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PubMed1998

Levels of histamine and histamine-producing bacteria in smoked fish from New Zealand markets.

Smoked fish has been the most commonly implicated product in presumptive cases of scombroid poisoning in New Zealand. One hundred seven samples of smoked fish were purchased from Auckland retail markets between July 1995 and March 1996, and their histamine and bacterial levels were determined. Eight samples, obtained from five of the nine retail outlets sampled, had histamine levels which exceeded 50 mg/kg, the level set by the FDA as an indicator of decomposition. Histamine levels in only 2 samples (346.4 and 681.8 mg/kg) exceeded a hazard level of 200 mg/kg. Thirty-three of the smoked fish were held at 20 degrees C for 2 days, and 8 of these developed histamine levels above 50 mg/kg with 4 exceeding 200 mg/kg (maximum 1,659.4 mg/kg). The stored samples that exceeded 200 mg/kg were all obtained from two outlets. Within or between fish species there were no consistent relationships between levels of histamine in the samples and either the total aerobic plate counts or the numbers of histamine-producing bacteria. To the contrary, there was evidence that histamine had been formed prior to smoking and that histamine-producing bacteria were eliminated during smoking.

Bacteria↗

PubMedDate not supplied

Gastric mucosal exposure to histamine in rats is followed by absorption of histamine but not mucosal hyperemia.

BACKGROUND/AIMS: Superficial mucosal damage is associated with mucosal hyperemia and release of histamine into venous blood and gastric lumen. This study was designed to examine if histamine administrated directly to gastric mucosa becomes absorbed and transported away with blood, and if so whether it is capable of increasing gastric mucosal blood flow. METHODOLOGY: Superficial mucosal injury was induced by exposing chambered rat stomachs to 2 M NaCl for 10 min, and 45 min later 4.5 x 10(-2) or 4.5 x 10(-3) M histamine was instilled into the chamber. Mucosal blood flow was determined by radioactive microspheres and continuously by Laser Doppler flowmetry. RESULTS: Histamine concentration in arterial blood was markedly increased 15 min after administration of histamine. The mucosal blood flow did not increase after application of histamine. Significant increase in heart rate and fall in arterial blood pressure were observed. Similar results were obtained after application of histamine to normal mucosa. CONCLUSIONS: Histamine applied to injured or normal gastric mucosa of rats becomes transported via capillaries and venules to the systemic circulation, but does not reach terminal arterioles in quantities large enough to cause vasodilatation.

Absorption↗

PubMed1991

The stimuli releasing histamine from murine bone marrow-derived mast cells. 2. Mechanisms involved in histamine release induced by extracellular ATP and its metabolites.

Extracellular ATP stimulated histamine release and generation of leukotrience C4 (LTC4) accompanied with the formation of inositol phosphates and a rapid increase in intracellular Ca2+ ([Ca2+]i) in mouse bone marrow-derived cultured mast cells (BMMC). The rank order of histamine-releasing potency of ATP and its metabolites is ATP greater than ADP greater than AMP greater than adenosine. Nonhydrolyzable ATP analog, adenosine-5'-O-[2-thiotriphosphate] (ATP-S) released more histamine from the cells than ATP. On the other hand, simultaneous addition of adenosine analogues at micromolar concentrations potentiated histamine release from the cells induced by ATP (50 microM) or DNP-HSA antigen (0.1 ng/ml) in the following rank order: adenosine greater than AMP much greater than ADP = ATP. Histamine release potentiated by adenosine was blocked by the treatment with pertussis toxin, whereas histamine release induced by ATP was not affected by the toxin, suggesting that extracellular ATP stimulate histamine release from BMMC probably via mechanisms independent of the potentiation of histamine release induced by adenosine.

Adenosine↗

PubMed1985

Binding of histamine and histamine analogs to lymphocyte subsets analyzed by flow cytometry.

