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Biomedical subjects

R Arnold

Publications and source records attributed to R Arnold.

At least 307 records · Page 17Linked to original sources
PubMed1992

Effect of gastrin receptor antagonists on gastric acid secretion and gastrin and somatostatin release in the rat stomach.

The effects of two recently developed gastrin receptor antagonists, PD 136450 and L-365,260, on pentagastrin-stimulated acid secretion were investigated in rats. PD 136450 at a dose of 6 mg/kg s.c. (9.6 mumol) completely abolished acid secretion induced by pentagastrin. The inhibition of 18 mg/kg PD 136450 s.c. lasted for at least 8 h and was still effective after 14 days of treatment (18 mg/kg s.c. every 8 h). Acute application of L-365,260 at a dose of 3.8 mg/kg, which is equimolar (9.6 mumol) to 6 mg/kg PD 136450 reduced acid responses slightly. However, when L-365,260 was administered intravenously at a dose of 3 mg/kg, this antagonist completely abolished the pentagastrin-stimulated acid secretion. Furthermore, the effect of PD 136450 on endogenous gastric somatostatin and gastrin releases was tested in the isolated, vascularly perfused rat stomach. PD 136450 perfused at a concentration of 1 microM slightly increased somatostatin secretion after stimulation with a high dose of isoproterenol (10(-7) M). There was no effect of PD 136450 on basal or acetylcholine-stimulated gastrin secretion.

Animals↗
PubMed1992

Influence of stress on the healing and relapse of duodenal ulcers. A prospective, multicenter trial of 2109 patients with recurrent duodenal ulceration treated with ranitidine. RUDER Study Group.

The influence of psychologic factors on the healing and relapse of duodenal ulcers under treatment with ranitidine was studied in a prospective, multicenter trial in 2109 patients with an endoscopically proven duodenal ulcer (DU) and a history of recurrent duodenal ulceration. All patient received ranitidine (300 mg daily), and, after healing, 1899 patients continued maintenance treatment (ranitidine, 150 mg daily) for 2 years. A physician's assessment of stress (stress or no stress) was made at every consultation. In the healing phase an overall classification of stress as absent, intermittent, or continuous was made, and in the maintenance phase patients were classified dichotomously as having stress (stress on at least half of the follow-up consultations) or no stress. In addition, at the start of the healing phase stress was measured by means of a standardized questionnaire. Continuous stress, as assessed by the physicians, was associated with a lower 14-day healing rate (35.7%) than intermittent or absent stress (42.4%; relative risk (RR) for delayed healing in patients with continuous stress, 1.19; 95% confidence interval (CI), 1.06-1.33; P < 0.02). Differences in the 14-day healing rate for patients with low and moderate stress scores (43.1%) compared with those with high and very high stress scores (37.9%) just failed to reach statistical significance (RR for patients with stress, 1.14; 95% CI, 0.998-1.29; P = 0.051). During the 1st year of maintenance treatment 18.3% of patients with stress, but 10.9% of patients without stress, had a DU relapse (RR of stress for DU relapse during the first year, 1.73; 95 CI, 1.44-2.09; P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Adaptation and renewal of the endocrine stomach.

At present at least seven different endocrine cell types have been identified in the stomach. According to their relative frequency and secretion products the antral gastrin producing G cell and somatostatin producing D cell and the fundic histamine producing ECL cell are the best characterized cell types. Total endocrine cell mass is controlled by various factors from inside and outside the stomach. Density of antral G and D cells depends on the presence and absence of food, on the antral pH and on additional humoral and/or neural factors. Gastrin and not gastric pH has been identified as the most important factor regulating the density of fundic ECL cells. Adaptation of gastric endocrine cells to gastric pH and to the presence, abundance or absence of humoral and neural regulators are well known phenomena though only partially understood. Antral G cells increase and antral D cells decrease during long-term achlorhydria which as a consequence leads to hypergastrinaemia. Examples are pernicious anaemia in man and drug-induced acid suppression under experimental conditions. Interestingly, achlorhydria-induced G cell hyperplasia never progresses to gastrinomas. Fundic ECL cell density increases markedly in the presence of long-lasting hypergastrinaemia independently of gastric pH. In contrast to G cells ECL cell hyperplasia may progress to rarely occurring ECLomas. However, this depends on additional conditioning factors as the presence of severe atrophic gastritis as in pernicious anaemia or a specific genetic trait present in patients with gastrinomas associated with the MEN I syndrome.

Adaptation, Physiological↗
PubMed1992

ABO-incompatible bone marrow transplantation.

