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PubMed1986

Regulation by serine esterase of histamine release from human leukocytes--I. Direct release of histamine by the serine esterase inhibitors diisopropyl fluorophosphate (DFP) and soman (GD).

The serine esterase inhibitor diisopropyl fluorophosphate (DFP) had been reported previously to inhibit IgE-dependent histamine release. Recently, it has been demonstrated that lower concentrations of DFP enhance IgE-dependent histamine release and inhibit desensitization. This manuscript describes the abilities of several esterase inhibitors to cause release of histamine from human leukocytes (basophils), by a process that is IgE-independent. This esterase inhibitor-induced histamine release appears to be by a non-cytotoxic mechanism that requires calcium and is temperature dependent. These histamine release processes occurred over a longer period of time than IgE-dependent release. Direct release of histamine by these small molecular weight inhibitors and inhibition of desensitization both suggest that one or more serine esterases are involved in the regulation of histamine release from human basophils.

Edetic Acid↗
PubMed1977

Histamine, histamine antagonists and regional blood flow.

The effects of mepyramine, a selective histamine H1-receptor antagonist, and metiamide, a selective histamine H2-receptor antagonist, have been determined on the cardiovascular response to intravenous infusions of a large dose of histamine, 1 X 10(-7) mol/kg/min. Pretreatment with either mepyramine, 2.5 X 10(-6) mol/kg, or metiamide, 2 X 10(-6) mol/kg/min, had no significant effect on the fall in blood pressure or fall in total peripheral resistance during histamine infusion. Pretreatment with mepyramine, 2.5 X 10(-6) mol/kg, and metiamide, 2 X 10(-6) mol/kg/min, abolished the fall in blood pressure and total peripheral resistance during infusion of histamine. Histamine-induced vasodilatation in the stomach was unaltered by pretreatment with mepyramine but abolished by pretreatment with metiamide. Histamine-induced coronary vasodilation was reduced slightly by pretreatment with mepyramine and substantially by pretreatment with metiamide. Coronary vasodilatation was abolished by treatment with mepyramine and metiamide.

Animals↗
PubMed1986

Monoclonal anti-histamine antibody. Preparation, characterization and application to enzyme immunoassay of histamine.

An enzyme immunoassay to measure histamine has been developed. A histamine-bovine serum albumin conjugate was prepared using 1,4-benzoquinone as the coupling agent and was employed to immunize mice for the preparation of monoclonal antibodies against histamine. After an initial screening to identify antigen-binding monoclonal antibodies the clones were isolated by limiting dilution cloning, grown in ascites and antibodies which had been secreted into the ascitic fluid were precipitated by ammonium sulphate at 50% saturation. A systematic approach for the determination of epitope specificities of monoclonal antibodies was performed. It was found that for the most specific antibody the main epitope encompassed the 2-histaminyl-1,4-benzoquinone moiety and that the KD value determined by indirect ELISA was 1.5 X 10(-8) M for the hapten part of the immunogen and 4.6 X 10(-10) M for a histamine-Bq-ovalbumin conjugate. The selected monoclonal antibody could not recognize histidine or methyl-histamine. Using this antibody, we developed an enzyme immunoassay for histamine and pg amounts could be detected. The same assay was used to quantify the allergic release of histamine from guinea pig lung mast cells. Results obtained either by the present enzyme immunoassay or by a fluorometric assay were closely correlated (correlation coefficient r = 0.9702, n = 37).

Animals↗
PubMed2004

Unusual functional properties of homo- and heteromultimeric histamine-gated chloride channels of Drosophila melanogaster: spontaneous currents and dual gating by GABA and histamine.

Histamine acts as a neurotransmitter of photoreceptors in insects and other arthropods, where it directly activates a chloride channel and mediates rapid inhibitory responses. Homo- and heteromultimeric histamine-gated ion channels formed by HisCl-alpha2 or HisCl-alpha1 + alpha2 subunits from Drosophila melanogaster were characterized by two-electrode voltage-clamp measurements of functionally expressed ion channels in Xenopus laevis oocytes. The sensitivity of heteromultimeric histamine receptors with an EC(50) of 2.3 microM is lower than that of either homomultimeric receptor. They can be further distinguished from the homomultimeric channels by their reduced sensitivity to d-tubocurarine. Heteromultimeric channels generate a spontaneous current in the absence of any agonist. This spontaneous current can be blocked in the absence of an agonist by d-tubocurarine and the histamine antagonists cimetidine, thioperamide and pyrilamine. Homomultimeric HisCl-alpha2 channels are dually gated by histamine (IC(50)=9.4 microM) and GABA (IC(50)=1.0mM), both of which are full agonists. The action of both agonists can be blocked with comparable IC(50) values by the histamine antagonists cimetidine, thioperamide and pyrilamine but not by the GABA antagonist bicuculline. Picrotoxin blocked with an IC(50) of 403 microM. Our data show that histamine and GABA act on the same ion channel, which thus might function as a site of integration of the action of different neurotransmitters.

