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PubMed1978

The mechanism of histamine release induced by the ionophore X537A from isolated rat mast cells. II. The relationship between increase of cell volume and histamine release.

The ionophore X537A induced swelling of isolated rat mast cells parallel to histamine release. Both actions were depressed by extracellular calcium and BSA, temperatures below 37 degrees C, NEM, PMSF, and TTX, and were enhanced by high potassium and pretreatment of the cells with ATP. DSCG, theophylline, and DFP enhanced the histamine release noted after 10 min of incubation without influencing the swelling action of X537A. The swelling action could not be separated from histamine release and it is suggested that it might be inherent in the mechanism of secretion induced by X537A. The present results further distinguish histamine release induced by the two ionophores X537A and A23187.

Animals↗
PubMed1984

A sensitive double isotopic, chromatographic method for the determination of histamine. I: Studies with authentic histamine.

This paper presents a method for the determination of histamine using an internal standard of 14C-labelled histamine, which together with an unknown sample of unlabelled histamine is dansylated with 3H-labelled dansyl chloride. The products of this dansylation are then separated on thin-layer-chromatographic plates coated with micropolyamide. The spot of dansylhistamine is scraped off and the content of histamine in the unknown sample is calculated from the 3H/14C-ratio in the spot.

Chemical Phenomena↗
PubMed1984

Gastric histamine methyltransferase: different methylation rates for enantiomers of side-chain methylated histamine analogues using a highly purified enzyme preparation.

The inhibitor/activator and substrate properties of enantiomers of two methylated histamines (MH) were investigated using a histamine methyltransferase preparation which was purified 1207-fold from pig fundic mucosa by ultracentrifugation, ion-exchange chromatography on DEAE-cellulose and preparative electrofocusing. In 1-100 microM concentrations, S-alpha-MH and R-alpha-MH were acceptor substrates as good as histamine itself. When substrate concentrations were increased to 1 mM these substances were methylated to an even greater extent than histamine, since they did not exert substrate inhibition on HMT. Introduction of a further methyl-group into the N alpha-position reduced acceptor substrate properties drastically. A difference in methylation was then seen since R-alpha,N alpha-DMH was a better substrate than S-alpha,N alpha-DMH. Whereas alpha-MH's could not activate HMT the alpha,N alpha-DMH's did. The poorer the substrate affinity of the investigated substances was, the better they were able to activate HMT.

Animals↗
PubMed1989

Increased levels of histamine observed in the skin of adrenaline-treated rats or mice are not the result of histamine synthesis by mast cells.

Like the skin of rats and mice injected with adrenaline (AD), rat isolated peritoneal mast cells display increased levels of perchloric acid-soluble histamine following incubation with AD. Although pre-exposure to alpha-fluoromethyl histidine (FMH), an inhibitor of histidine decarboxylase, prevented the effect of AD in vivo and in vitro, this compound was also found to inhibit mast cell granule swelling evoked by AD, a response linked to histamine changes. Absence of increased levels of isotopic histamine in mast cells incubated with labelled histidine in the presence of AD, as well as the insufficient amounts of would-be precursor histidine found in untreated mast cells, confirm the conclusion that AD does not increase mast cell histamine by stimulating its synthesis.

Animals↗
PubMed1985

Inhibition of in vivo histamine metabolism in rats by foodborne and pharmacologic inhibitors of diamine oxidase, histamine N-methyltransferase, and monoamine oxidase.

When [14C]histamine was administered orally to rats, an average of 80% of the administered radioactivity was recovered in the urine at the end of 24 hr. About 10% of the total dose was excreted via the feces. Analysis of 4-hr urine samples found imidazoleacetic acid to be the predominant metabolite (60.6%), with N tau-methylimidazoleacetic acid (8.6%), N tau-methylhistamine (7.3%), and N-acetylhistamine (4.5%) to be the minor metabolites. Histamine metabolism was inhibited by simultaneous oral administration of aminoguanidine, isoniazid, quinacrine, cadaverine, putrescine, tyramine, and beta-phenylethylamine. The administration of inhibitors resulted in an increased amount of unmetabolized histamine and a decreased amount of metabolites reaching the urine. Pharmacologic inhibitors were found to be more potent and have a longer duration of action than foodborne ones. The inhibitors could potentiate food poisoning caused by histamine by inhibiting its metabolism.

Administration, Oral↗
PubMed1998

Histamine receptor-independent muscle relaxation elicited by a series of histamine H2-receptor agonists on the isolated guinea pig duodenum: a study into the mechanism of action.

