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Biomedical subjects

R Arnold

Publications and source records attributed to R Arnold.

At least 433 records · Page 24Linked to original sources
PubMed1988

[Reduced suppression of gastric acid by ranitidine in severe reflux esophagitis. A pilot study].

Repeated intragastric long-term pH recordings for 24 h were conducted in 13 patients with reflux oesophagitis grade III and IV (Savary and Miller) during treatment with ranitidine 150 mg b.i.d. and 300 mg b.i.d. and omeprazole 40 mg mane (n = 5). Ranitidine led to a significantly less pronounced increase in median gastric pH in oesophagitis than in healthy controls. The magnitude of intragastric pH increase showed parallelism to symptomatic response and healing. Omeprazole increased intragastric pH above 4 for 24 h and caused rapid healing in non-responders. It is concluded that in patients with severe reflux oesophagitis ranitidine is less effective in increasing intragastric pH than in controls, whereas omeprazole reveals potent antisecretory activity accompanied by rapid healing.

Adult↗
PubMed1988

Total anomalous pulmonary venous drainage. Seventeen-year surgical experience.

Between 1968 and 1985, 80 children underwent correction of total anomalous pulmonary venous drainage. There were 47 boys and 33 girls whose ages ranged from 3 days to 16 years (median 2 months, interquartile range 5 years). Seventy (87.5%) were less than 1 year of age at operation. Fifty-eight (72.5%) weighed less than 5 kg, the range being 1.6 to 42 kg (median 3.7 kg, interquartile range 2.4 kg). Forty-five (56%) patients had supracardiac, 14 (17.5%) cardiac, 15 (19%) infracardiac, and 6 (7.5%) had mixed total anomalous pulmonary venous drainage. Follow-up was complete in 78 (97.5%) and ranged from 6 to 189 months (median 58 months, interquartile range 59 months). There were 14 (17.5%) early and six (7.5%) late deaths. Analysis by various factors revealed year of operation as the only factor to affect survival at the 5% level of significance. Early mortality was 29% between 1968-1977 and 11% between 1978-1985 (p = 0.04). Postoperative pulmonary venous obstruction occurred in five (6%) patients between 6 weeks and 3 months after operation. All 5 died, three after reoperation. Five (6%) other children had reoperations, four for residual shunts and one for superior vena caval obstruction.

Adolescent↗
PubMed1987

Cytomegalovirus (CMV) infections in patients receiving CMV-IgG-hyperimmunoglobulin prophylaxis after bone-marrow transplantation.

Conditioning therapy with aggressive chemotherapy and irradiation induces a state of transient combined immunodeficiency in bone-marrow transplant recipients. This promotes the occurrence of severe cytomegalovirus (CMV) infections, the most frequent lethal complication after bone-marrow transplantation (BMT) at present. Forty-four BMT recipients received CMV-IgG-hyperimmunoglobulin for CMV prophylaxis intravenously. The efficacy of this prophylaxis and possible risk factors for the occurrence of CMV-induced interstitial pneumonia (IP) were analyzed. Risk factors for the promotion of a CMV-IP were: additional immunosuppressive therapy after BMT, CMV-positive serostatus of the recipient, CMV-seropositive granulocyte transfusion, CMV infection immediately prior to BMT, and HLA-haploidentical BMT. In this study the incidence of graft-versus-host disease was low and was not associated with the incidence of CMV infections. The use of T-cell-depleted grafts did not result in increased CMV infections or IP and may possibly have improved the immunological reconstitution.

Adolescent↗
PubMed1987

Influence of chronic omeprazole treatment on gastric endocrine function.

The influence of a 4-week treatment with the substituted benzimidazole omeprazole (20 mg daily) or placebo on gastric endocrine function was tested in healthy male volunteers. Compared with placebo-treated subjects basal serum gastrin levels were slightly but significantly increased after treatment with omeprazole from 10 to 22 pg/ml (medians; P less than 0.05) but returned to pretreatment values after 2 weeks recovery (9 pg/ml). Antral gastrin tissue concentration increased and was still elevated after recovery; however, antral gastrin concentrations also increased in placebo controls, and increments immediately after cessation of omeprazole treatment (2.58 micrograms/g; median) were not significantly over control values (1.92 micrograms/g; P greater than 0.1). Postprandial gastrin release, basal and food-stimulated insulin release, antral somatostatin concentration, and volume densities of antral G and D cells were unaffected. It is concluded that, due to incomplete inhibition of gastric acid secretion at the omeprazole dose studied, only slight effects on the endocrine stomach are to be expected after 4 weeks of administration of omeprazole.

