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Biomedical subjects

B Ryberg

Publications and source records attributed to B Ryberg.

At least 37 records · Page 2Linked to original sources
PubMed1988

Serum antibodies to peripheral nerve tissue in acute Guillain-Barré syndrome in relation to outcome of plasma exchange.

Mixed haemagglutination and complement fixation tests were used to detect serum antibodies to peripheral nerve in 36 patients with acute Guillain-Barré syndrome. Twenty patients were treated with plasma exchange, 16 served as controls. A significant antibody titre was found in 19 patients with the haemagglutination test; 30 had complement-fixing antibodies. Patients lacking complement-fixing antibodies were less disabled at entry (P less than 0.01). However, there was no correlation between the course of the disease and any of the antibodies in the two patient groups. The two tests were therefore not able to select patients for treatment by plasma exchange.

Adult↗
PubMed1988

Gastrin and somatostatin in the rat antrum. The effect of removal of acid-secreting mucosa.

Female rats were subjected to operations aimed at reducing the amount of oxyntic gland mucosa draining its acid secretion to the antrum. The rats were provided either with Heidenhain or Pavlov pouches reducing the oxyntic mucosa draining its secretion to the antrum by about 50% or subjected to various degrees (75, 90 and 100%) of fundectomy. Ten weeks following surgery, plasma levels of gastrin and somatostatin were assayed. At the same time, antral mucosal content of gastrin and somatostatin was determined as well as the mucosal density of these hormone-producing cells. There was a relationship between the amount of acid-secreting mucosa removed and the ensuring plasma concentration of gastrin. Thus, a stepwise increase in plasma gastrin was found with the highest levels obtained in rats subjected to 90 or 100% fundectomy. The somatostatin concentration in plasma was reduced only in rats subjected to fundectomy with the most sustained decrease in animals in which all oxyntic gland mucosa had been removed. There was also a relationship between the amount of acid-secreting mucosa removed and the gastrin content of the antral mucosa. An inverse relationship seemed to exist between antral gastrin and somatostatin concentrations. However, a significant decrease in somatostatin concentration of the antral mucosa was seen only in rats subjected to a fundectomy. The number of gastrin cells in the antral mucosa was increased in fundectomized rats only, with the largest density seen in rats deprived of all oxyntic mucosa. A corresponding decrease in the number of somatostatin cells was noticed. Our results would suggest an apparent functional relationship between antral gastrin and somatostatin cells, where the antral acid load (or pH) appears to be the major factor of physiological significance.

Animals↗
PubMed1988

Rat parietal cell function after prolonged inhibition of gastric acid secretion.

Female rats were treated orally for 3 mo with omeprazole (40 and 400 mumol/kg). Both doses caused total inhibition of gastric acid secretion and recovery was parallel to that of H+-K+-ATPase activity (30-50 and 60-80% inhibition 24 h after doses, respectively). The H+-K+-ATPase activity returned to control levels within 1 wk after the last dose. Plasma gastrin levels were dose-dependently increased during treatment but reversed to control levels within 9 days after the last dose. Parallel with a general increase in corpus mucosal mass, both pepsinogen and H+-K+-ATPase total content increased. However, their tissue concentrations did not differ from control values, suggesting that neither parietal nor chief cell density are changed by omeprazole treatment and also that their growth is parallel to the general hyperplasia. In contrast, the oxyntic mucosal histamine concentration was increased, indicating an increase in the enterochromaffin-like (ECL) cell density. Maximal capacity of the mucosa to secrete acid increased in parallel with the increase in mucosal mass and total H+-K+-ATPase content. However, basal acid secretion did not differ between treatment groups. Increased capacity slowly declined toward control levels over the 70-day recovery period after withdrawal of omeprazole. These results suggest that hypergastrinemia, induced in the rat by pharmacological inhibition of gastric acid secretion, causes a hyperplasia of oxyntic mucosal cells, ECL cells growing faster than the others. The hyperplastic mucosa has an increased capacity to produce acid and is functionally normal.

Adenosine Triphosphatases↗
PubMed1988

Effects of omeprazole and ranitidine on gastric acid secretion, blood gastrin levels and [3H]-thymidine incorporation in the oxyntic mucosa from dogs and rats.

Dogs provided with a gastric fistula were treated orally for 1 week either with the H+, K+-ATPase inhibitor omeprazole, 80 mumol/kg once daily, or with the histamine H2 receptor antagonist ranitidine, 85-175 mumol/kg every 8 h. Acid secretion, serum gastrin levels and [3H]-thymidine incorporation in the corpus mucosa were determined before, during and after the treatment period. In order to examine differences between species, plasma gastrin levels and [3H]-thymidine incorporation in the oxyntic mucosa were also determined in female rats treated up to 1 week with omeprazole, 400 mumol/kg orally once daily. Histamine-stimulated gastric acid secretion in dogs treated with omeprazole or ranitidine was almost completely inhibited during the whole treatment period. As a consequence of that, the meal-stimulated gastrin levels were increased (7-fold) during treatment by both compounds. [3H]-thymidine incorporation in the dog corpus mucosa was increased approximately 4 times on day 5 both with omeprazole and ranitidine. After the treatment was stopped, gastric acid secretion, serum levels of gastrin and the rate of [3H]-thymidine incorporation were back to control level in both groups within 11 days. In the rats, the plasma gastrin levels increased 10-fold and the rate of [3H]-thymidine incorporation in the corpus mucosa increased 3-fold during treatment with omeprazole. In conclusion, a pronounced suppression of gastric acid secretion over the day with antisecretagogues results in hypergastrinemia in both dogs and rats. As a consequence of the trophic effect of gastrin, the incorporation of [3H]-thymidine in the oxyntic mucosa is increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Omeprazole: its influence on gastric acid secretion, gastrin and ECL cells.

