[Determination of the histamine level in the skin. II. The level of free histamine in the skin in normal rats and rabbits and its relation to the total histamine level].
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Animals↗
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Histamine receptor-bearing leukocytes (HRL). I. Detection of histamine receptor-bearing cells by rosette formation with histamine-coated erythrocytes.
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AKR murine leukemia virus↗
Intravenous histamine test with fixed doses of histamine. Minimal dose of histamine for maximal acid secretion.
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Adult↗
[Studies on histamine metabolism in childhood. I. Histamine content in the blood and histamine excretion in healthy children].
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Adolescent↗
Possible participation of histamine H3-receptors in the regulation of anaphylactic histamine release from isolated rat peritoneal mast cells.
Anaphylactic histamine release from isolated rat peritoneal mast cells was concentration-dependently blocked by a 5-min treatment with exogenous histamine at 0.9 and 9 microM and enhanced by a 20- to 30-min treatment with thioperamide (H3-antagonist) at 3 microM with significance, but little affected by mepyramine (H1-antagonist) and cimetidine (H2-antagonist) at the cell concentration of 10(6) mast cells/ml. At a low concentration of mast cells (10(4) mast cells/ml), (R)-alpha-methylhistamine (alpha-MH), an H3-agonist, at 0.9-90 microM also inhibited the release in a concentration-dependent fashion. Thioperamide, but neither mepyramine nor cimetidine, significantly restored the decreased release by alpha-MH. However, the complete restoration by thioperamide could not be achieved because the drug itself slightly but concentration-dependently inhibited anaphylactic histamine release. On the other hand, not only betahistine and dimaprit but also alpha-MH did not suppress histamine release from the mast cells induced by compound 48/80. In rat plasma, considerable levels of histamine were detected. From these results, it is strongly suggested that histamine H3-like receptors are largely responsible for the negative feedback regulation of the anaphylactic histamine release from rat peritoneal mast cells.
Anaphylaxis↗
Improved detection of the histamine receptor on human peripheral blood mononuclear cells by crosslinking using tritiated as compared with radioiodinated histamine.
In order to detect histamine receptors on the surface of human peripheral blood mononuclear cells, the cells were incubated in the presence of radiolabelled histamine and then the bifunctional crosslinker disuccimidyl suberate was added in various concentrations. They were then solubilized with sodium dodecyl sulphate, boiled, reduced and the lysate separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Both 3H and 125I-radiolabelled ligands bound to a 16 kDa band, to be defined although a much clearer and obviously unequivocal signal was obtained with 3H-labelled histamine. This molecule migrated with the same mass on sodium dodecyl sulfate-polyacrylamide gel electrophoresis as a 16 kDa subunit which had been purified on a histamine affinity column from Triton X-100 solubilized mononuclear cells, indicating it to be the ligand-binding subunit for the histamine receptor on these cells. For 3H, fluorography with Entensify was required to obtain an autoradiographic signal. Although 3H took much longer to give a signal than 125I, the considerable background, artefacts and heavy lane trailing seen with [125I] histamine were completely abrogated when [3H]histamine was used. In addition, the distinction between specific and nonspecific binding was more clearly seen using [3H]histamine. The modifications reported here which improve signal detection for 3H should encourage the use of tritiated ligands in radioreceptor crosslinking, particularly those of low molecular weight which might otherwise undergo steric modification due to iodination, this having the potential for interfering with receptor ligand binding.
Autoradiography↗
Histamine, histidine decarboxylase and histamine-N-methyltransferase in brain areas of spontaneously hypertensive rats.
Histamine levels, histidine decarboxylase and histamine-N-methyltransferase activities were determined in various brain areas of young (9-week old) and adult (18-week old) normotensive rats (WKY) and hypertensive rats (SHR). When compared with WKY, histamine levels were increased in the anterior and posterior hypothalamus of young and adult SHR, as well as in the brainstem of young SHR. Histidine decarboxylase activity was unchanged in the posterior hypothalamus and in the medulla oblongata of young and adult SHR as well as in the anterior hypothalamus of young SHR, but it was slightly decreased in the anterior hypothalamus of adult SHR. Histidine decarboxylase activity was enhanced in the cortex-midbrain of young, as well as adult SHR, histamine-N-methyltransferase in the cortex-midbrain of young SHR. The following differences were found between young and adult rats: histamine levels were elevated in the cortex-midbrain of adult WKY and SHR. In the cortex-midbrain and brainstem of adult WKY and SHR histidine decarboxylase activity was also increased, while histamine-N-methyltransferase activity was elevated in the cortex-midbrain of adult WKY. The findings show changes in histamine levels, histidine decarboxylase and histamine-N-methyltransferase activities in SHR and suggest involvement of histaminergic neurons in hypertension. The activity of histaminergic neurons of adult rats seems to be higher than that of young animals.
Age Factors↗
The effect of hypertonic saline administration or stalk transection on histamine and histamine N-methyltransferase in the rat posterior pituitary.