In the past 10 years 201 HLA-identical bone marrow transplantations (BMT) were performed with major ABO incompatibility in 41 (20%) and minor ABO incompatibility in 35 (18%) patients. ABO compatibility between donor and recipient showed no influence on granulocyte and platelet recovery after BMT. Erythrocyte reconstitution was significantly (p < 0.01) delayed for about 1 week in major ABO-incompatible BMT. In addition, a pure red cell aplasia lasting for 2-5 months occurred in 6 out of 21 blood group 0 patients who received transplants of group A. The rate of graft rejection, incidence of graft-versus-host disease as well as the leukemic relapse rate were similar in ABO-compatible and ABO-incompatible BMT. The probability of a 10-year survival after BMT is independent of ABO compatibility between donor and recipient.

ABO Blood-Group System↗
PubMed1992

[Phases in the rehabilitation of male and female bone marrow transplant patients].

Teamwork is essential when investigating the long-term adoption of such medical intervention that are highly demanding on patients, physicians and nursing staff. Bone marrow transplantation represent such an intervention for a series of well defined hematological diseases. The contribution demonstrates the multiple perspective approach of the Ulm team. A case report illustrates the multiplicity of clinical issues. The state of research allows the sketching of a process model on rehabilitation.

Adaptation, Psychological↗
PubMed1992

Morphology of the ventriculoaortic junction in critical aortic stenosis. Implications for hemodynamic function and clinical management.

The clinical presentation of infants with critical aortic stenosis, as well as the results of surgical treatment, differs from obstruction of the left ventricular outflow tract in older children. To investigate a possible anatomic basis for this situation, we performed a detailed morphometric study of 21 hearts from infants who had critical aortic stenosis and 11 normal hearts from infants less than 3 months of age. In each of the hearts with critical aortic stenosis, only one commissure extended to the sinutubular ridge. The other two commissures were represented by folds in the aortic wall that suspended the leaflet below the level of the sinutubular junction. The leaflet thus had a free edge shorter than the circumference of the sinus, in contrast with the normal valve, in which leaflets always were longer than the circumference of their supporting sinus. Analysis of the fibrous triangles on the ventricular aspect of abnormal valves showed a symmetric three-sinus arrangement. In all but one specimen, however, only the triangle related to the mitral valve was fully developed. Although incision of both rudimentary commissures to the aortic wall should achieve some relief of obstruction, these morphologic features strongly mitigate against surgical restoration of normal function or growth in aortic valves having the morphology observed in this series of hearts.

Aortic Valve↗
PubMed1991

[Conservative treatment of florid peptic esophageal stenosis. Complete elimination by dilatation and omeprazole in H2-blocker refractory cases].

23 patients with severe reflux oesophagitis complicated by peptic erosive strictures requiring dilatation and resistant to H2-blocker therapy were treated with the proton pump inhibitor omeprazole (initial dosing: 40 mg daily) and dilated. Combination of dilatations (median 2, range 1 to 12 courses) and omeprazole therapy facilitated complete resolution of strictures and disappearance of peptic lesions after four and eight weeks in 30% and 70%, respectively. In all remaining cases healing could be achieved by perpetuation of omeprazole therapy though three patients (13%) required omeprazole doses higher than 40 mg daily for healing and maintenance. Follow-up investigations available in 17 patients during continuation of omeprazole therapy revealed no recurrence of strictures. It is concluded that more pronounced and particularly longer lasting inhibition of acid secretion is effective even in these most severe cases of reflux oesophagitis.

Adolescent↗
PubMed1991

Characterization of glucagon-like peptide-I(7-36)amide receptors of rat lung membranes by covalent cross-linking.

125I-labelled GLP-I(7-36)amide was cross-liked to a specific binding protein in rat lung membranes using disuccinimidyl suberate. A single radio-labelled band at Mr 66,000 was identified by SDS-PAGE after solubilization of the ligand-binding protein complex which is consistent with the presence of a single class of binding sites on rat lung membranes. The band was undetectable when 1 mumol/l GLP-I(7-36)amide was included in the binding assay. No change in the mobility of the band was observed under reducing conditions suggesting that the binding protein in the receptor is not part of a larger disulphide-linked protein. The intensity of the radiolabelled protein band was reduced when the incubation with 125I-labelled GLP-I(7-36)amide was carried out in the presence of guanine nucleotides suggesting that the GLP-I(7-36)amide receptor is coupled to the adenylate cyclase system.

Animals↗
PubMed1991

Aortico-left ventricular tunnel: long-term outcome after surgical repair.

