Histamine release from the mast cells of guinea-pig lung

Eilbeck, J. F.; Smith, William G.

doi:10.1111/j.2042-7158.1967.tb09563.x

Cited by 8 publications

(4 citation statements)

References 15 publications

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“…In the trachea it is possible that some of the fluorescent cells seen in the connective tissue could have been mast cells which had taken up noradrenaline. The presence of mast cells in the guinea-pig trachea is rarely described although guinea-pig lung is believed to have a high mast cell count (Eilbeck & Smith, 1967). The toluidine blue stain used for staining cartilage also stains mast cells but only a few mast cells were ever seen in the tracheal sections.…”

Section: Discussionmentioning

confidence: 99%

A histochemical study of extraneuronal accumulation of noradrenaline in the guinea‐pig trachea

O’Donnell

Saar

1973

British J Pharmacology

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Summary Accumulation of noradrenaline in extraneuronal tissue of the guinea‐pig trachea has been studied by the use of the fluorescence histochemical technique of Falck and Hillarp. After incubation in solutions of noradrenaline, fluorescence developed in cellular structures (tracheal smooth muscle, vascular smooth muscle and endothelium, fibroblasts and chondroblasts), in the intercellular matrix of the cartilage and throughout the loose connective tissue of the adventitia and submucosa. The effect of various experimental procedures on the development of this fluorescence has been examined i.e. incubation with noradrenaline at reduced temperature (0° C), removal of fluorescence by washing with Krebs solution at 37° C or 0° C, incubation with phenoxybenzamine (10−4m) or metanephrine (10−4m). From these observations it has been concluded that noradrenaline accumulates in the trachea: (a) in cellular structures where it is firmly bound, i.e. not easily removed by washing at 0° C, and where the accumulation is prevented by phenoxybenzamine, metanephrine or cold. (b) in the intercellular matrix of the cartilage where it is also firmly bound, but where the accumulation is not prevented by phenoxybenzamine, metanephrine or cold. This probably represents binding to sulphated mucopolysaccharides. (c) in the adventitia and submucosa where it is loosely bound and easily removed by washing. Some implications of these findings in pharmacological experiments with guinea‐pig trachea are discussed.

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Section: Discussionmentioning

confidence: 99%

A histochemical study of extraneuronal accumulation of noradrenaline in the guinea‐pig trachea

O’Donnell

Saar

1973

British J Pharmacology

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“…However, there is evidence for an inhibitory effect of the glucocorticoids on antigen-induced histamine release from guinea pig mesentery [7[ and lung [8][9][10] as well as on hypoxia mediated histamine release [1 11. Also antigen-induced histamine release from human tissue is inhibited by the glucocorticoids, e.g.…”

Section: Introductionmentioning

confidence: 99%

Influence of glucocorticoids on histamine release and45Calcium uptake by isolated rat mast cells

Grosman

Jensen

1984

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Hydrocortisone and prednisolone inhibited the histamine release from isolated rat mast cells induced by antigen, the ionophore A23187, and compound 48/80 in the absence and in the presence of calcium. Hydrocortisone reduced the response to the different releasing agents by 50% in the concentration range 2-6 X 10(-4) M, whereas prednisolone was about 1.5 times more potent. The inhibitory effect of hydrocortisone had a rapid onset of action and maximal inhibition was observed after preincubation for 20 minutes. The effect of hydrocortisone was reversed by including 2 mM glucose in the medium. The reversal was only partial with antigen and the ionophore A23187, indicating a greater energy requirement of these releasing agents compared with compound 48/80. The inhibition of the histamine release was accompanied by a concentration-related inhibition of the 45Ca uptake, except with the ionophore. The inhibition of the 45Ca uptake was also reversed by glucose, but differences were noted concerning the influence of preincubation time. The observations are explained by an association of 45Ca to cellular material, e.g. granules, secondary to the release process. The effects of hydrocortisone and prednisolone were qualitatively identical and were not observed with estriol. The glucocorticoid inhibition of histamine release does not seem to be caused by effects on phospholipase activity or cyclic AMP metabolism. The present observations are fully consistent with an impaired mitochondrial function as the mechanism for the mast cell effects of the glucocorticoids.

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“…Several authors have observed a correlation between the histamine release and the formation of spasmogenic lipids in anaphylaxis; some reports also include a correlation between the amounts of substances released and the number of mast cells in the tissue (Borgus and Chakravarty 1960, Eilbeck andSmith 1967). This has led to the suggestion that the release of both histamine and spasmogenic lipids is the result of a common mechanism, and that the mast cell is the source of both.…”

Section: Discussionmentioning

confidence: 99%

Release of Histamine and Formation of Smooth‐Muscle Stimulating Principles in Guinea‐Pig Lung Tissue Induced by Antigen and Bee Venom Phosphatidase A

Strandberg

1969

Acta Physiologica Scandinavica

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Release of histamine and formation of smooth‐muscle stimulating principles (spasmogenic lipids) occurred when minced guinea‐pig lung tissue was exposed to antigen or to bee venom phosphatidase A. In agreement with earlier reports the anaphylactic histamine release was a rapid process, and it could be inhibited by anoxia in the absence of glucose, and by potassium cyanide, ninhydrin and A’‐ethyl‐maleimide. The histamine release induced by phosphatidase A was not influenced by these inhibitors or by anoxia, and the release was slower than in anaphylaxis. The spasmogenic lipids formed had similar chromatographic and biological properties to those reported for the corresponding principles formed in anaphylaxis, and the process of formation was inhibited by oxygen lack and by the above enzyme inhibitors. One noteworthy feature of the spasmogenic lipid formation was that the inhibition caused by anoxia could not be counteracted by glucose. The results support earlier hypotheses regarding the mode of action of phosphatidase A on guinea‐pig lung tissue. It is suggested that mast cells are not necessarily involved in the formation of spasmogenic lipids occurring in connection with histamine release induced by phosphatidase A in the guinea‐pig lung. The bee venom fraction F II, which liberates histamine from rat tissues by a mechanism resembling that of compound 48/80, did not cause release of histamine or formation of spasmogenic lipids from the guinea‐pig lung tissue in concentrations up to 100 mug/ml.

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Histamine release from the mast cells of guinea-pig lung

Cited by 8 publications

References 15 publications

A histochemical study of extraneuronal accumulation of noradrenaline in the guinea‐pig trachea

A histochemical study of extraneuronal accumulation of noradrenaline in the guinea‐pig trachea

Influence of glucocorticoids on histamine release and45Calcium uptake by isolated rat mast cells

Release of Histamine and Formation of Smooth‐Muscle Stimulating Principles in Guinea‐Pig Lung Tissue Induced by Antigen and Bee Venom Phosphatidase A

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