The binding of histamine, 4-methylhistamine (a histamine type 2 receptor agonist), cimetidine (a histamine type 2 receptor antagonist), and telemethylhistamine (an inactive analog) to human peripheral blood mononuclear cell subsets was investigated by flow cytometry by using conjugates of these ligands coupled to fluorescein-labeled human serum albumin. Our results indicate that binding of fluorescent protein conjugates of histamine and its analogs does not selectively identify a lymphocyte subset(s) that mediates the immunomodulatory effects of histaminergic ligands. Conjugates with both low (2.5 to 2.8:1) and high (28 to 57:1) ligand to protein coupling ratios were used. No binding above background could be detected for the low mole ratio reagents. The high mole ratio reagents were bound by 95 to 99% of all lymphocytes when used at ligand concentrations of 50 microM or greater. At lower ligand concentrations, the number of lymphocytes exceeding a set fluorescence threshold was decreased, but fluorescence distributions remained unimodal at all concentrations used (1 to 500 microM). Monocytes also bound the high mole ratio reagents and gave rise to a second high-intensity peak in the fluorescence distribution unless they were excluded by other means. Levels of conjugate binding detected by flow cytometry did not parallel ligand potencies at classical histamine type 2 receptors; at equivalent ligand concentrations, approximately equal amounts of histamine or 4-methylhistamine conjugate were bound per lymphocyte, and only 30% less telemethylhistamine conjugate was bound. Competition with free ligands (10(2)- to 10(4)-fold excess histamine, 4-methylhistamine, cimetidine, or telemethylhistamine) did not significantly decrease the level of binding observed for the high mole ratio reagents at bound ligand concentrations of 1 to 25 microM. Dual staining with fluorescein-labeled conjugate and phycoerythrin-labeled monoclonal antibodies Leu-3ab (anti-helper T), Leu-2a (anti-suppressor T), Leu-M3 (anti-monocyte), or anti-HLA-DR (B cells and monocytes) was also carried out. The extent of conjugate binding to helper and suppressor cells was identical for each of the ligands used, but higher levels of conjugate binding were seen for monocytes and B cells than for T cells in every case. Our data do not exclude the possibility of enhanced conjugate binding to small numbers of activated (HLA-DR positive) T cells that might be involved in mediation of histamine effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Binding Sites↗

PubMed1983

The lack of effect of histamine--protein conjugates on human lymphocyte responses to concanavalin A and histamine.

We have studied the effect of depleting human peripheral blood lymphocytes (PBL) on plates coated with histamine-rabbit serum albumin (H-RSA) or control (E-RSA) conjugates, on the concanavalin A (Con A) response and the histamine suppression of Con A responses. Low H10-RSA-substituted conjugate depletion had little effect on [3H]-thymidine incorporation of Con A-stimulated cells compared to control (E10-RSA) conjugates and unseparated cells, but significantly increased unstimulated cell counts, therefore reducing stimulation index (SI). Highly histamine-substituted (H30-RSA) and control (E30-RSA) conjugates decreased SI in a similar way, but also decreased the [3H]-thymidine incorporation of Con A-stimulated cells. Histamine suppression of Con A responses was reduced by both E10- and H10-RSA-coated plates at suboptimal but not optimal mitogen concentrations. The induction of Con A-induced suppressor cells was unaffected by prior depletion of cells on H10- or E10-RSA conjugate-coated plates. Addition of H10- and E10-RSA to Con A cultures had a slight enhancing effect on transformation, but no effect on histamine suppression of the Con A response. Thus, whilst it is clear from other studies in vitro that functional histamine receptors are present on suppressor T cells, the results presented here show that histamine-protein conjugates do not specifically bind to histamine receptor-bearing human peripheral blood suppressor T lymphocytes.

Concanavalin A↗

PubMed1983

Changes in histamine synthetic activity, histamine content and responsiveness to compound 48/80 with maturation of rat peritoneal mast cells.