Over a 14 year period, four children (three male, one female) underwent surgical correction of an aortico-left ventricular tunnel. All presented in infancy (age range 5 days to 9 months). The presenting feature was a systolic and diastolic murmur in all, one of whom developed heart failure within 2 weeks of presentation. In the first two patients, the echocardiographic findings were inconclusive and the diagnosis was confirmed at cardiac catheterization (at 10 and 23 months of age, respectively); the other two were diagnosed echocardiographically by two-dimensional and Doppler color flow imaging. All four patients underwent surgery by patch closure of the aortic end of the tunnel (three patients) or direct suture closure (one patient) and there were no deaths. The mean age at operation was 11 months. During a mean follow-up period of 71 months (range 2 to 157), three patients have clinical and echocardiographic evidence of trivial aortic valve regurgitation, which was noted in the immediate postoperative period in one and at early (less than 6 months) follow-up study in the other two. All are symptom-free, are taking no medications and are growing and developing normally. Aortico-left ventricular tunnel can be accurately diagnosed by echocardiography. In patients presenting in infancy, echocardiography also provides the necessary morphologic information to enable surgical correction without angiography. Early operation is associated with an excellent outcome, whereas repair at a later age is associated with a high incidence of residual aortic regurgitation requiring further surgery.

Aorta↗
PubMed1991

Role of cholecystokinin in the control of gastric somatostatin in the rat: in vivo and in vitro studies.

Cholecystokinin (CCK) has been shown to be a powerful stimulus for somatostatin release from isolated canine fundic D-cells in short-term culture. The influence of the CCK analogue caerulein on the secretory activity of the D-cell in the intact stomach in vitro and the effect of elevated plasma levels of endogenous CCK on gastric somatostatin stores in vivo were investigated in the rat. Basal somatostatin secretion from the isolated, vascularly perfused rat stomach preparation was not affected by various doses of caerulein. Slight stimulation of somatostatin-like immunoreactivity (SLI) release by epinephrine was significantly inhibited by caerulein, whereas caerulein did not alter half-maximal stimulation of SLI secretion by isoproterenol. Rats with chronically elevated plasma CCK levels induced by experimental exocrine pancreatic insufficiency did not show any change in tissue concentrations of SLI or in D-cell number, both in the antrum and corpus. These data suggest that CCK--in contrast to dogs--is not an important modulator of gastric somatostatin in the rat.

Animals↗
PubMed1991

Priming effect of glucagon-like peptide-1 (7-36) amide, glucose-dependent insulinotropic polypeptide and cholecystokinin-8 at the isolated perfused rat pancreas.

The priming effect of glucagon-like peptide-1 (7-36) amide (GLP-1 (7-36) amide), glucose-dependent insulin-releasing polypeptide (GIP) and cholecystokinin-8 (CCK-8) on glucose-induced insulin secretion from rat pancreas was investigated. The isolated pancreas was perfused in vitro with Krebs-Ringer bicarbonate buffer containing 2.8 mmol/l glucose. After 10 min this medium was supplemented with GLP-1 (7-36) amide, GIP or CCK-8 (10, 100, 1000 pmol/l) for 10 min. After an additional 10 min period with 2.8 mmol/l glucose alone, insulin secretion was stimulated with buffer containing 10 mmol/l glucose for 44 min. In control experiments the typical biphasic insulin response to 10 mmol/l glucose occurred. Pretreatment of the pancreas with GIP augmented insulin secretion: 10 pmol/l GIP enhanced only the first phase of the secretory response to 10 mmol/l glucose; 100 and 1000 pmol/l GIP stimulated both phases of hormone secretion. After exposure to CCK-8, enhanced insulin release during the first (at 10 and 1000 pmol/l CCK-8) and the second phase (at 1000 pmol/l) was observed. Priming with 100 pmol/l GLP-1 (7-36) amide significantly amplified the first and 1000 pmol/l GLP-1 (7-36) amide both secretion periods, 10 pmol/l GLP-1 (7-36) amide had no significant effect. All three peptide hormones influenced the first, quickly arising secretory response more than the second phase. Priming with forskolin (30 mM) enhanced the secretory response to 10 mM glucose plus 0.5 nM GLP-1 (7-36) amide 4-fold. With a glucose-responsive B-cell line (HIT cells), we investigated the hypothesis that the priming effect of GLP-1 (7-36) amide is mediated by the adenylate cyclase system. Priming with either IBMX (0.1 mM) or forskolin (2.5 microM) enhanced the insulin release after a consecutive glucose stimulation (5 mM). This effect was pronounced when GLP-1 (7-36) amide (100 pM) was added during glucose stimulation. Priming capacities of intestinal peptide hormones may be involved in the regulation of postprandial insulin release. The incretin action of these hormones can probably, at least in part, be explained by these effects. The priming effect of GLP-1 (7-36) amide is most likely mediated by the adenylate cyclase system.

