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At least 37 records · Page 2Linked to original sources
PubMed1954

Cytological and pharmacological observations on the release of histamine by mast cells.

Experimental solutions known to affect mast cells or to cause liberation of histamine from the tissue were introduced into the peritoneal cavity of rats. Samples of the peritoneal fluid were withdrawn at intervals afterward and assayed for histamine and the condition of the mast cells was subsequently ascertained by microscopic examination of stained spreads of the mesenteries. Intraperitoneal injection of distilled water caused osmotic disruption of the mast cells and the appearance of an appreciable amount of histamine in the peritoneal fluid. Injection of Tyrode solution alone was not particularly damaging to the mast cells and little or no histamine was released. Injection of Tyrode solution containing compound 48/80 resulted in extensive release of granules from mast cells and the appearance of large amounts of histamine in the fluid. Solution of 48/80 failed however to cause histamine release when injected into rats whose subserosal mast cells had previously been destroyed. A series of increasing doses of compound 48/80 had a graded morphological effect upon mast cells and resulted in a graded increase in the amount of histamine that appeared in the peritoneal fluid. It is unlikely therefore that this compound acts by simply lysing the plasma membrane. It is concluded that mast cells in the rat are extraordinarily rich in histamine which is liberated under conditions which cause mast cells to release their granules. The histamine set free by the potent histamine liberator, compound 48/80, appears to come principally from the tissue mast cells.

Animals↗
PubMed1955

Mast cells as sources of tissue histamine.

Enumeration of mast cells and determination of histamine in sections of dog skin and dog lung have shown that the regions of the tissue rich in mast cells are also rich in histamine. In the skin, the outer layers of the dermis contain higher concentrations of histamine and mast cells than any other region. Average values of the histamine content and mast cell count for dog liver, heart, muscle, and kidney, and for beef liver parenchyma and capsule, also exhibit a positive relationship between these two parameters, although the amount of histamine found per mast cell varied from 7 micromicrog. in dog skin to 32 micromicrog. in beef liver capsule. When the size of the mast cells was taken into account, the intracellular concentration of histamine was found to be of the same order (about 0.4 molar) for all the tissues examined except skin and kidney. In both dog skins analyzed, the intracellular concentration was about 0.1 molar. In kidney both mast cell and histamine values were too low for accurate estimation. The concentration of histamine in the mast cells investigated was much greater than the concentration in human basophils, the blood elements richest in histamine. The mechanism of the localization of histamine in mast cells is briefly considered.

Animals↗
PubMed1956

5-Hydroxytryptamine and histamine as mediators of the vascular injury produced by agents which damage mast cells in rats.

Each of the four agents, ovomucoid, dextran, 48/80, and testis extract, when injected beneath the skin of the dorsa of the paws of rats produces a local vascular injury characterized by a protein-rich edema. Each agent also produces damage to mast cells. Either 5-hydroxytryptamine or histamine produces a response similar in the gross to that elicited by the agents which damage mast cells; however, neither of these two agents produces mast cell damage. On a weight basis 5-hydroxytryptamine is a much more potent edema-producing agent than histamine. The edema-producing action of 5-hydroxytryptamine can be differentiated from the similar action of histamine by the use of specific antagonists; dibenamine is a 5-hydroxytryptamine antagonist and pyrilamine a histamine antagonist. The edema produced by the mast cell-damaging agents is partially inhibited by dibenamine but is not diminished by pyrilamine. It is completely inhibited by treatment of rats with both drugs. The drugs which inhibit edema do not prevent mast cell damage by ovomucoid, dextran, 48/80, or testis extract. The observations are consistent with the hypothesis that agents which damage mast cells, "release" both 5-hydroxytryptamine and histamine and that in the rat the edema associated with mast cell damage is mediated largely by 5-hydroxytryptamine.

Animals↗
PubMed1961

Anaphylaxis in chopped guinea pig lung. I. Effect of peptidase substrates and inhibitors.

