated enzyme secretion and increased plasma CCK. We concluded that the intraduodenal perfusion of camostate stimulated pancreatic secretion by a feedback mechanism that is not mediated by CCK. The repeated oral administration of camostate did not induce adaptive changes in pancreatic secretion.

Cholecystokinin↗
PubMed1988

Norfloxacin for prevention of bacterial infections during severe granulocytopenia after bone marrow transplantation.

48 patients treated with bone marrow transplantation (BMT) received the quinolone norfloxacin (NOR) in a total decontamination (TD-NOR, n = 36) or selective decontamination (SD-NOR, n = 12) regimen and were compared with a historical control group of 48 BMT patients receiving oral non-absorbable antibiotics (TD-NAA, n = 31 and SD-NAA, n = 17). 17/36 patients (47%) of group TD-NOR and 16/31 patients (52%) of group TD-NAA remained free of febrile episodes and infections. 4/12 patients (33%) of group SD-NOR and only 1/17 patients (6%) of group SD-NAA remained free of fever and infections. The use of norfloxacin in selective decontamination resulted in a statistically significant lower incidence of fever days than in patients receiving SD-NAA (p less than 0.001). These data suggest that norfloxacin may replace non-absorbable antibiotics in total and in selective decontamination regimens used for infection prophylaxis in BMT recipients.

Adolescent↗
PubMed1988

[The entero-insular axis: the new incretin candidate glucagon-like peptide-1(7-36)amide (GLP-1(7-36))amide].

The functional connection between the gut and pancreatic islets is described by the term "enteroinsular axis". A humoral factor of the gut that might enhance the glucose-induced secretion of insulin is named "incretin". For many years glucose-dependent insulin-releasing polypeptide (GIP) was the strongest incretin candidate. However, recent evidence suggests that glucagon-like peptide-1(7-36)amide represents a more potent physiological incretin. The sequence of GLP-1 is identical in various mammals including man. The 7-36 sequence of the original peptide is a potent insulin-releasing peptide in vitro and in vivo. GLP-1(7-36)amide was found in the human bowel; its circulating level rises in answer to oral glucose and after meals. Recently, specific high-affinity binding sites for GLP-1(7-36)amide were demonstrated on rat insulinoma-derived RINm5F cells. In this model system for B-cell studies the peptide has potent stimulatory effects on cAMP formation, insulin-mRNA transcript synthesis, and insulin release. Further studies in the insulinotropic action of GLP-1(7-36) amide in health and disease will be of great importance.

Animals↗
PubMed1988

Influence of prolonged antacid administration on rat gastric mucosa.

The effect of long-term administration of an antacid preparation on the gastric mucosa was investigated in rats, special attention was directed towards hypergastrinaemia and density of argyrophil cells. One ml of an Al (OH)3- and Mg (OH)2-containing antacid (in vitro neutralization capacity 28 mmol/die) or water was administered intragastrically 4 times daily. An additional group of rats remained untreated. Twelve hours after the final dose serum gastrin levels were significantly (p less than 0.001) elevated (113 +/- 28 pg/ml) compared to the control groups (33 +/- 1 and 22 +/- 2 pg/ml). Antral gastrin (G)-cell density was also increased after antacids by 58% whereas the somatostatin (D)-cell density and the somatostatin concentration in antral tissues were decreased. The number of fundic D- and argyrophil cells were not altered by antacid treatment. The number of parietal cell declined significantly in response to antacids. The foveolar gland region was almost doubled after antacids. It is concluded that in the rat 1. despite persistent hypergastrinaemia due to chronic antacid administration increases in argyrophil cell densities are not to be found; 2. long-term administration of antacids exert a trophic effect on the corpus mucosa predominantly by an increase of mucus neck cells.

Aluminum Hydroxide↗
PubMed1988

Influence of experimental hyperthyroidism on the adult rat pancreas, small intestine, and blood gastrin levels.

Thyroxine modulates the ontogenic changes of animal tissues. In this study, the effects of experimental hyperthyroidism on the adult rat pancreas, small intestine, and serum gastrin were evaluated. Hyperthyroidism was induced by oral feeding of thyroxine (T4) in increasing dosages (150-450 micrograms/kg body weight; 3 weeks) and controlled by measurements of the circulating hormones. The increase of thyroid hormones in blood (T4 ng/dl: thyroxine-treated rats 10.8 vs. controls 3.3; p less than 0.01; given are means) was accompanied by hypergastrinemia (IR-gastrin pg/ml: T4-treated rats 169 vs. controls 25; p less than 0.05). The T4-treated animals consumed more food but lost about 20 g of their initial body weight. Pancreatic wet weight (g: T4-treatment 1.72 vs. controls 1.42; p less than 0.05), DNA (micrograms/g body weight: T4-treatment 2.42 vs. controls 1.5; p less than 0.05), and protein (micrograms/g body weight: T4-treatment 131.7 vs. controls 63.5; p less than 0.05) were increased, whereas no pronounced influence on pancreatic amylase, trypsin, and chymotrypsin was found. The gut wet weight after thyroxine administration (18.1 g vs. 15.4 g of controls; p less than 0.05) was elevated, but length, DNA, protein, and brush border enzyme activities remained unaltered. Our data demonstrate in adult rats a small but significant trophic response of pancreas and gut to repeated oral thyroxine administration.

Animals↗