1-Methyl-3-isobutylxanthine↗
PubMed1991

The sphinctometer: a new device for measurement of lower oesophageal sphincter function.

Current evidence suggests that lower oesophageal sphincter (LOS) competence depends upon both pressure and length. Existing devices can measure length and pressure, but not simultaneously. This methodological problem is a fundamental drawback to understanding LOS function and its role in oesophageal disease. A 'sphinctometer' has been developed, consisting of an oil-filled 3-mm diameter Silastic chamber, 6 cm in length, incorporating a pressure microtransducer designed to provide an integrated pressure reading as a function of length. Its performance has been tested in vitro using human cadaver oesophagus in a specially constructed chamber in which sphincter length and pressure can be varied independently. Comparisons were made with a conventional pull-through technique. Sphinctometer response was linear throughout the LOS pressure range of 0 to 50 mmHg at a fixed LOS length (RS = 0.99; P less than 0.001). Sphinctometer response was also linear at fixed LOS pressure for sphincter lengths from 1 to 6 cm (RS = 0.99; P less than 0.001). This device thus appeared suitable for monitoring function of the human LOS, and has subsequently been successfully incorporated into an ambulatory system for patient use.

Biometry↗
PubMed1991

Dissociation of cholecystokinin and pancreaticobiliary response to intraduodenal bile acids and cholestyramine in humans.

The role of intraduodenal bile acids in the regulation of cholecystokinin (CCK), pancreatic polypeptide (PP), and secretin as well as exocrine pancreatic and biliary secretion was investigated by means of a duodenal marker perfusion technique in volunteers. The following solutions were perfused: (1) liquid test meal, (2) test meal with 6 g cholestyramine, (3) test meal with 2 g chenodeoxycholic acid (CDC), (4) test meal with 6 g cholestyramine and 2 g CDC, (5) 6 g cholestyramine alone, and (6) 2 g CDC alone. The test meal caused an immediate increase in CCK and PP plasma levels, whereas secretin was not significantly altered. CCK release was further enhanced by addition of cholestyramine, whereas CDC inhibited release. The stimulatory effect of cholestyramine was abolished by CDC. CDC alone and in combination with the test meal stimulated secretin release. The response of PP to the test meal was not altered by addition of either compound. Cholestyramine and CDC alone caused only a very small increase in CCK levels, whereas PP was stimulated to nearly postprandial values. Meal-stimulated pancreatic and biliary secretion was significantly enhanced by cholestyramine, CDC, and the combination of both. CDC and cholestyramine alone each stimulated enzyme and bile secretion to a greater extent than the test meal. We conclude that intraduodenal bile salts are a modulator of postprandial CCK release. Changes in exocrine pancreatic and biliary and PP secretion do not necessarily parallel CCK concentrations, suggesting that different mediators are involved in the observed bile acid-induced changes in humans.

Adult↗
PubMed1991

Long-term maintenance treatment of reflux esophagitis with omeprazole. Prospective study in patients with H2-blocker-resistant esophagitis.

Thirty-four patients with H2-blocker-resistant reflux esophagitis subsequently healed by 40 mg omeprazole daily entered a maintenance study with 20 mg omeprazole. In 31 evaluable cases the observation period was at least 12 months (mean 24 months). Esophagitis remained in remission in two thirds of patients despite dose reduction. Relapses of esophagitis occurred in 10 cases within six months, which rapidly healed by increasing the omeprazole dose to 40 mg. No further recurrence with 20 mg omeprazole was found later than six months. Peptic strictures primarily requiring repeated dilatation in six patients during healing with omeprazole did not reappear while on omeprazole maintenance. Major side effects that could be attributed to omeprazole were not observed. Gastrin levels remained within or slightly above the normal range in the vast majority. It is concluded that omeprazole maintenance treatment in severe reflux esophagitis is an effective and safe therapy.

Adult↗
PubMed1991

Fatal B-cell lymphoproliferative syndrome in allogeneic marrow graft recipients. A clinical, immunobiological and pathological study.