1. The histamine H2 receptor agonists, dimaprit, impromidine, amthamine, and several dimaprit- and impromidine-analogues were investigated for their spasmolytic activity on the guinea pig duodenum, precontracted with acetylcholine or KCl. 2. Almost all the H2 receptor agonists exerted a histamine H2 receptor-independent muscle relaxation, which was more evident on acetylcholine- than on KCl-precontracted preparations. 3. The relaxing activity of these compounds was independent of inhibitory receptors, like beta-adrenergic, GABA-ergic, serotoninergic, etc. Similarly, modifications of cyclic nucleotide metabolism and nitric oxide production did not appear to be involved. 4. The behavior of histamine H2-receptor agonists was shared only by the Na+-blocker procaine, the intracellular Ca2+-antagonist ruthenium red and, at least in terms of efficacy, by the protein kinase C inhibitor, chelerithrine. 5. This spasmolytic effect is probably due to an impairment of receptor-mediated depolarization at the plasma membrane level and/or an inhibitory activity on the protein kinase C-dependent activation of the contractile machinery. 6. Finally, our findings suggest that the histamine H2 receptor-independent muscle relaxation is a general feature shown by H2 receptor agonists endowed with different chemical structure and the putative spasmolytic "receptor" prefers a (substituted) thiazole over a (substituted) imidazole.

Animals↗
PubMed1975

Conformation of histamine derivatives. 5. Molecular orbital calculation of the H1-receptor "essential" conformation of histamine.

Conformational energies of histamine and 4-methylhistamine monocations are calculated using the EHT molecular orbital procedure; the results are expressed as potential energy surfaces in which bond rotations (theta1 for ring-Cbeta, theta2 for Cbeta-Calpha) are measured along the axes, and energy variation is indicated by contours. Using the classical Boltzmann partition function and Simpson's rule for normalization, corresponding probability surfaces are generated which take account of the potential surface entropy. Comparing the two surfaces provides regions which are within a given probability contour of histamine but outside this contour for 4-methylhistamine. Thus, at the 99% probability level, three conformational regions defined by the bond rotation angles are indicated as possible "H1-essential" conformations of histamine: viz. trans (theta1=290-330 degrees, theta2=150-210 degrees) and gauche (theta1=260-280 degrees, theta2=30-90 degrees and theta1=290-320 degrees, theta2=270-320 degrees). This procedure provides a quantitative basis for comparison with other histamine derivatives and may have a general value for studying relationships between conformation and biological activity of closely related small molecules.

Energy Transfer↗
PubMedDate not supplied

The importance of endogenous histamine relative to dietary histamine in the aetiology of scombrotoxicosis.

Deliberately spoiled mackerel samples and mackerel samples implicated in outbreaks of scombrotoxicosis were, under medical supervision, tested blind on normal, healthy volunteers of both sexes. These experiments identified batches of fish which could induce nausea/vomiting and/or diarrhoea when 50 g samples were consumed. It was also established that the fillets in a batch were neither of equal potency nor homogeneous with respect to histamine content. Strong evidence was obtained that dietary histamine is not a major determinant of scombrotoxicosis since potency was not positively correlated with the dose, and volunteers appeared to fall into susceptible and non-susceptible subgroups. However, there is no reason to suspect allergy as being solely responsible for these differences in sensitivity. It is also possible to discount body weight as a factor. While the data suggest that females may be more susceptible than males, this effect cannot be confirmed at the present time. Studies with susceptible volunteers predosed with either placebo or H1 antagonist (chlorpheniramine 4 mg) demonstrated convincingly that the antihistamine can abolish vomiting and diarrhoea associated with the ingestion of 50 g of scombrotoxic fish. It is therefore postulated that endogenous histamine released by mast cell degranulation has a significant role in the aetiology of scombrotoxicosis, whereas the role of dietary histamine is minor. The nature and origin of the agent responsible for mast cell degranulation is being investigated.

Chlorpheniramine↗
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↗
PubMed1985

Sensitive glass microfibre-based histamine analysis for allergy testing in washed blood cells. Results compared with conventional leukocyte histamine release assay.

The new microfibre method for allergy testing is based on basophil histamine release after challenge with suspected allergens in samples of 50 microliter washed blood cells. Released histamine is bound to microfibres and measured after removal of interfering substances by washing. The microfibre method was compared with the conventional leukocyte histamine release assay in 18 allergic patients tested with 10 different allergens. It was found that the same individuals responded with histamine release to the same allergens in both assays, and the number of responders was almost identical. Also the dose-response curves and the cell sensitivity were almost identical, which further substantiated identity between the results obtained by the new microfibre method and the conventional assay. A comparison between the microfibre method and in vivo provocation tests showed good agreement when comparing the number of positive and negative responses in these test. The new method overcomes the problems in allergy testing, where only small amounts of blood are available and many tests have to be carried out.

Allergens↗
PubMed2005

Validation of basophil histamine release against the autologous serum skin test and outcome of serum-induced basophil histamine release studies in a large population of chronic urticaria patients.