The H+,K+-ATPase inhibitor omeprazole is a highly effective gastric antisecretory agent, both in animals and man, with a long duration of action. These properties are shared by a number of recently described histamine H2-receptor antagonists. In life-long oncogenicity studies of these H2-receptor antagonists, as well as with the H+,K+-ATPase inhibitor omeprazole, gastric enterochromaffin-like cell (ECL cell) hyperplasia and carcinoids have been found. The purpose of this paper is to summarize available evidence for the "Gastrin Hypothesis" to explain the development of ECL-cell hyperplasia. The hypothesis may be outlined as follows: 1) Inhibition of gastric acid secretion leads to elevated antral pH and, secondarily, to release of gastrin from the antral gastrin cells into the blood stream. 2) Gastrin causes both general hypertrophy of the oxyntic mucosa and hyperplasia of the ECL cells in the oxyntic mucosa. That this sequence of events occurs not only with omeprazole but also with other effective gastric antisecretory agents has been verified in the rat by giving the H2-receptor antagonist ranitidine as a continuous infusion. Ranitidine caused a hypergastrinemia of a similar magnitude as that seen after omeprazole, provided that the acid secretion was inhibited to a similar degree. At similar gastrin levels, ECL-cell hyperplasia of the same magnitude developed during both ranitidine and omeprazole treatment. Antrectomy prevented the development of ECL-cell hyperplasia during omeprazole treatment, indicating that the hyperplasia was not due to the drug treatment per se, but rather to the hypergastrinemia. Both the hypergastrinemia and the ECL-cell hyperplasia were found to be reversible.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Hypergastrinaemia produces trophic effects in stomach but not in pancreas and intestines.

Hypo- or anacidity, caused by antisecretagogues, stimulates gastrin release and leads to hypergastrinaemia. If drug treatment is maintained over a period of time, the hypergastrinaemia can be expected to give rise to trophic effects. We examined the trophic consequences of the very marked hypergastrinaemia produced by long-term treatment (16-20 weeks) of rats with large doses of the substituted benzimidazole, omeprazole, a potent and long-acting blocker of acid secretion. The weight of the stomach and the oxyntic mucosal thickness were increased, whereas the weight of the pancreas and the intestines and the thickness of the mucosa of the antrum and small and large intestine were unaffected. The number of exocrine cells (parietal, zymogen and mucous cells) were uniformly increased by 25-30%. The density of parietal and zymogen cells, expressed as number of cell nuclei per mm2 epithelium, was unchanged. The volume density of parietal cells, expressed as % of epithelial volume, was also unchanged, implying that the volume of the individual parietal cell had not increased. The density of endocrine ECL cells in the stomach increased 5-fold. Thus, the findings demonstrate a growth-promoting effect of the hypergastrinaemia on the oxyntic mucosa, the ECL cells in particular, and the lack of such an effect on the antrum, pancreas and intestines.

Animals↗
PubMed1986

Are anti-brain antibodies in multiple sclerosis directed to myelin basic protein? Studies employing the Shiverer mouse mutant.

The dysmyelinating mouse mutant Shiverer has a severe and relatively selective deficiency of myelin basic protein (MBP) in the central and peripheral nervous system. Nevertheless, Shiverer brain and control-mouse brain showed similar antigenic titers when tested by a complement fixation assay against a panel of 14 multiple sclerosis (MS) sera and 6 MS CSF samples known to represent several specificities of antibrain antibodies. By analogy with experimental allergic encephalomyelitis, a sensitization to MBP has been proposed in MS. Our results, however, show that antibodies to other CNS antigens are quantitatively more important in this disease.

Animals↗
PubMed1986

Pharmacology and toxicology of omeprazole--with special reference to the effects on the gastric mucosa.

Omeprazole is a long acting inhibitor of gastric acid secretion in different species including rat and dog. Due to the long duration of action, steady state inhibition at repeated once daily administration is reaches within 4-5 days in dogs and in about 3 days in rats. Daily dosing at high dose levels results in virtually complete 24-hour inhibition of acid secretion in experimental animals. The elimination of the inhibitory feedback effect of acid on gastrin secretion leads to hypergastrinaemia. Because gastrin has a trophic effect on the oxyntic mucosa, the hypergastrinaemia results in a reversible hypertrophy of the oxyntic mucosa and an increased capacity to produce acid following maximal stimulation with exogenous secretagogues after discontinuing treatment. Despite the increased capacity to produce acid, basal acid secretion seems to be unchanged. The pronounced hypergastrinaemia which occurs during long-term treatment with high doses rapidly normalizes after discontinuing treatment. The hyperplasia of the oxyntic endocrine ECL cells, and the eventual development of gastric ECL cell carcinoids after lifelong treatment of rats with high doses, can also be attributed to the hypergastrinaemia developing after almost complete elimination of gastric acid secretion in these animals.