The quantitative release of histamine by specific antigen from perfused, chopped, sensitized guinea pig lung has been used to study the effect of peptidase substrates and inhibitors on the anaphylactic reaction. The anaphylactic release of histamine is prevented by chymotrypsin substrates and inhibitors but not by trypsin, carboxypeptidase, or leucine aminopeptidase substrates or the soybean trypsin inhibitor. The chymotrypsin substrates and inhibitors appear to be acting on an antigen-antibody-activated step because these substances fail to inhibit if the tissue is washed free of them prior to antigen addition, and because there is complete desensitization of the tissue without histamine release when the antigen is added in the presence of these inhibitors. The inhibitors work equally well in tissue from passively sensitized animals or in tissue from animals actively sensitized with either ovalbumin or bovine gamma globulin. These observations suggest that activation of a chymotrypsin-like enzyme is a necessary condition for the anaphylactic release of histamine in guinea pig lung. Diisopropylfluophosphate is inhibitory when present at the time of antigen addition but not when the tissue is washed free of unfixed diisopropylfluophosphate prior to adding antigen. This indicates that diisopropylfluophosphate must be acting exclusively on an enzyme which exists in lung tissue in a precursor form resistant to diisopropylfluophosphate until activated by the antigen-antibody interaction. Thiol alkylating or oxidizing agents also prevent the anaphylactic release of histamine, but in contrast to the situation with diisopropylfluophosphate and the other chymotrypsin inhibitors, the phase of the anaphylactic reaction inhibited by N-ethylmaleimide is available prior to the antigen-antibody interaction. The similarities and differences between immune hemolysis and anaphylaxis in chopped guinea pig lung are considered in detail.

Amino Acids↗
PubMed1961

Anaphylaxis in chopped guinea pig lung. II. Enhancement of the anaphylactic release of histamine and slow reacting substance by certain dibasic aliphatic acids and inhibition by monobasic fatty acids.

The quantitative release of histamine and slow reacting substance by specific antigen from perfused, chopped, sensitized guinea pig lung has been used to study the opposing effects of monobasic and certain dibasic fatty acids on the anaphylactic reaction. The anaphylactic release of histamine and slow reacting substance is doubled by the addition of 0.5 mM of succinic or maleic acid to the reaction mixture, and enhancement is definite with as little as 0.05 mM of succinic acid. Prolonged preincubation of the tissue with the dibasic acids is not required, for 60 to 90 per cent of maximal enhancement is apparent when the antigen is added to the tissue only 10 seconds after succinic or maleic acid. The increased histamine release is not due to a qualitative change in the time course of histamine release, is not the result of increased histamine formation, and cannot be attributed to an effect on the tricarboxylic acid cycle. The enhancement seems to be due to potentiation of some step activated by the antigen-antibody interaction and common to both the release of histamine and slow reacting substance. The structural configuration required for a dibasic acid to enhance the anaphylactic reaction in guinea pig lung is quite specific; the carboxyl groups should be separated by a two carbon chain, and must be free or fixed in the cis position. The monobasic fatty acids from valeric to dodecanoic inhibit the anaphylactic release of histamine, and the concentration needed to produce 50 per cent inhibition decreases with increasing chain length. The introduction of a polar group, amino or carboxyl, into the hydrocarbon residue diminishes or abolishes inhibitory capacity. The inhibition produced by the fatty acids is neither due to calcium binding nor due to prevention of effective antigen-antibody interaction; the fatty acids probably inhibit by acting on an antigen-antibody-activated step. The inhibition of the anaphylactic release of histamine and slow reacting substance produced by caproic or decanoic acid can be reversed by the enhancing effect of succinic acid, and vice versa. Thus, compounds normally present in mammalian tissue can greatly influence the intensity of the in vitro anaphylactic reaction in the guinea pig.

Anaphylaxis↗