Animals↗
PubMed1997

Histamine content in colorectal cancer. Are there sufficient levels of histamine to affect lymphocyte function?

Histamine has been found to stimulate growth of colorectal cancer in vitro and in vivo. Histamine has also been found to inhibit lymphocyte activity in vitro at concentrations greater than 10(-7) M. The aim of our study was to determine if the histamine concentrations in human colorectal cancer were sufficient to achieve these effects. We measured the histamine content in 31 colorectal cancer specimens using a radioenzymatic assay. Results were expressed as microgram histamine per gram of fresh tissue weight. Recovery and reproducibility studies were also carried out. The median histamine concentration in colorectal cancer tissue was 8.4 micrograms/g [7.6 x 10(-5)M], ranging from 0.3 microgram/g to 20.6 micrograms/g. The high concentration of histamine in colon cancer is enough to be locally immunosuppressive.

Adult↗
PubMed1977

Vascular reactions to histamine and compound 48/80 in human skin: suppression by a histamine H2-receptor blocking agent.

1 The ability of a specific competitive histamine H2-receptor antagonist, cimetidine, to inhibit vascular responses to histamine in human skin provides new evidence that skin blood vessels possess histamine H2 receptors. 2 Simultaneous systemic administration of cimetidine and chlorpheniramine (an H1-receptor antagonist) was more effective than either drug alone in inhibition of the erythematous reaction both to exogenous histamine, and endogenous histamine secreted by skin mast cells in response to compound 48/80. 3 These results suggest that combined therapy of histamine-mediated skin diseases included urticaria and dermatitis using a combination of H1- and H2-histamine receptor antagonists may be more effective than either class of drug alone.

Adult↗
PubMed1985

Reproducibility of histamine skin prick test. Inter- and intravariation using histamine dihydrochloride 1, 5, and 10 mg/ml.

The reproducibility of skin prick test using histamine dihydrochloride 1, 5, and 10 mg/ml was tested by three nurses in five non-atopics in a double-blind trial. The variations day-to-day, within-day, between and for the same tester were calculated. Seventy-five percent of wheal reactions obtained by histamine 1 mg/ml were less than 15 mm2. With histamine 5 mg/ml there were only a few wheals less than 15 mm2 and none at all with histamine 10 mg/ml. The mean coefficient of variation of wheals greater than 15 mm2 was between 20-30%, in contrast to figures between 30-60% with wheals less than 15 mm2. No significant day-to-day or within-day variation was shown concerning histamine wheal areas. It is suggested that histamine dihydrochloride 10 mg/ml should replace histamine dihydrochloride 1 mg/ml as the positive reference in routine skin prick tests and biological standardization.

Adult↗
PubMed1986

Influence of bacterial endotoxins on basophil histamine release. Potentiation of antigen- and bacteria-induced histamine release.

The histamine-releasing capability of lipopolysaccharides (LPS) was examined in human leukocyte suspensions. LPS alone did not release histamine, but was found to enhance the histamine release caused by anti-IgE. Also the IgE-mediated histamine release caused by specific antigens (allergens or bacteria) in sensitized individuals was enhanced by LPS. The potentiating effect of LPS was observed in grass pollen and dog dander allergic patients as well as in patients sensitized to E. coli or Staph. aureus bacteria. No potentiation was obtained by exposure to unspecific allergens or bacteria to which the persons were not sensitized. Bacteria can release histamine by immunological or nonimmunological mechanisms, and only the immunological histamine release was found to be potentiated by LPS. It is speculated that endotoxins reinforce release of histamine caused by allergens in allergic patients or by bacteria in persons sensitized to these microorganisms.