BACKGROUND: Endogenous histamine-releasing factors (HRFs) are involved in 30-60% of patients with chronic urticaria (CU). Evidence for their existence comes from in vivo studies of autoreactivity with the autologous serum skin test (ASST), in vitro immunoassays demonstrating autoantibodies against the immunoglobulin E (IgE) or the high affinity IgE receptor (FcepsilonRI) and serum-induced histamine release (HR) from basophils and mast cells. We have examined the correlation between the ASST and a new basophil histamine-releasing assay (the HR-Urtikaria test) in a group of well-characterized CU patients and subsequently determined the frequency of HR-Urticaria-positive sera from a larger population of CU patients. SUBJECTS: Group 1 consisted of 28 patients with CU (16 were ASST-positive) 20 patients with atopic dermatitis, 24 patients with allergy to birch and nine healthy controls. Group 2 consisted of 873 unselected CU patients. METHODS: White blood cells containing 1-2% basophils from a healthy nonatopic donor were incubated with patients sera in the presence of interleukin (IL)-3. Histamine was measured by the glass fibre method. RESULTS: Using the ASST as the true outcome, the HR-Urticaria test showed a sensitivity and specificity of 75% in group 1 using a cut-off value for HR of >16.5%. None of the controls was positive in the HR-Urticaria test. In group 2, we found no difference in the frequency of positives between male (34.6%, n = 254) and female adults (35.1%, n = 576) but twice as many females as males were tested. CONCLUSIONS: Our studies have shown that the HR-Urticaria test has a good sensitivity and specificity for endogenous HRFs demonstrated by the ASST in patients with CU and that about one-third of unselected patients with CU have a positive result.

Adolescent↗
PubMed1975

The effects of histamine and some histamine-like agonists on blood pressure in the cat.

1. The effects of histamine on blood pressure have been compared with the effects caused by four histamine-like agonists in anaesthetized cats. 2. It has been confirmed that the depressor responses to histamine involve both H1- and H2-receptors: depressor responses also follow the administration of selective H1- and H2-receptor agonists. 3. 2-Methylhistamine, in doses up to 1 X 10(-7) mol/kg, lowers blood pressure by interaction with H1-receptors. Larger doses of 2-methylhistamine also lower blood pressure but this may involve H2-receptors. 4. 4-Methylhistamine, in doses up to 1 X 10(-7) mol/kg, lowers blood pressure by interaction with H2-receptors. Larger doses of 4-methylhistamine also lower blood pressure but this may involve H1-receptors. 5. 2-(2-Aminoethyl)pyridine and 2-(2-aminoethyl)thiazole both lower blood pressure by interaction with H1-receptors only. 6. The potential value and limitations of these compounds as tools to investigate the cardiovascular effects of histamine are discussed.

Animals↗
PubMed2002

Klebsiella pneumoniae produces no histamine: Raoultella planticola and Raoultella ornithinolytica strains are histamine producers.

Histamine fish poisoning is caused by histamine-producing bacteria (HPB). Klebsiella pneumoniae and Klebsiella oxytoca are the best-known HPB in fish. However, 22 strains of HPB from fish first identified as K. pneumoniae or K. oxytoca by commercialized systems were later correctly identified as Raoultella planticola (formerly Klebsiella planticola) by additional tests. Similarly, five strains of Raoultella ornithinolytica (formerly Klebsiella ornithinolytica) were isolated from fish as new HPB. R. planticola and R. ornithinolytica strains were equal in their histamine-producing capabilities and were determined to possess the hdc genes, encoding histidine decarboxylase. On the other hand, a collection of 61 strains of K. pneumoniae and 18 strains of K. oxytoca produced no histamine.

Animals↗
PubMed1985

Assessment of histamine release and kinin formation in man: identification of kinin degradation products and characterization of a lymphocyte-dependent histamine releasing factor.

Factors traditionally associated with histamine release include IgE antibody plus antigen and the anaphylatoxins C3a, C4a, and C5a. Yet histamine release is thought to occur in disorders such as chronic urticaria, atopic dermatitis, and contact dermatitis in which the above mechanisms do not appear operative. We have partially purified a factor from stimulated human mononuclear cells which causes basophil histamine release. It is homogeneous by gel filtration with a molecular weight of about 35,000 daltons and has two molecular forms when assessed by ion exchange chromatography, isoelectrofocusing in gels and chromatofocusing. The purified material, when radiolabeled, gives a single band upon two-dimensional gel electrophoresis and radioautography. This factor may therefore represent one mechanism in which delayed hypersensitivity and histamine release are linked. We are also developing methods to better assess the kinin-forming system in allergic diseases. Assays for enzyme inhibitor complexes are the most sensitive and specific methods for inferring activation in plasma. These include quantitation of activated Hageman factor-C1 INH complexes and kallikrein-C1 INH complexes each of which appears elevated in cutaneous late-phase reactions. However, bradykinin assessment is fraught with difficulties including spurious generation and rapid inactivation. Using high performance liquid chromatography we have separated bradykinin from kallidin, des-Arg9-bradykinin (the degradation product of carboxypeptidase N) as well as the fragments Arg-Pro-Pro-Gly-Phe, Ser-Pro, and Phe-Arg, the degradation products formed by angiotensin-converting enzyme. These can be assayed in purified mixtures, can be detected upon addition of bradykinin to human plasma and are formed by kaolin treatment of plasma.