Animals↗
PubMed1985

Persistence of antibrain antibodies in cerebrospinal fluid during plasmapheresis for multiple sclerosis.

A man with chronic progressive multiple sclerosis received a 10 day course of treatment with adrenocorticotrophic hormone without beneficial effect. He then received six sessions of plasmapheresis, again without improvement. Treatment with adrenocorticotrophic hormone had no effect on serum antibrain antibody titres, but plasmapheresis virtually eliminated the antibodies from serum and caused a fall in serum IgG concentrations; neither treatment had any effect on the IgG concentration and antibody titre in the cerebrospinal fluid. Treatment with plasmapheresis may fail in patients with multiple sclerosis because it does not remove antibrain antibodies from the intrathecal space.

Adrenocorticotropic Hormone↗
PubMed1984

Antineural antibodies in Guillain-Barré syndrome and lymphocytic meningoradiculitis (Bannwarth's syndrome).

Antineural antibodies occur in Guillain-Barré syndrome (GBS), but have not been studied in lymphocytic meningoradiculitis (Bannwarth's syndrome), which has clinical features in common with GBS. Employing a sensitive complement-fixation assay with homogenates of nerve root and brain as antigens, we recorded positive serum reactions to either tissue in 14 of 18 samples from patients with GBS during the first three weeks of the disease. Five of nine samples were positive during the fourth to eighth weeks, whereas all seven patients sampled thereafter had negative reactions. Four GBS serum samples reacted only with nerve root, seven reacted only with brain, and eight reacted with both antigen preparations. One of 12 patients with meningoradiculitis and one of 50 supposedly healthy blood donors had serum antibodies to brain. Our results support the concept of an autoimmune mechanism in GBS, while in Bannwarth's syndrome an infectious cause related to that of Lyme disease may be suspected.

Antibodies, Anti-Idiotypic↗
PubMed1984

Extra- and intrathecal production of antinerve and antibrain antibodies in Guillain-Barré syndrome: evaluation by an antibody index.

In serum and CSF samples from 19 patients with the Guillain-Barré syndrome (GBS), we assayed complement-fixing autoantibodies that react with peripheral and central nervous tissue. About two thirds of the serum and CSF samples reacted with preparations of one or both tissues. The distribution of antibodies, evaluated by the antibody index (CSF/serum titer divided by CSF/serum albumin), suggested predominantly extrathecal production in most patients, but an intrathecal contribution was also seen. Thus, the possible pathogenic effects of antineural antibodies in GBS may be exerted on both sides of the blood-brain barrier.

Antibodies↗
PubMed1983

Immunocytochemical identification of polypeptide YY (PYY) cells in the human gastrointestinal tract.

Various parts of the human gastrointestinal tract were investigated immunocytochemically for the occurrence of polypeptide YY (PYY) and pancreatic polypeptide (PP). PYY-immunoreactive cells were observed in the lower part of the ileum, in the colon and in the rectum, and PP-immunoreactive cells were found in the colon and rectum. Both cell types were of the open type, i.e. they extended from the basal lamina to the gut lumen. PYY-immunoreactive cells were seen to emit cytoplasmic processes to the neighbouring goblet cells. This latter observation suggests that PYY cells may exert a paracrine action on the mucus-secreting goblet cells. Staining of consecutive thin plastic sections and staining of the same section simultaneously for two peptides showed that PYY-immunoreactivity did not occur in PP- or enteroglucagon-immunoreactive cells. On the ultrastructural level PYY-immunoreactivity was localized in basal granulated endocrine cells. These cells contained round or slightly oval electron dense granules with a mean diameter of 150 nm (range 100-300 nm).

Digestive System↗
PubMed1983

Anticomplementary activity in multiple sclerosis.

Anticomplementary activity (ACA) is a common problem in serological work. Often it is regarded as an indicator of circulating immune complexes and has been clinically used as such. In a longitudinal study (Ryberg 1982b) ACA was determined in heated (56 degrees C for 30 min) sera from 35 MS patients followed for up to 5 years; in 18 of them ACA in heated CSF was also assayed. Persistent or transitory ACA of low titre was found in some sequences, usually without evident correlation with clinical events. Marked ACA in unheated sera was found more often in MS patients than in controls and showed dramatic changes in most of 15 sequences studied for this property, sometimes in a way suggesting a correlation with clinical exacerbations. This activity was heat labile and was not bound by an immunosorbent with affinity to human IgG and, therefore, is not likely to represent IgG containing aggregates or immune complexes.

Adult↗