Allergens↗
PubMed1983

Effect of alpha-fluoromethylhistidine on the histamine content of the brain of W/Wv mice devoid of mast cells: turnover of brain histamine.

In the brains of W/Wv mutant mice that have no mast cells, the histidine decarboxylase (HDC) level is as high as in the brain of congenic normal mice (+/+), but the histamine content is 53% of that of +/+ mice. The effects of alpha-fluoromethylhistidine (alpha-FMH) on the HDC activity and histamine content of the brain of W/Wv and +/+ mice were examined. In both strains, 30 min after i.p. injection of alpha-FMH the HDC activity of the brain had decreased to 10% of that in untreated mice. The histamine content decreased more gradually, and after 6 h about half of the control level remained in +/+ mice, whereas histamine had disappeared almost completely in W/Wv mice. It is concluded that the portion of the histamine content that was depleted by HDC inhibitor in a short time is derived from non-mast cells, probably neural cells. The half-life of histamine in the brain of W/Wv mice was estimated from the time-dependent decrease in the histamine content of the brain after administration of alpha-FMH: 48 min in the forebrain, 103 min in the midbrain, and 66 min in the hindbrain.

Animals↗
PubMed1973

Concentration of histamine in different parts of the brain and hypophysis of rabbit: effect of treatment with histidine, certain other amino acids and histamine.

1. Estimates have been obtained by biological assay of the histamine concentration in different parts of the rabbit brain and hypophysis.2. Mean values (ng/g) for the brain were: hypothalamus, 660; central grey matter and medial thalamus, 275; tegmental region of mid-brain, the hind-brain and caudate nucleus, 140 to 170; hippocampus and cerebral cortex, 90 to 110; cerebellum (vermis), 60.3. The mean value (ng/g) for the anterior lobe of the hypophysis was 650; for the posterior lobe, 400.4. In conscious rabbits, intravenous infusion of histidine in the dose range 62 to 1,500 mg/kg, raised significantly (P<0.01) the concentration of histamine in all regions of the brain examined, the pattern of distribution remaining unchanged. The largest increases occurred in the mid brain (90 to 320%) and in the hypothalamus (50 to 250%); in these areas the higher doses produced higher concentrations. Elsewhere in the brain the concentration rose in response to the lowest dose of histidine, but was not increased when higher doses were given. Concentrations in the anterior lobe of the hypophysis were unaltered.5. The infusion of histidine, unlike that of amino acid precursors, of the monoamines, produced no obvious disturbance in the animals.6. The rise in brain histamine after dosage with histidine persisted for several hours, depending on the dose; with 500 mg/kg, the rise was virtually unchanged after 16 hours.7. Histamine (5 mg/kg by intravenous infusion) raised the concentration of histamine in the hypophysis but not in the brain.8. After the infusion of DOPA, alpha-methyldopa or 5-hydroxytryptophan, the histamine concentration rose in the mid-brain but not in other parts of the brain.9. These amino acids, when infused singly with histidine, did not interfere with the histidine-induced rise of brain histamine.

5-Hydroxytryptophan↗
PubMed1979

Inhibition of guinea-pig lymphocyte activation by histamine and histamine analogues.

1 The incorporation of [3H]-thymidine into guinea-pig lymphocytes stimulated by a plant lectin (concanavalin A), soluble antigen (tuberculin (P.P.D.)) and syngeneic hepatoma cells, was partially inhibited (50%) by histamine in vitro. 2 The effect of histamine on both mitogen and antigen dose-response curves suggests a non-competitive, probably physiological antagonism. 3 The inhibitory dose range of histamine lay between 10 nM and 30 microM with an ID50 of approximately 400 nM. 4 The potency order for histamine analogues for the inhibition of lymphocyte activation was histamine greater than or equal to 4-methylhistamine greater than 2-methylhistamine greater than 3-methylhistamine. This is in accord with the mediation of the response through an H2-receptor. 5 H2-receptor antagonists reversed the inhibitory effect of histamine in a dose-related manner, but both metiamide and burimamide, in high concentrations, augmented lymphocyte activation in their own right. This precluded the determination of affinity constants and made it impossible to state with certainty that the inhibition of lymphocyte activation by histamine was mediated by an H2-receptor.

Animals↗
PubMed1977

Metabolism of histamine in myotonic dystrophy a dual pattern of inactivation of intestinal histamine.