Adult↗
PubMed1987

Calcitonin gene-related peptide stimulates rat gastric somatostatin release in vitro.

The influence of rat calcitonin gene-related peptide (rCGRP) on the secretion of gastric somatostatin and gastrin was studied in vitro using the isolated, vascularly perfused rat stomach preparation. rCGRP stimulated somatostatin secretion dose-dependently reaching 3-fold stimulation at 1 microM. The kinetics of somatostatin response were characterized by a sharp increase in the initial phase of rCGRP perfusion followed by sustained elevated levels. Gastrin secretion was moderately suppressed at 1 nM to 100 nM CGRP. Somatostatin responses to half-maximal stimulation with 100 nM CGRP were not affected by concomitant perfusion of atropine, propranolol, and tetrodotoxin. It is concluded that increases in somatostatin release in response to CGRP are probably due to a direct effect on the gastric somatostatin-producing D-cell and may be important for the potent acid-inhibitory activity of CGRP.

Animals↗
PubMed1987

Elimination of the low-molecular weight proteinase inhibitor camostate (FOY 305) and its degradation products by the rat liver.

The elimination of the low molecular weight proteinase inhibitor camostate (FOY 305) was studied in rats after oral administration and in the the situ perfused rat liver. After feeding of camostate (400 mg/kg b.w.) only the metabolites (FOY 251, GBA) were detected in blood samples withdrawn from the portal and hepatic vein. This indicated a rapid degradation of FOY 305 after absorption from the gut lumen. The hepatic extraction of the anti-proteolytic active metabolite FOY 251 during a single liver passage was 23%. It remained almost constant over the period of 120 min. In the perfused rat liver, FOY 305 was given in concentrations comparable to the in vivo studies. It was eliminated by 20%. In these experiments, the compound was metabolized to FOY 251 and in minor amounts to guanidino-benzoate (GBA), the latter being an anti-proteolytic ineffective degradation product. In conclusion, a low hepatic extraction of FOY 305 led to pharmacologically effective concentrations of the active metabolite FOY 251 in the circulation after oral ingestion of the proteinase inhibitor.

Administration, Oral↗
PubMed1987

Influence of chronic drug-induced achlorhydria by substituted benzimidazoles on the endocrine stomach in rats.

The release of gastric somatostatinlike immunoreactivity and gastrin was studied in rats with chronic achlorhydria induced by the substituted benzimidazole BY 308. In vitro, stimulation of gastrin release by acetylcholine was slightly enhanced after 1 day of treatment but no further effects were observed compared to placebo controls. Four weeks of treatment evoked marked gastrin hypersecretion, which was atropine-resistant. Stimulation of gastrin release was inversely correlated to enhancement of basal gastrin levels. Chronic achlorhydria distinctly reduced somatostatin responses to isoproterenol, whereas potent stimulation was observed in controls. Treatment with BY 308 for 1 wk was associated with fully developed gastrin hypersecretion but isoproterenol-stimulated somatostatin release was still unaffected. Hypergastrinemia accompanied by increased antral gastrin and reduced antral and fundic somatostatin concentrations was also found in vivo after 4 wk of treatment with BY 308. It is concluded that chronic achlorhydria not only enhances storage and secretion of gastrin but also diminishes the secretion and tissue stores of somatostatin; adaptive changes of the somatostatin cell occur, however, with a much longer delay.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1987

Chromosome studies in patients with acute nonlymphocytic or acute lymphocytic leukemia submitted to bone marrow transplantation--results of a European cooperative study.

The chromosomal data of 58 acute nonlymphocytic leukemia (ANLL) patients and of 32 acute lymphocytic leukemia (ALL) patients submitted to bone marrow transplantation and collected from nine institutions are reported. Chromosomal studies were available at diagnosis in 19 cases with ANLL: seven had a partially or completely abnormal pattern. Forty-one patients had a chromosome study before bone marrow transplantation and all had a normal pattern. Thirteen patients with ALL were studied at diagnosis: five had a partially or completely abnormal karyotype. Of 20 cases analyzed before bone marrow transplantation, only one has maintained the abnormal pattern of diagnosis in part of the cells. Karyotypes were available in nine ANLL patients relapsed after bone marrow transplantations. Two showed the same clonal abnormalities seen at diagnosis; in three other cases the leukemic clone of relapse carried an additional chromosome abnormality with respect to the pattern at diagnosis and four more cases presented at relapse complex abnormalities; two of them had a cytogenetically normal pattern at diagnosis. In four of ten relapsed ALL cases chromosomes analyses were available. A relapse in donor cells and a hyperdiploid pattern were observed in two cases, respectively, while a normal, recipient pattern was documented in the other two cases. Serial chromosome studies performed in acute leukemia patients after bone marrow transplantation may allow the detection of different chromosomal patterns of relapse. In those cases who relapsed with a cell clone cytogenetically different from the pattern at diagnosis, a direct role played by the conditioning treatment in the pathogenesis of the relapsing disease may be hypothesized.

