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At least 487 records · Page 27Linked to original sources
PubMed1978

[Thrombocyte functional resistance and histamine and serotonin metabolism in ischemic heart disease].

The functional resistance of blood platelets, the reserve and active forms of histamine and serotonin, and the activity of monoamine oxidase and histaminase were studied in 5 healthy subjects, in 64 patients with acute, subacute and rehabilitation stages of myocardial infarction, and in 33 patients during frequent attacks of angina pectoris and after their total subsidence. On the grounds of the data obtained, the authors conclude that: (1) the drastically disturbed blood platelet resistance, megathrombocytosis, and marked decrease in the content of reserve amine forms in ischemic heart disease should be considered an additional risk factor; (2) agents which improve blood platelet vital activity and/or block the release reaction should be included in the therapeutic program for patients suffering from ischemic heart disease with heightened risk factors.

Adult↗
PubMed1978

Urinary methylhistamine as an index of histamine formation during histidine decarboxylase inhibition in the rat.

A new method is described for the evaluation in vivo of histidine decarboxylase inhibitors. Urinary methylhistamine excretion is approximately trebled in rats treated simultaneously with the histaminase inhibitor aminoguanidine and the monoamine oxidase inhibitor pargyline, thus providing a high base-line against which inhibiton of methylhistamine formation, and hence of histamine formation, can be measured. Variations in the recovery of methylhistamine are compensated for by addition of a standard amount of radioactive methyl-histamine to each urine sample. The method has the advantage over previously described methods of requiring less radioactive material and fewer animals which, moreover, do not have to be killed and so can be re-used. In addition, the time course of inhibition can be assessed.

Animals↗
PubMed1980

[Role of sodium nitrite in histamine urticaria of dietary origin].

Although genuine gastro-intestinal allergy is sought as the cause of chronic urticaria or repeated vaso-motor headaches, a non-allergic intolerance of one or more ingested substances, additives to foodstuffs (colourants and conserving agents) are likely to be implicated. Dietary histories from such patients often reveal heavy consumption of charcuterie. Oral provocation tests, performed using additives and placebo, can reproduce symptoms reliably. The substance most frequently incriminated is sodium nitrite (E 250): out of 76 tests, 4 were positive and 4 doubtful. In these cases complete avoidance of E 250 led to significant improvement or cure. We discuss various hypotheses on the harmful effects of sodium nitrite, such as denaturation of histamine-binding SH-group rich mucoproteins, direct toxicity on microvilli or inhibition of intestinal histaminase.

Adult↗
PubMed1980

[The effect of experimentally induced histamine deficiency on growth and rate of taking of model tumours (author's transl)].

From oncolytically effective clostridial strains, the intact washed or fractionated material of the spores and vegetative forms and culture media were examined for histamine decomposing activity in previous in vitro experiments (14). In a fractionated state, all strains cause a reduction of histamine activity. Therefore histaminases are present as endozymes. When the spores germinate to vegetative forms on the tumour following i.v. injection, the cell wall breaks open and the enzymes are released. Möse et al. (13) described rapid and nearly complete decomposition of plasmakinins (specifically bradykinin) by means of the above mentioned special preparations of clostridial strains with oncolytical effect (culture media partially excepted). Bradykinin and histamine are vasoactive substances, which are significant in terms of fine regulation of the capillary circulation. Continuous inactivation of these tissue hormones effected by the (clostridial) vegetative forms concentrated in the tumour may decrease the capillary circulation and thereby favour necrotization or decomposition of the tumour. In this animal experiment the effect of this biogenic amine on growth and rate of taking of tumours by means of artificially produced changes in the flowing equilibrium of the histamine metabolism was to be shown. Mice: While feeding mice a pyridoxal phosphate-free diet, a Harding-Passey melanoma was inoculated: The tumour weights were slightly lower in the case of animals put on the diet than in controls. Rats: Histamine-free diet and treatment with semicarbazide (in the course of the treatment implanzation of a Walker tumour). The taking of the tumours was significantly delayed or their growth reduced as a result of the diet or the treatment with semicarbazide or both.

Animals↗
PubMed1976

Modulation of human eosinophil polymorphonuclear leukocyte migration and function.