The catabolism of orally and subcutaneously administered 14C histamine was studied in myotonic dystrophy patients. No definite abnormalities were observed as for subcutaneously administered histamine. The catabolism of orally administered histamine followed two distinct patterns: In patients with a relatively low endogenous urinary conjugated histamine excretion at the time of testing, small quantities of radioactivity were excreted in the stools (mean 0.25 per cent), whereas the quantity of exhaled 14CO2 was in the control range (mean 14.4 per cent), and the exhalation curve diphasic as in controls. In patients with a relatively high urinary conjugated histamine excretion, the catabolic pattern differed: There was a relatively high faecal excretion of radioactivity (mean 20.1 per cent), whereas the exhalation of 14CO2 was markedly reduced (i.e. mean 0.5 per cent, versus a mean control level of 8.9 per cent). Diphasicity of the exhalation curve was not present in these patients. It has previously been demonstrated that a patient with myotonic dystrophy may shift between being a normal and a high conjugated histamine excretor. It is thus possible that all patients with myotonic dystrophy may pass through phases with abnormal catabolism of intestinal histamine.

Administration, Oral↗
PubMed1986

Comparison of human bronchial muscle responses to histamine in vivo with histamine and isoproterenol agonists in vitro.

In an effort to explain the large variation of airway reactivity to histamine in human subjects in vivo, we have examined the relationship between histamine responses in vivo and isoproterenol in vitro. The bronchial reactivity in patients with lung carcinoma was assessed prior to surgery by measuring the provocative concentration of histamine that resulted in a 20 or a 40% reduction in either forced expiratory volume in one second or specific airway conductance (SGaw). We also determined the pD2 value (-Log EC50 molar) to histamine and isoproterenol in isolated bronchial muscle preparations from these subjects. A wide range of histamine responsiveness was observed in vivo for the 17 patients (PC40 SGaw: 1.3 to greater than 64 mg/ml of histamine). There was no correlation between this latter parameter and the bronchial histamine sensitivity in vitro. However, isolated bronchial muscle preparations from asthmatic subjects were less sensitive to isoproterenol than were those preparations from nonasthmatic subjects.

Adult↗
PubMed2000

Histamine release induced by antimicrobial agents and effects of antimicrobial agents on vancomycin-induced histamine release from rat peritoneal mast cells.

Vancomycin and certain fungicides may cause anaphylactoid reactions. We investigated the effects of vancomycin, miconazole and fluconazole on histamine release in rat peritoneal mast cells. Vancomycin and miconazole provoked histamine release in a dose-dependent manner. In contrast, fluconazole did not provoke histamine release at concentrations of 3 x 10(-6)-3 x 10(-3) M. Vancomycin is efficacious in the treatment of gram-positive bacterial infections; patients presenting themselves with mixed infections require concomitant therapy with a second antimicrobial agent. We investigated the effect of fosfomycin sodium, cilastatin sodium or fluconazole on vancomycin-induced histamine release. Fosfomycin sodium inhibited vancomycin-induced histamine release but neither cilastatin sodium nor fluconazole inhibited it in the mole ratios of daily doses used in humans. These results suggest that vancomycin and miconazole provoke histamine release in rat mast cells, but that fluconazole probably does not, while fosfomycin sodium may inhibit vancomycin-induced histamine release.

Animals↗
PubMed1980

Effect of cimetidine treatment on parietal and chief cell sensitivity to histamine and on catabolism of histamine in duodenal ulcer patients.

Gastric acid and pepsin output in response to a low and a maximal dose of histamine was studied before and 60 h after cessation of 4 weeks of cimetidine treatment, 1 g/day, in 11 duodenal ulcer patients. Plasma histamine concentrations were measured in eight patients and the urinary excretion of intravenously injected 14C-histamine and its metabolites in two patients. Acid and pepsin output in response to the low dose of histamine as a percentage of the maximal response was on average 41.3% +/- 4.4% (S.E.M.) and 46.3% +/- 3.5% before treatment and 40.4% +/- 4.8% and 38.8% +/- 4.5% after cessation of treatment, respectively (p greater than 0.10). Thus, a course of treatment with cimetidine does not influence the sensitivity of the parietal and chief cells to histamine stimulation in duodenal ulcer patients. No significant change of plasma histamine concentrations and of catabolism of radiolabelled histamine was observed after cessation of cimetidine treatment.