Intact rat peritoneal mast cells were separated by elutriation into fractions differing in cell size, the smallest cells (less than 12 microns) exhibited high histamine synthetic activity (200-300 pmol of histidine decarboxylated per hr/10(6) cells) and contained little histamine (less than 2 pg/cell). With increasing cell size, histamine synthetic activity diminished to less than 20 pmol/hr/10(6) cells and histamine content increased to greater than 12 pg/mast cell. A gradation in histamine release in response to Compound 48/80 was also observed; small mast cells were resistant, those of intermediate size (12-13 microns diameter) were partially responsive and large mast cells (14-17 microns) were fully responsive to Compound 48/80. These changes were related to the state of maturity of the mast cells as indicated by their histochemical reactions to Alcian blue and safranin, which stain nonsulfated heparin precursors and heparin, respectively. Fractions of small mast cells were predominantly immature cells (70-85% of the cells were Stage I) with few granules, whereas fractions of large cells contained mostly mature cells (greater than 80% Stages III and IV) with numerous heparin-containing granules. Fractions in between contained mast cells at intermediate stages (Stages II and III) of development. Degenerative changes, namely decreased viability and diminished responsiveness to Compound 48/80, were evident, however, in fractions of the largest cells (greater than 17 microns). This and other work indicate that, even in adult rats, peritoneal mast cells are heterogeneous and can be separated on the basis of size into subpopulations that differ markedly in histamine content, histamine synthetic activity and ability to release histamine in response to Compound 48/80.

Animals↗

PubMed1991

The antiproliferative potency of histamine antagonists correlates with inhibition of binding of [3H]-histamine to novel intracellular receptors (HIC) in microsomal and nuclear fractions of rat liver.

Previously, we identified in rat liver microsomes, low (microM) affinity histamine receptors (HIC), associated with antiestrogen binding sites (AEBS). N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine HCl (DPPE), a potent AEBS ligand, is a specific HIC antagonist. Through binding HIC, newly-formed intracellular histamine mediates, and DPPE inhibits, human platelet aggregation. We now provide evidence that histamine, mobilized from cytoplasmic stores, is a mediator of the mitogenic response to concanavalin A in mouse spleen cells. DNA synthesis and intracellular histamine levels are decreased over time by the histidine decarboxylase inhibitor, alpha-fluoromethylhistidine. For DPPE, H1 and H2 antagonists, rank order of potency to inhibit [3H]-histamine binding to HIC in rat liver microsomes correlates with antiproliferative potency. DPPE also competes for [3H]-histamine binding at low and high affinity sites in rat liver nuclei (IC50 approximately 2 microM). Thus, histamine may mediate growth through two intracellular subtypes of HIC.

Animals↗

PubMed1995

Famotidine, a histamine-2-receptor antagonist, inhibits the increase in rat gastric H+/K(+)-ATPase mRNA induced by intravenous infusion of gastrin 17 and histamine.

We examined the effects of gastrin and histamine on rat gastric H+/K(+)-ATPase, the enzyme responsible for H+ secretion, gene expression in vivo. Gastrin 17 (G 17) or histamine dihydrochloride (histamine) was continuously infused through the femoral vein of anesthetized rats. Gastric H+/K(+)-ATPase mRNA levels were measured using northern blot analysis. Infusion of G 17 and histamine increased the H+/K(+)-ATPase mRNA level significantly compared with basal control level or vehicle control level (P < 0.01). However, pretreatment with famotidine, a potent histamine-2 (H2)-receptor antagonist, inhibited the increase of rat gastric H+/K(+)-ATPase mRNA following G 17 and histamine infusion. These findings indicate that both histamine and G 17 increase expression of H+/K(+)-ATPase mRNA by activating H2 receptor on the parietal cell.

Actins↗

PubMed2002

Endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats--studies with histamine N-methyltransferase inhibitor SKF 91488.