We have studied four cases of fatal B-cell lymphoproliferative syndrome (LPS) developing among 333 patients (incidence 1.2%) treated with allogeneic bone marrow transplantation (BMT). All four patients had received a T-cell depleted graft. Onset of the first clinical symptoms (palpable lymph node enlargement in three and IgA-lambda paraproteinemia in two patients) occurred between 41 and 188 days post-BMT (median 76 days). The course of the LPS was rapidly progressive in all cases, leading to death in 2-5 weeks. The peripheral blood showed progressive pancytopenia with disproportionally high numbers of activated NK cells, apparently compensating for the T-cell deficiency. Post-mortem histological studies disclosed polymorphic B-cell proliferations, most pronounced in the lymph nodes, spleen, liver, lungs and kidneys. Lymphohemopoietic cells were of donor origin in three patients. In the fourth patient, graft failure suggested a host origin for the proliferating cells. Immunophenotyping and gene rearrangement analysis revealed polyclonal proliferation in one patient, monoclonal proliferation in another patient, and an oligoclonal pattern in the other two patients. The clinical behavior of the LPS was independent of clonality. Immunohistologically, the proliferating cells showed characteristics of relatively mature B-cells in three cases, and pre-B-cell features in one case. Epstein Barr virus (EBV) serology indicated seroconversion (primary infection) in one child, and chronic active EBV infection in both adults. EBV DNA as well as EBV nuclear antigen (EBNA) were detected in infiltrated tissues of all four patients. The labeling pattern on in situ hybridization suggested a replicative EBV infection comparable to that in lymphoblastoid cell lines. We conclude that EBV-associated LPS developing as a result of post-transplant immunodeficiency is a distinct clinicopathologic entity, differing from non-Hodgkin's lymphoma (including Burkitt's lymphoma) and infectious mononucleosis of the immunocompetent host.

Adult↗
PubMed1991

Helodermin and islet hormone release in isolated rat pancreas.

The effect of helodermin (1,10,100 pmol/L), a new member of the VIP/secretin/glucagon peptide family, was investigated in glucose- (10 mmol/L) and arginine- (10 mmol/L) induced insulin, glucagon, and somatostatin secretion from the isolated perfused rat pancreas. Helodermin stimulated the somatostatin release in a concentration-dependent manner during the first (controls, 100%; 1 pmol/L, 113%, ns; 10 pmol/L, 175%, p less than 0.05; 100 pmol/L, 233%, p less than 0.05) and the second secretion phases (controls, 100%; 1 pmol/L, 117%, ns; 10 pmol/L, 210%, p less than 0.05; 100 pmol/L, 362%, p less than 0.05). There was a biphasic glucagon response with an inhibition during the first phase (controls, 100%; 1 pmol/L, 92%; 10 pmol/L, 63%, p less than 0.05; 100 pmol/L, 52%, p less than 0.05%) and a stimulation during the second phase (controls, 100%; 1 pmol/L, 117%, ns; 10 pmol/L, 210%, p less than 0.05; 100 pmol/L, 362%, p less than 0.05). Helodermin had weak stimulatory effects on pancreatic beta cells with a maximum at 10 pmol/L (first phase: controls, 100%; 1 pmol/L, 96%, ns; 10 pmol/L, 148%, p less than 0.05; 100 pmol/L, 136%, ns; second phase: controls, 100%; 1 pmol/L, 104%, ns; 10 pmol/L, 170%, p less than 0.05; 100 pmol/L, 136%, ns).

Animals↗
PubMed1991

Interaction of the cholinergic system and cholecystokinin in the regulation of endogenous and exogenous stimulation of pancreatic secretion in humans.

Pancreatic enzyme secretion is regulated in humans by the cholinergic system and by cholecystokinin (CCK). The interaction between both regulatory systems in response to exogenous and endogenous stimulation was analyzed in the present study using the cholinergic antagonist atropine and the CCK antagonist loxiglumide. A dose-dependent stimulation of pancreatic enzyme output was achieved either by duodenal perfusion of graded caloric loads or by IV infusion of increasing doses of cerulein. Prestimulated pancreatic secretion was inhibited by atropine and loxiglumide. Atropine furthermore almost completely blocked meal-stimulated pancreatic secretion, whereas loxiglumide caused 60% inhibition. The enzyme response to graded doses of exogenous CCK was significantly inhibited by atropine and loxiglumide. Plasma levels of CCK were not altered by atropine but increased with infusion of loxiglumide. This study supports the concept that pancreatic enzyme secretion is predominantly dependent on a cholinergic tone and that CCK modulates the enzyme-secretory response.

Adult↗