Adult↗
PubMed1990

Histamine, histamine formation capacity and gastrin in cysteamine-induced peptic ulcer.

We attempted to induce chronic peptic ulcer in the rat by injection of consecutive doses of cysteamine. We investigated the incidence of peptic ulceration and measured gastric mucosal histamine, histamine formation capacity (HFC), plasma gastrin and tissue (oesophagus, duodenum, liver and lung) histamine in rats 1, 7, 14, 21, and 28 days after injection of cysteamine-HCl (300 mg/kg s.c. and 100 mg/kg 8 h later). Saline injections were used in control rats. After 24 h all rats given cysteamine had duodenal ulcers and the ulcer incidences after 7 and 14 days were 60 and 40%, respectively. After Day 21 no ulcers were found. Microscopy revealed ulcer healing seen as epithelialized scars from Day 14 onwards. A rising incidence of gastric metaplasia of the duodenal mucosa was noted from Day 7 after cysteamine treatment, which may have pathophysiological significance. Gastric mucosal histamine was higher and plasma gastrin was lower after 24 h compared with controls and values obtained later in the study. Rats with duodenal ulceration had significantly higher gastric mucosal histamine than those without lesions and control rats. A direct relationship was found between plasma gastrin and HFC in rats given cysteamine. A small but significant increase in histamine content of the liver was also observed after 24 h. No significant changes were found in other tissue specimens. Thus, a rise in gastric histamine is associated with duodenal ulcers in this model.

Animals↗
PubMed1976

Complement-induced histamine release from human basophils. II. Mechanism of the histamine release reaction.

The activation of human serum complement by incubation with zymosan generates C5a which releases histamine from autologous basophils. The characteristics of the C5a-induced histamine release were investigated. It is similar to IgE-mediated reactions in requiring Ca++ and in being inhibited by EDTA. However, it has marked differences from IgE-mediated reactions. C5a, at all concentrations, released histamine completely in less than 2 min. The C5a reaction has a narrow pH optimum that antigen-induced release and occurs well at 17 degrees to 37 degreesC but not at 0 degreesC. The optimal reaction temperature is 25 degrees to 30 degrees C. Unlike the antigen-induced release, no two-stage activation with C5a for the release of histamine could be demonstrated. There was additive release between C5a- IgE-mediated reactions. Leukocytes could be desensitized to the C5a-mediated reaction by 1) incubating the cells at 37 degrees C for 45 min, 2) pretreating the leukocytes with activated serum in the presence of EDTA, and 3) adding the activated serum to the leukocytes at 0 degrees C before transferring to the optimal reaction temperatures. Cells desensitized to the complement-induced release have normal reactions to IgE-mediated histamine release. In parallel experiments, cells from allergic donors desensitized for IgE-mediated reactions by incubation with antigen under sub-optimal conditions release histamine normally upon the addition of C5a. The results indicate that histamine release by C5a involves a mechanism of basophil activation that is different from the pathway involved in the IgE-induced reaction.

Antigens↗
PubMed1978

Effect of histamine and histamine antagonists on human lower esophageal sphincter function.

The purpose of this study was to evaluate the effect of histamine phosphate and specific histamine antagonists on human lower esophageal sphincter (LES) pressure. Continuous intravenous infusions of histamine at doses of 2.0 to 40.0 microgram/kg-hr gave graded increases in LES pressure with a peak response of 378 +/- 4.6 mm Hg at 20.0 microgram kr-hr. The LES response was not altered by an H1-antogonist, diphenhydramine (50 mg, intravenously), but was completely blocked by infusion of the H2-antagonist, cimetidine (4.0 mg/kg-hr). Also, oral cimetidine (300 mg) antagonized any increase in LES pressure during histamine infusion at a dose shown to give the maximal LES response. Despite this effect of cimetidine in antagonizing the maximal LES response to histamine, oral cimetidine at 200, 300, and 400 mg failed to alter basal LES pressure over a 3-hr period. Cimetidine also failed to alter the LES response to intravenous pentagastrin or oral beef hydrolysate. These studies suggest that: (1) human LES pressure increases in response to intravenous histamine phosphate through its action at an H2-receptor; (2) the H1-receptor has no apparent role in the human LES response to histamine; and (3) H2-antagonism with cimetidine has no effect on the human LES basal pressure or its response to gastrin stimulation.

Cimetidine↗