Acute Disease↗
PubMed1987

Captopril in treatment of infant heart failure: a preliminary report.

We have studied retrospectively 18 infants who have received captopril for treatment of severe heart failure due to left-to-right shunts with pulmonary hypertension. Captopril has been administered in doses of up to 3.5 mg/kg/day (mean 2.47 mg/kg/day). Maintenance treatment with digoxin and frusemide was continued but potassium-sparing diuretics were stopped in most patients. The mean period of assessment was 19 days before and 27 days after commencing captopril. The mean daily weight gain before captopril was -7 g and after its introduction was + 13 g (P less than 0.001). There were statistically significant (P less than 0.05) falls in mean heart rate and respiratory rate and rises in plasma sodium concentration and feeding score. Plasma urea concentration fell but this did not reach statistical significance. Two patients suffered hypotension after increments in captopril dosage and subsequently had a rise in plasma urea and creatinine values. This adverse reaction may be linked to the presence of hyponatraemia. This preliminary report shows captopril may be useful in the control of severe heart failure in infancy.

Body Weight↗
PubMed1987

Pulmonary artery tear following balloon valvoplasty in Fallot's tetralogy.

A 3-year-old girl with Fallot's tetralogy underwent balloon pulmonary valvoplasty without any obvious complications. Elective total correction was performed 15 months later. At operation, a well-healed longitudinal tear measuring 2 cm was noted in the posterior wall of the main pulmonary artery 1 cm from the pulmonary valve extending into the right pulmonary artery.

Cardiac Catheterization↗
PubMed1987

Coagulation factor XIII A and B subunits in bone marrow and liver transplantation.

The polymorphism of the coagulation factor XIIIA and B subunits was determined before and after bone marrow or liver transplantation. It could be shown that the FXIIIA phenotype of the recipient was replaced by donor phenotype after bone marrow transplantation, whereas the phenotype of FXIIIB remained of recipient origin. In contrast, the FXIIIB phenotype changed to donor type after orthotopic liver transplantation but not the FXIIIA phenotype. The results indicate that the FXIIIA protein is produced in hemopoiesis, most likely in megakaryocytes and FXIIIB protein in the liver. Depending on the site of synthesis, FXIII alleles can be used as a marker in engraftment of FXIIIA-incompatible bone marrow transplantation or as a marker in FXIIIB-incompatible orthotopic liver transplantation.

Alleles↗
PubMed1987

Evidence for the involvement of host-derived OKT8-positive T cells in the rejection of T-depleted, HLA-identical bone marrow grafts.

The recent introduction of a variety of techniques for removing T cells from bone marrow grafts has reduced the incidence of graft-versus-host disease (GVHD)-associated morbidity and mortality. Whether this advance will be translated into improved patient survival is unclear at present, mainly because these procedures increase the risk of graft failure. Since 1983 we have transplanted 25 consecutive leukemia patients with HLA-identical sibling grafts purged of T cells by a single incubation with the monoclonal antibody Campath-1 and donor complement. This approach was successful in reducing T cell contamination of the graft and preventing acute and chronic GVHD. In this group of patients two suffered irreversible graft failure and one developed reversible graft failure. In a similarly sized group of patients previously transplanted with unpurged marrow according to the Seattle protocol, no episodes of graft failure occurred. Since other causes of graft failure, such as drug toxicity or viral infections, could be largely excluded, this suggested that the graft failures were specifically related to the purging process. In haploidentical bone marrow transplantation (BMT) O'Reilly has identified residual host-versus-graft activity (HVG) as a cause of graft failure. The causes and mechanisms of graft failure in T-depleted HLA-identical sibling transplants have not been extensively investigated to date. In the three graft failures observed by us, the loss of the graft was preceded by the appearance of a population of activated lymphocytes. We have determined the phenotype and origin of this population and investigated its interactions with donor hemopoietic tissue in vitro.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1987

Increased visualization of antral gastrin-producing G-cells after acute stimulation of gastrin release in the rat.