Basophils↗
PubMed1988

Role of cyclic AMP during histamine release. Histamine release is not directly related to increase in cyclic AMP levels in rat mast cells activated by concanavalin A, anti-IgE, antigen, prostaglandin D2 and isoproterenol.

Activation of mast cells by bridging of IgE-receptors or concanavalin A (Con A) results in a rapid initial rise and fall in cyclic AMP (cAMP) levels followed by a second rise in cAMP levels and histamine release (Sullivan, T. et al. (1976) J. Immunol. 117, 713-716; Lewis, R.A. et al. (1979) J. Immunol. 123, 1663-1668; Ishizaka, T. et al. (1981) Proc. Natl. Acad. Sci. U.S.A. 78, 6812-6816). trans-4-Guanidinomethylcyclohexanecarboxylic acid 4-tert-butylphenyl ester (GMCHA-OPhBut), a strong trypsin inhibitor and an anti-allergic agent (Muramatu, M. et al. (1982) Hoppe-Seyler's Z. Physiol. Chem. 363, 203-211; Takei, M. et al. Agents Actions, in press), strongly and dose-dependently inhibited the initial and second rises in cAMP levels, and release of histamine from rat mast cells by Con A, anti-IgE and antigen. Addition of GMCHA-OPhBut after the initial rise in cAMP inhibited the second rise in cAMP and histamine release. These results suggested a possible participation of a trypsin-like proteinase, probably pH 7 tryptase present in rat mast cells, in the activation of adenylate cyclase by the above secretagogues, and the initial rise in cAMP was not directly related to the latter events. The second rise in cAMP is induced by prostaglandin D2 (PGD2), a metabolic product of arachidonic acid. PGD2 elevated the cAMP levels in mast cells whereas no histamine was secreted. GMCHA-OPhBut did not inhibit the increase in cAMP by PGD2. Therefore, the strong inhibitory effect of GMCHA-OPhBut on the second rise in cAMP might depend on the inhibition of an earlier process than the activation of adenylate cyclase by PGD2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Effect of histamine application on diamine oxidase activity in kidneys and histamine level in urine].

Histamine or cadaverine or both amines jointly were given to guinea pigs for 7 weeks. The histamine content was determined in urine and the diamine-oxidase activity in the kidneys. Histamine excretion by the kidneys occurred 4 hours after introduction of the amine into the stomach. In the animals receiving histamine the activity of diamine-oxidase was greatly enhanced.

Amine Oxidase (Copper-Containing)↗
PubMed1988

[The blood histamine level of patients with bronchial asthma and their skin vascular reaction to histamine].

The relation between the pathochemical phase and the histaminergic reactivity of the effector structures in asthmatic patients was studied. In 124 asthmatic patients classified into two groups the skin vascular reaction to histamine by mediaphoresis and the histamine blood level by two different methods for each group (spectrophotometric and spectrofluorometric) were examined. A linear relation was established between the histamine blood level and the histamine skin vascular reaction.

Adolescent↗
PubMed1987

Quantitation of histamine-induced angiogenesis in the chick chorioallantoic membrane: mode of action of histamine is indirect.

Histamine was chosen as a standard chemical suitable for the development of new methods of assessing vascularity in the chick chorioallantoic membrane (CAM). When applied in liquid form to the entire 'dropped' area of CAM at day 10 of growth, a sublethal dose was required before a convincing appearance of increased vascularity was produced by day 15. Computer-assisted morphometry, using osmium-stained CAMs viewed en face, demonstrated a progressive increase in both length (21%) and number (59%) of arterial branches over 5 days relative to buffer only controls. A 56% increase in number of mesenchymal vessels seen in cross-section was also detected and this method is the quickest and easiest. No increase in the number of capillaries in the surface plexus of the ectoderm was found but this may be attributable to inadequate technique due to the already high density of capillaries present even in control CAMs using thin resin sections. However a 21% increase in the haemoglobin content of the CAM 4 days after histamine is consistent with an overall increase in the vascular bed. A rapid fall in DNA synthesis by 6 h (-48%) was produced by histamine, followed by a slow rebound to a peak at 36 h (74%). This contrasts with the growth factor type of pattern seen previously with fibrin degradation products giving a progressive rise to a major peak of DNA synthesis at 18 h. These effects indicate two mechanisms of induction of angiogenesis, and that the action of histamine is indirect.

Animals↗