Eosinophil migration toward a concentration gradient of a chemotactic factor is regulated at four levels. Diverse immunologic pathways generate stimuli with eosinophil chemotactic activity, including the complement products C5a and a fragment of C3a and the peptide products of mast cells and basophils activated by IgE-mediated reactions, such as eosinophil chemotactic factor of anaphylaxis (ECF-A) and other oligopeptides. The intrinsic preferential leukocyte activity of the chemotactic stimuli represents the second level of modulation, with ECF-A and other mast cell-derived peptides exhibiting the most selective action on eosinophils. The third level of control of eosinophil chemotaxis is composed of inactivators and inhibitors of chemotactic stimuli and is exemplified by degradation of C5a by anaphylatoxin inactivator or chemotactic factor inactivator and of ECF-A by carboxypeptidase-A or aminopeptidases. The activity of ECF-A is uniquely suppressed by equimolar quantities of its NH2- terminal tripeptide substituent, presumably by eosinophil membrane receptor competition. Factors comprising the fourth level of regulation, which alter eosinophil responsiveness to chemotactic stimuli, include the chemotactic factors themselves, through deactivation; nonchemotactic inhibitors such as the COOH-terminal tripeptide substituent of ECF-A, the neutrophil-immobilizing factor (NIF), the phagocytosis-enhancing factor Thr-Lys-Pro-Arg, and histamine at concentrations greater than 400 ng/ml; and nonchemotactic enhancing principles represented by ascorbate and by histamine at concentrations of 30 ng/ml or less. Local concentrations of eosinophils called to and immobilized at the site of a hypersenitivity reaction may express their regulatory functions by degrading the chemical mediators elaborated including histamine, slow-reacting substance of anaphylaxis (SRS-A), and platelet-activating factor (PAF) by way of their content of histaminase, arylsulfatase B, and phospholipase D, respectively. Immunologic pathways may thus provide the capability for early and specific host defense reactions with a later influx of eosinophils preventing irreversible local tissue alterations or distant organ effects.

Anaphylaxis↗
PubMed1994

Diamine oxidase is the amiloride-binding protein and is inhibited by amiloride analogues.

Diamine oxidase (histaminase), an enzyme that oxidatively deaminates putrescine and histamine, was purified from human placenta and from pig kidney. Both NH2-terminal sequences are highly homologous to the human kidney amiloride-binding protein, previously thought to be a component of the amiloride-sensitive Na+ channel. Monoclonal antibodies raised against the pig kidney amiloride-binding protein immunoprecipitate a polypeptide with the same M(r) (105,000) as that of pig kidney diamine oxidase. That polypeptide has both diamine oxidase activity and the capacity to bind [3H]phenamil, a tritiated amiloride derivative. Cells stably transfected with human kidney amiloride-binding protein cDNA express a high diamine oxidase activity. In transfected cells as well as with the purified enzyme, this activity was inhibited by amiloride and by some of its derivatives, such as phenamil and ethylpropylamiloride. Amiloride inhibition seems to be due to drug binding at the active site of the enzyme. These data indicate that human placental diamine oxidase is identical to the human kidney amiloride-binding protein and that amiloride analogues may have wider physiological effects besides those on epithelial ion transport.

Amiloride↗
PubMedDate not supplied

Isolation and characterization of monoamine oxidase from hyperfunctioning human thyroid.

Human thyroid monoamine oxidase from hyperfunctioning thyroids was isolated and purified by separating the mitochondria by differential centrifugation followed by ultrasonication. The suspension containing the active enzyme from the DEAE-column, on passing through a Sephadex G-200 column gave three peaks corresponding to molecular weights of approximately 220,000, 23,000 and 4000 of which the component with molecular weight 4000 showed enzyme activity. The blood of the patients was analyzed for plasma MAO, RBC cholinesterase, plasma histaminase and plasma catecholamines. Histology and histochemistry of the thyroid tissues were also done. The data are examined from the point of view of the prevalent idea of the possible existence of MAO in multiple forms.

Adolescent↗
PubMed1976

Metabolic studies of guinea pig basophilic leukocytes in short-term tissue culture. I. Measurement of histaminesynthesizing capacity by using an isotopic-thin layer chromatographic assay.

Mature circulating guinea pig basophils, purified to comprise 25% or more of leukocytes, have been successfully maintained in short-term tissue culture for up to 72 hr. These cells were found to retain the ability to synthesize histamine, as assayed by a new isotopic-thin layer chromatographic assay which can reliably detect as little as 0.5 pg of 3H-histamine. Cell-associated, newly synthesized histamine was detectable as early as 1 hr of culture, was substantially increased at 6 hr, and reached maximal levels at 24 hr, when it accounted for approximately 6.5% of total cell histamine. Newly synthesized histamine was still detectable at 48 and 72 hr of culture. Histamine synthesis was decreased by lwoering the concentration of histidine in the culture medium, and was markedly reduced by all the specific histidine dedarboxylase (HDC)3 inhibitors tested, but not by alpha-methyl-DOPA, pyrilamine maleate, or metiamide. Increasing the concentration of pyridoxal phosphate, the HDC coenzyme, above that normally present in culture medium resulted in only an equivocal increase in the amount of newly synthesized histamine, whereas aminoguanidine, an inhibitor of histaminase, had no detectable effect. Uptake of exogenous histamine by cultured basophils was trivial compared to histamine synthesis. Both newly synthesized and previously manufactured, nonisotopic, histamine seemed to be stored in the same pool, as the same proportion of both was released by concanavalin A (Con A). Cellular histamine was largely conserved, with little or no spontaneous release into the medium of detectable isotopic or nonisotopic histamine. These techniques provide a model for studying granulocyte metabolic processes in vitro, and should assist in the direct investigation of a variety of their physiologic functions.

Animals↗