The effect of acute stimulation of gastrin release on the number of antral gastrin-producing G-cells stained by conventional immunohistology was investigated in two experimental models. The substituted benzimidazole derivate BY 308 was administered at a dosage that induces complete achlorhydria and thereby led to marked hypergastrinaemia. Two hours after drug administration, antral G-cell density was increased by 14% and 35% in 12-h and 48-h fasted rats, respectively. Both serum gastrin levels and G-cell density further increased after 3 and 8 days' treatment with BY 308 whereas the somatostatin (D)-cell count did not change prior to 8 days' administration. In the isolated, vascularly perfused rat stomach, acetylcholine was perfused for 36 min; this regimen increased gastrin release four-fold and enhanced the G-cell count by 24% whereas 8 min acetylcholine perfusion did not alter G-cell density significantly but stimulated gastrin output. The results of this study suggest that acute changes in the secretory activity of the gastrin cell are accompanied by an alteration of the staining characteristics thus indicating that an increase in the antral G-cell count does not solely depend upon formation of new cells.

Acetylcholine↗
PubMed1987

Effect of pancreatic atrophy and hypertrophy on the small intestine.

Intestinal enzyme activities were investigated in mice with spontaneously occurring exocrine pancreatic insufficiency (EPI), in rats after induction of pancreatic insufficiency by intraductal injection of oleic acid, and in rats after feeding a proteinase inhibitor (Camostate) which induced a marked pancreatic hypertrophy. An increase in saccharase activity and in vitro uptake of L-phenylalanine was found in EPI mice, while activities of alkaline phosphatase and lactase were not altered. In oleic acid induced pancreatic insufficiency and in pancreatic hypertrophy no alterations in enzyme activities were observed. Morphometric analysis revealed no alterations in mucosal surface of EPI mice. It was suggested that the small intestine adapts fuctionally to severe and long lasting pancreatic insufficiency, but not to pancreatic hypertrophy.

Adaptation, Physiological↗
PubMed1987

Tryptophan rich diet as a new approach to study the serotoninergic enteropancreatic axis.

The influence of a tryptophan enriched diet (L-tryptophan added as 1% of total diet), fed over 10 days, on the rat duodenum and pancreas was studied by immunohistology, measurements of serotonin and tryptophan tissue concentrations by HPLC, and incubations of pancreatic lobules. Ingestion of a tryptophan enriched diet resulted in increased contents of tryptophan and serotonin in the duodenum that was not accompanied by a significant change of the serotonin cell density. Neither basal nor CCK-stimulated amylase release from isolated pancreatic lobules was altered after tryptophan enriched food. Although serotonin could be extracted from the pancreas, no increase in serotonin concentration was detected after ingestion of the tryptophan diet. A 'serotonin loading' diet may be a useful tool to study the significance of amines produced by gut endocrine cells in respects to enteropancreatic connections.

Animals↗
PubMed1987

Endocrine pancreatic morphology and function in exocrine insufficiency in rats.

Exocrine pancreatic insufficiency was induced in rats by injection of oleic acid into the pancreatic duct. Six weeks after a single injection of 50 microliters oleic acid, the exocrine tissue was reduced by 98%. The islets of Langerhans remained intact and showed no changes in the relative distribution of beta-, alpha-, D-, and PP-cells. In rats fed ad libitum, plasma insulin levels and pancreatic insulin content did not differ between oleic acid-treated animals and controls. The dynamic insulin response was evaluated in the isolated perfused pancreas. The biphasic pattern of insulin release after stimulation by glucose was preserved. The half-maximal (10 mM) glucose-induced insulin release was reduced to 49% after onset of exocrine atrophy. After stimulation of insulin secretion by a maximal glucose load (20 mM), the insulin output from the perfused pancreas was reduced to 56%. A reduction in insulin release to 24% occurred with respect to the arginine (15 + 10 mM glucose)-stimulated secretion. To evaluate the significance of these findings in intact animals, glucose tolerance tests were performed. There were no differences between oleic acid-, saline-, or untreated animals with respect to serum glucose or plasma insulin levels during the oral glucose tolerance test. The insulin response after intravenous glucose in oleic acid-treated rats was not statistically different from controls. Nevertheless, the serum glucose levels in rats with exocrine atrophy were above controls, indicating a slight impairment of glucose tolerance.

Animals↗