OBJECTIVE AND DESIGN: Activation of the histaminergic system is associated with mobilisation of compensatory mechanisms in response to the action of stimuli which disturb homeostasis. Therefore, the effects of endogenous histamine in central cardiovascular regulation were studied in a rat model of irreversible haemorrhagic hypotension. MATERIAL: Cardiovascular parameters were measured in 66 and central histamine concentrations in 12 male Wistar rats anaesthetised with ketamine/xylazine. TREATMENT: Haemorrhage-shocked rats with mean arterial pressure (MAP) 20-25 mmHg were injected intracerebroventricularly (icv) with histamine N-methyltransferase inhibitor SKF 91488 after icv pre-treatment with H, H2 and H3 histamine receptor antagonists--chlorpheniramine (100 nmol), ranitidine (200 nmol) and thioperamide (100 nmol), respectively, or saline. METHODS: Arterial pressure and heart rate (HR) changes were monitored within 2 h after icv treatment, or to death if it occurred earlier. Histamine concentrations were measured using enzyme immunoassay. ANOVA followed by a test of Neuman-Keules, and Fisher's exact test were used to compare the results. RESULTS: SKF 91488 produced dose-dependent, significantly higher compared to normovolaemic animals, increases in MAP and HR with the improvement in survival rates. The action of SKF 91488 (100 microg) was associated with an increase in endogenous histamine concentrations in the cerebral cortex (1.19 +/- 0.09 vs. 0.77 +/- 0.21 nmol/g; p < 0.05), hypothalamus (5.62 +/- 0.68 vs. 4.18 +/- 0.45 nmol/g; p < 0.01) and medulla oblongata (0.53 +/- 0.17 vs. 0.29 +/- 0.05 nmol/g; p < 0.05) in comparison to saline-treated animals. SKF 91488-induced effects were inhibited by chlorpheniramine, whereas neither ranitidine nor thioperamide influenced the action. CONCLUSION: Endogenous central histamine, after SKF 91488 treatment, via activation of H, receptors produces reversal of hypotension, with improvement in the survival rate at 2 h after treatment, in rats subjected to critical haemorrhagic hypovolaemia.

Animals↗

PubMed1986

Effects of eight-week treatment with histamine H2-antagonists or an antacid on plasma levels of histamine and serotonin in duodenal ulcer patients.

The effects of 8-week treatment with oral histamine H2-antagonists (ranitidine or cimetidine) or an antacid on plasma levels of histamine and serotonin were studied in duodenal ulcer patients. Histamine H2-antagonists significantly elevated plasma histamine levels, however, they markedly decreased serotonin concentrations by the 4th week of treatment. Antacid treatment similarly increased histamine levels without significantly affecting blood serotonin. It is concluded that changes in intragastric or intraduodenal acidity affect histamine release, as reflected by increased blood levels; serotonin secretion could be influenced by blocking histamine H2-receptors, possibly those located mainly in the gastrointestinal tract.

Antacids↗

PubMed1986

The effects of combined H1 and H2 histamine antagonists on alterations in nasal airflow resistance induced by topical histamine provocation.

A clinical trial was undertaken to assess the effects of oral H1 (diphenhydramine hydrochloride) and H2 (cimetidine) histamine blockade on nasal resistance induced by topical histamine. Ten adult volunteers were tested on two separate occasions. Their noses were pretreated by oral administration of either combined H1 and H2 histamine antagonists or H1 antagonist and placebo. The nasal airflow resistive response to topical histamine was then determined. Combined histamine antagonism was significantly more effective in reducing the nasal resistive response to topical histamine than H1 antagonist alone (p less than 0.0001). Furthermore, ingestion of the oral H1 histamine antagonist, diphenhydramine hydrochloride, alone led to an increase in resistance of the unprovoked nose, whereas combined H1 and H2 antagonism did not lead to a significant change.

Adult↗

PubMed2005

Marked increase in the histamine content of neointima after stent implantation of pig coronary artery and growth-promoting effects of histamine in cultured smooth muscle cells.