There is evidence to suggest that histamine is a neurotransmitter in the CNS and functions in the regulation of arg-vasopressin (AVP) secretion. The posterior pituitary contains high levels of histamine and histamine N-methyltransferase (HNMT). Therefore, posterior pituitary histamine could also modulate the release of AVP. Paralleling the effect on AVP levels, the concentration of histamine in the rat posterior pituitary decreased from 18.8 +/- 2.7 ng/mg protein (x +/- SEM) to 12.9 +/- 1.9 ng/mg protein following 2 days of 2% (w/v) hypertonic saline administration and to 11.5 +/- 0.9 ng/mg protein with 7 days of treatment. Conversely, posterior pituitary HNMT activity was significantly elevated after hypertonic saline administration. Pituitary stalk transection did not reduce the concentration of histamine in the rat posterior pituitary although HNMT activity was reduced from 18.8 +/- 0.82 munits/gland to 9.22 +/- 1.56 munits/gland (x +/- SEM). These results indicate that histamine released from posterior pituitary mast cells could facilitate AVP release as part of the overall mechanism for osmotic stimulation of AVP secretion and support the concept that most posterior pituitary histamine is not neuronally derived from the brain. HNMT, on the other hand, may be contained in neurons disrupted by stalk section.
Animals↗
Histamine and histamine-N-methyltransferase in the goat brain.
Histamine concentrations and histamine-N-methyltransferase (HMT) (EC 2.1.1.8) activities were assayed in the goat brain, since this animal has been used for the purpose of assessing the physiological role of histamine in the central nervous system. The highest histamine concentrations were found in the hypothalamus (616 +/- 88 ng/g), 'thalamus' (244 +/- 41), preoptic area (242 +/- 95) and 'area postrema' (170 +/- 52), and are three to tenfold higher than the average concentration in the whole brain (76 +/- 9). The pineal body and choroid plexus contained very high concentrations of histamine (5800 and 5400 ng/g, respectively) and the pituitary gland had about the same as the hypothalamus (564 +/- 248 ng/g). There was little variation in the HMT activity in various parts of the brain and in the glands. In the cerebrospinal fluid both histamine concentration and HMT activity were very low, some increase occurred post mortem, but not within 20 minutes of death. The results indicate that the distribution of histamine and that of HMT in the goat brain are fairly similar to those in other mammalian brains, supporting the assumption that histamine might have a physiological function in the brain, especially in the hypothalamus.
Animals↗
A relatively specific and quantitative assay for histamine H2-receptor blocking activity by determination of inhibition of histamine-induced gastric acid secretion in the rat.
A relatively specific method for the quantitative assay of histamine H2-receptor antagonists has been developed. The method is based on the antagonism of the histamine-induced, and the spontaneous, gastric acid secretion in the stomach-perfused, urethane-anesthetized acute rat. For the induced gastric acid secretion, the animal received two consecutive equal injections of histamine (2 mg/kg, intrajugularly), the second 1.7 h after the termination of the first histamine-induced acid hypersecretion. Atropine (5 mg/kg), chlorisondamine (2 mg/kg), imipramine (10 mg/kg) and tripelennamine (5 mg/kg), administered i.p., failed to inhibit the histamine-induced, or the spontaneous, gastric acid secretion. Metiamide inhibited the histamine-induced acid secretion (ED50 1.85 mg/kg, i.p.) and the spontaneous acid secretion (10 mg/kg, i.p.). These results suggest that in the rat model employed in this study, histamine and H2-receptors play a very important role in the regulation of the gastric acid secretion. Other mechanisms involving cholinergic tone, biogenic amine uptake and histamine H1-receptors do not seem to intervene.
Animals↗
Spontaneous histamine release and histamine content in normal subjects and subjects with asthma.
Spontaneous histamine release (SHR) from basophils by simple incubation at 37 degrees C for 60 minutes and histamine content of basophils were assessed in normal subjects, patients with asthma, and methacholine-sensitive subjects without asthma (NAMS). SHR from basophils of normal subjects did not exceed 10% of the total histamine. A significantly higher SHR was observed in basophils from subjects with asthma than from normal subjects (p less than 0.002). Basophil SHR in patients with asthma not receiving medication was significantly greater than that in patients with asthma receiving medication (p less than 0.05). SHR from basophils in NAMS subjects was similar to that in normal subjects. SHR was highly dependent on temperature and Ca++ and Mg++ ions and appeared to be a slower event than anaphylactic release. The mean histamine content per basophil from normal subjects was 1.48 +/- 0.13 pg (mean +/- SEM). Basophils from subjects with asthma contained significantly less histamine than basophils from normal subjects (p less than 0.002). Histamine content per basophil from NAMS subjects was slightly lower than histamine content per normal basophil. No apparent relationship was found between the magnitude of SHR and the histamine content per basophil in the patients with asthma not receiving medication. Hypersensitivity to food or exercise does not appear to be essential for high SHR. High SHR appears to bear little, if any, relationship to cell damage or cell death. High SHR may be a factor that could serve as a marker for bronchial asthma. Further studies are needed to define the clinical relationship and pathophysiologic mechanism of SHR.
