Search PubMed⌕ Search

Biomedical subjects

S Norn

Publications and source records attributed to S Norn.

At least 127 records · Page 7Linked to original sources
PubMed1980

Histamine H2 receptor-mediated cyclic AMP formation in human platelets.

The influence of histamine on the level of cyclic AMP was studied in human platelets. A dose-related accumulation of cyclic AMP was obtained, culminating at about 10 microM of histamine. The response was blocked by the H2 antagonist cimetidine, but neither by H1 antagonists nor by alpha- or beta-adrenergic antagonists. The results suggest that histamine causes an accumulation of cyclic AMP in human platelets by stimulation of H2 receptors. Cyclic AMP accumulation is supposed to be associated with a depression of the platelet function, and a reduced platelet release reaction was actually demonstrated by our results.

Blood Platelets↗
PubMed1979

3H-histamine release from human leukocytes. A new method for detecting type I allergy compared with basophil histamine release technique.

A rapid, simple, and inexpensive method for large scale screening of patients suspected of type I allergy has been developed. The method is based on in vitro incorporation of 3H-histamine in the leukocytes of the patient, whereafter release of labelled histamine is measured after provocation of the cells with the suspected allergen. The new method was compared with the conventional basophil histamine release technique by in vitro provocation of six asthmatic patients under suspicion of type I allergy against animal dander, house dust, and mite, and an almost identical release of histamine was observed in both assays.

Allergens↗
PubMed1979

Binding of antigen to surface Ig during in vitro hyposensitization of isolated rat mast cells.

The mechanism of in vitro hyposensitization was examined in isolated rat mast cells. Surface distribution of immunoglobulin was examined by immunofluorescence technique. Hyposensitization could be ascribed neither to changes in the distribution of surface immunoglobulins nor to capping or shedding phenomena. The distribution of cell-bound antigen and the number of antigen-positive cells (patch-bearing cells) was not changed by hyposensitization. The binding of antigen to surface Ig was quantitated by I125-labelled antigen. In rats sensitized to two different antigens, hyposensitization of the mast cells with one of these inhibited the subsequent histamine release induced by either of the two antigens, whereas no changes were observed in the antigen binding capacity. The present investigation indicates that the mechanism of in vitro hyposensitization is the result of events secondary to the initial binding of antigen to the mast cell surface immunoglobulin.

Animals↗
PubMed1978

Basophil histamine release by RNA, DNA and aggregated IgG examined in rheumatoid arthritis and systemic lupus erythematosus. Results compared with basophil counts and antinuclear antibodies.

Basophils from patients with rheumatoid arthritis (RA) respond to RNA, DNA and immune complexes (aggregated IgG) with histamine release. The RNA response was well correlated to the clinical activity of the disease, since histamine liberation was found in all patients with severe activity, whereas no liberation was observed in patients with moderate or quiescent activity. A less significant correlation was obtained with DNA and aggregated IgG. In contrast, no response was obtained with RNA, DNA and aggregated IgG in patients with systemic lupus erythematosus (SLE) or in controls. In the RA and the SLE groups no significant correlation was found between the response of RNA, DNA and aggregated IgG and the serum titres of anti-DNA and antinuclear antibodies. No difference in basophil cell count in peripheral blood and basophil histamine content was found between RA, SLE and controls. Our results point to an involvement of an autoimmune type I reaction in the pathogenesis of RA directed against the nuclear components RNA and DNA and against immune complexes.

Adolescent↗
PubMed1978

Binding of antigen to surface Ig on isolated rat mast cells.

This study concerns observations on isolated rat mast cells sensitized to specific antigen. Specific binding of antigen to the surface immunoglobulins of these cells could be demonstrated by immunofluorescence technique as well as by radiolabelled antigen binding and the degree of binding parallelled the allergic reaction as judged by histamine release. Exposure of mast cells to antigen at both low and high antigen concentrations did not change the distribution of the surface immunoglobulins. Furthermore, neither capping not shedding could be induced, even by excessive antigen stimulation. The amount of antigen molecules bound to surface Ig was linearly correlated to the allergic histamine release. When mast cells were sensitized to two antigens of different molecular weight, the cells showed the highest sensitivity to the antigen having the highest molecular weight. These results indicate that both the amount of antigen and the molecular weight of the antigen bound to surface Ig are important factors in the allergic histamine release from mast cells, whereas surface Ig redistribution is not.

Anaphylaxis↗
PubMed1977

Allergic reactions, cyclic AMP and histamine release.

Both isobutylmethylxanthine and theophylline increased the level cyclic AMP in the mast cell. Theophylline reduced the allergic histamine release, whereas isobutylmethylxynthine caused a pronounced potentiation of the histamine release. This indicates that the hypothesis of an inverse relationship between the level of cyclic AMP in mast cells and histamine release is too simple.

Animals↗
PubMed1977

A simplified method for measuring basophil histamine release and blocking antibodies in hay fever patients. Basophil histamine content and cell preservation.

A simplified method for measuring basophil histamine release in grass pollen hay fever patients has been developed. Leukocytes were challenged in vitro with extracts of Phleum pratense (timothy) and the release of histamine was determined indirectly as the residual histamine in the cell sediment. Several steps to purify histamine thus became superfluous and histamine was directly conjugated with o-phthaldialdehyde to form a fluorophore. The simplified method showed a basophil histamine content which was in accordance with results obtained by more specific methods. No difference in basophil histamine content was found between normal and allergic persons. For the histamine liberation assay blood could be adequately preserved for transport for 48 h at room temperature by adding cell culture medium. Basophil histamine release technique allows evaluation of cell sensitivity for determination of the degree of allergy as well as the level of blocking antibodies.

Adult↗
PubMed1977

Cyclic AMP and allergic histamine release. Influence of methylxanthines on rat mast cells.

Both isobutylmethylxanthine and theophylline increased the level of cyclic AMP in rat mast cells. Theophylline reduced the allergic histamine release, whereas isobutylmethylxanthine caused a pronounced potentiation of the histamine release. This indicates that the hypothesis of an inverse relationship between the level of cyclic AMP in mast cells and histamine release is inadequate.

Animals↗
PubMed1976

Influence of hyposensitization of ATP level and CO2 production of mast cells in anaphylaxis.

Anaphylaxis in a glucose-free medium containing pyruvate caused a release of histamine and a significant decrease in the ATP level of rat mast cells. The fall was maximal after 10 min and it was found to reverse after 22 min. Glucose completely counteracted the ATP fall without changing the anaphylactic histamine release. Furthermore, the oxidative metabolism of exogenous pyruvate to CO2 was stimulated in the mast cell. A high level of protection of mast cells to antigen challenge was obtained following hyposensitization and only a small amount of the intracellular histamine was released in contrast to non-hyposensitized cells. Hyposensitization counteracted the ATP fall by antigen challenge but the increase in oxidative metabolism remained unchanged. The results indicate that hyposensitization exerts effects in the mast cell consistent with a reduced ATP utilization or with a reduced uncoupling of oxidative phosphorylation. The mechanism of the hyposensitization must be due to inhibition of one or more of the cellular steps leading to histamine release and subsequent morphological changes of the cell or to uncoupling of oxidative phosphorylation.

Adenosine Triphosphate↗