After coronary stent implantation, the unfavorable in-stent restenosis often occurs by the formation of neointima due to the proliferation of smooth muscle cells. Platelet-derived growth factor (PDGF) and other peptide growth factors contribute to this process, but little is known about the role of non-peptide factors in this process. In the present study, the role of histamine, a non-peptide factor, in the formation of neointima was investigated using a pig coronary model of in-stent restenosis and a culture system of coronary smooth muscle cells. A Palmaz-Schatz stent was implanted in the left anterior descending coronary artery of male pigs. At 1, 2 and 4 weeks after stenting, the histamine content of neointima was determined to be 326 +/- 82, 1427 +/- 280 and 440 +/- 69 pmol/mg protein, respectively, by HPLC fluorometry. In contrast, the histamine content of arterial media from the untreated control arteries was only 15.3 +/- 1.6 pmol/mg protein. These results demonstrate that the histamine content of neointima is about 20 to 90-fold that of the normal media. In vitro, histamine by itself did not stimulate the proliferation of cultured smooth muscle cells, but potentiated the PDGF-stimulated proliferation of the cultured cells via a mechanism independent of H1 and H2 histamine receptors. Thus, histamine may be an important non-peptide factor in the pathogenesis of in-stent restenosis.

Animals↗

PubMed1995

Histamine N-methyltransferase inhibitor potentiates histamine- and antigen-induced airway microvascular leakage in guinea pigs.

BACKGROUND: Histamine N-methyltransferase (HMT) modulates histamine- and antigen-induced bronchoconstriction. However, it is unclear whether vascular permeability evoked by an allergic reaction can be exaggerated by inhibition of HMT activity. METHODS: We studied the effects of intravenously injected SKF 91488, a specific HMT inhibitor, on increases in plasma extravasation induced by intravenously injected histamine in unsensitized guinea pigs and by intravenously injected ovalbumin antigen in guinea pigs sensitized to ovalbumin in vivo with Evans blue dye as a marker. RESULTS: Pretreatment with SKF 91488 shifted, in a dose-dependent fashion, the dose-response curves of the leakage of dye to histamine to lower concentrations in the trachea, main bronchi, and nasal mucosa. Likewise, pretreatment with SKF 91488 (20 mg/kg intravenously) significantly increased the leakage of dye induced by ovalbumin antigen (200 micrograms/kg intravenously) in three parts of the airway (p < 0.05). In contrast to SKF 91488, intravenously injected aminoguanidine, a specific inhibitor of diamine oxidase (16 mg/kg intravenously), did not alter the leakage of dye induced by histamine (from 0.001 microgram/kg to 10 micrograms/kg intravenously) (p < 0.20). HMT activities were observed in the nasal mucosa, as well as in the trachea and main bronchi, as shown in a previous study. CONCLUSION: These findings suggest that HMT modulates the effects of exogenous histamine and endogenously released histamine induced by antigen challenge on plasma extravasation in the airway in guinea pigs in vivo.

Amine Oxidase (Copper-Containing)↗

PubMed2002

Histamine inhibits KCNQ2/KCNQ3 channel current via recombinant histamine H(1) receptors.

A variety of agonists are capable of inhibiting M-type K(+) channels via the activation of G-protein coupled receptors which converge on phospholipase-C (PLC) via the activation of G(q/11). Histamine acting via H(1) receptors also activates PLC but to date has not been shown to produce M-current (I(M)) modulation. We postulated that histamine would modulate recombinant M-channels after expressing histamine H(1) receptors in heterologous systems. Expression of KCNQ2 and KCNQ3 K(+) channel subunits by transient transfection in HEK 293T and HeLa cells caused the induction of a slow time-dependent outward current characteristic of I(M). Application of histamine (10 microM) to cells transfected with KCNQ2 and KCNQ3 K(+) channel subunits and H(1) histamine receptors produced a rapid and reversible inhibition. I(M) modulation by histamine was concentration-dependent, half maximal inhibition occurring at 399 nM with a Hill coefficient of 1.09 and was completely abolished by the H(1) receptor selective antagonist, astemizole. Studies of the modulatory effects of histamine on I(M) may aid in elucidating the signal transduction pathway(s) involved in I(M) modulation.

Astemizole↗

PubMed1983

H1-histamine receptors may mediate the contractile response of guinea-pig ileum to 'histamine-free' splenic extracts.

A water-soluble splenic factor, which produces a contractile response of the guinea-pig ileum, that is resistant to cholinoceptor and adrenoceptor antagonists is described. The ileal contractions elicited by the splenic extract showed some significant differences from those elicited by 5-hydroxytryptamine. The responses to splenic extract were not affected by the D-tryptamine-receptor antagonist, methysergide. The effect of the splenic extract on the guinea-pig ileum was similar to that of histamine. The H1-histamine antagonists, (+)-chloropheniramine and diphenhydramine, caused a parallel shift to the right of the splenic extract dose-response curve without suppression of the maximum response. A pA2 value of 8.97 +/- 0.03 for (+)-chloropheniramine and 7.55 +/- 0.1 for diphenhydramine was calculated. Significant histamine levels, as determined by fluorometric methods, could not be detected in the splenic extract. Likewise, the splenic factor did not release histamine from the intestinal preparation. These results support the view that: (i) the splenic factor acts through H1-histamine receptors; (ii) it is not histamine; (iii) it does not have any histamine releasing effect on the ileal smooth muscle.

Animals↗

PubMed1979

Inhibition of rat mast cell degranulation and histamine release by histamine-rat gammaglobulin conjugate.

Histamin-rat-gamma-globulin conjugate inhibited degranulation and histamine release of rat peritoneal mast cells to a greater extent than the rat globulin or histamine alone. Since mast cells contain histamine receptors, it may be assumed that the histamine bound to the gamma-globulin combines with the rat mast cell histamine receptor and inhibits the degranulation and histamine release by a feedback mechanism.

Animals↗

PubMed1988

Detection of histamine in human placental perfusate and the effect of histamine releasers.

Studies on full-term human placentas were conducted to determine whether the vasogenic actions of certain agents on perfused placental vasculature are due to histamine release. Compound 48/80 and morphine were selected because they liberate the autacoid via different mechanisms. Initially, a control effluent was collected prior to each drug challenge and again collected throughout the rise and fall in perfusion pressure. The drugs were given alone and in the presence of a 50 mcg dose of histamine free base (HFB) to assess the release of stored histamine and also to serve as a control. Following extraction in n-butanol and recovery in 0.1 N HCl, all effluents were fluoresced with o-phthalaldehyde and assayed for histamine content via spectrophotofluorometry. A baseline histamine level was discovered in the majority of placental effluents collected prior to the administration of any agent. No significant increases above this initial level occurred following treatment with compound 48/80 alone. However, small but significantly elevated amounts of histamine appeared in the placental effluent when compound 48/80 was given 10 minutes after the initial 50 mcg dose of HFB. This agent also caused a slight increase in placental perfusion pressure after each administration. Results obtained with morphine do not appear to support the hypothesis that significant amounts of histamine are released by this agent in the perfused human placenta.

Female↗

PubMed1990

Basophil histamine release in the diagnosis of house dust mite and dander allergy of asthmatic children. Comparison between prick test, RAST, basophil histamine release and bronchial provocation.

The aim of the study is to compare the glass fibre-based basophil histamine release test with skin test (Phazet), RAST (Phadebas) and bronchial provocation test in children with allergic asthma. The study comprised 68 selected children with a case history of extrinsic allergic asthma to danders (cat and dog) and house-dust mite. Skin prick test, RAST, and histamine release were performed in all children and the bronchial provocation test was used as a reference of "true allergic asthma". A total of 81 allergen bronchial challenges were performed and 44 children experienced 49 positive provocations. In 2.9% (2/68) of the children histamine release could not be performed due to technical difficulties (low histamine release with anti-IgE). Concordances in the range 76-87% were observed with no significant difference between the tests. The highest concordance (87%) was found between histamine release and bronchial provocation test followed by skin prick test vs bronchial provocation (84%) and RAST vs bronchial provocation (80%). The sensitivity and specificity were calculated for each test. All tests showed sensitivities in the range 90-94% and no significant difference between them was observed. The specificity of histamine release, skin prick test, and RAST was 0.78, 0.69, and 0.63, respectively. The specificity of histamine release was better than RAST demonstrated by 95% confidence intervals. In conclusion, it was found that the histamine release test is a convenient diagnostic method and the study indicates a diagnostic value comparable to the common diagnostic methods in clinical allergy.

Animals↗