Adolescent↗
Reversal of histamine-mediated immunosuppression by structurally diverse histamine type II (H2) receptor antagonists.
The effect of a series of structurally-diverse histamine type II (H2)-receptor antagonists on histamine-mediated immunosuppression of human peripheral blood lymphocytes (HPBL) has been examined. This analysis of structure--activity relationships was undertaken to examine the validity of the recent proposal arising from clinical studies that H2-receptor antagonists containing a furan ring were devoid of the effects on lymphocyte function reported previously in studies using cimetidine and other H2-receptor antagonists containing an imidazole nucleus. Cimetidine and two furan-containing antagonists, ranitidine and SKF 93479, were found to be devoid of any effect on PHA-induced proliferation of human peripheral blood lymphocytes over a wide concentration range (10(-4) to 10(-10)M). At high drug concentrations (10(-3)M) significant suppression of mitogen stimulation was observed but this was accompanied by significant cytotoxicity. All three antagonists were effective in reversing the suppression of PHA-stimulation of HPBL induced by exogenous histamine. Reversal of histamine-induced immunosuppression was obtained at drug concentrations (2.0 X 10(-4) to 1.0 X 10(-6)M) which were non-toxic and did not affect PHA-induced proliferation in the absence of histamine. Ranitidine was the most potent antagonist in reversing histamine-mediated immunosuppression. The ability of structurally-diverse H2-receptor antagonists to modify the action of histamine on lymphocyte function lends support to the view that histamine exerts its effects via classical H2-receptors. The ability of ranitidine to alter lymphocyte responsiveness in analogous fashion to cimetidine indicates that the possibility of alterations in immune function should be considered in clinical studies using ranitidine and other furan-containing H2-receptor antagonists.
Animals↗
Histamine H1 receptor antagonist blocks histamine-induced proinflammatory cytokine production through inhibition of Ca2+-dependent protein kinase C, Raf/MEK/ERK and IKK/I kappa B/NF-kappa B signal cascades.
Histamine H1 receptor (H1R), a therapeutic target for alleviation of acute allergic reaction, may be also involved in mediating inflammatory responses via effects on cytokine production. However, the mechanisms whereby histamine induces cytokine production are poorly defined. In this study, we comprehensively investigated the signaling pathway involved in cytokine expression caused by histamine, using native human epidermal keratinocytes. We confirmed the expression of functional H1R by reverse transcription-polymerase chain reaction (RT-PCR), Western blotting and histamine-induced Ca(2+) elevation. Histamine induced concentration- and time-dependent production of granulocyte-macrophage-colony stimulating factor (GM-CSF), interleukin (IL)-8 and IL-6, which was completely blocked by olopatadine, an H1 antagonist. Histamine activated the phosphorylation of protein kinase C (PKC), c-Raf, mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK), extracellular signal-regulated kinase (ERK), I kappa B kinase (IKK), inhibitory kappa B (I kappa B)-alpha and nuclear factor-KB (NF-kappa B) p65, which was inhibited by Ro-31-8220, a PKC inhibitor. Also, Ro-31-8220 significantly suppressed the expression of these cytokines. BAPTA-AM, an intracellular Ca(2+) chelator, also reduced PKC phosphorylation and cytokine expression. PD98059, a MEK inhibitor, and BAY 11-8702, an I kappa B-alpha inhibitor, reduced ERK and NF-kappa B cascade activation, respectively, with little effect on PKC phosphorylation. PD98059 preferentially inhibited GM-CSF production whereas BAY 11-8702 prevented IL-8 and IL-6 production. Furthermore, in addition to the above cytokines, histamine stimulated the biosynthesis and/or release of numerous keratinocyte-derived mediators, which are probably regulated by the ERK or NF-kappa B cascades. Our study suggests that histamine activates Ca(2+)-dependent PKC isoforms that play crucial roles in the activation of Raf/MEK/ERK and IKK/I kappa B/NF-kappa B cascades, leading to up-regulation of cytokine expression. Thus, the anti-inflammatory benefit of H1 antagonists may be in part due to prevention of cytokine production.
Cells, Cultured↗
Skin reactivity to histamine and expression of histamine receptors mRNA in lymphocytes of healthy subjects and non-small-cell lung cancer patients before and after surgery.
Histamine modulates an immunological response through stimulation of appropriate receptor--H1R proinflammatory or H2R suppressive. The participation of histamine in regulation of an immunological response in the course of neoplastic disease is determined by the expression of particular receptor. The aim of our work was the investigation of the expression of mRNA of two types of histamine receptors in peripheral blood lymphocytes and the evaluation of skin-prick test with histamine in lung cancer patients before and after surgery. The investigation was performed on 15 patients qualified to surgery before and 7-10 days after treatment and on 12 healthy subjects. Reverse transcriptase polymerase chain reaction (RT-PCR) with primers labeled with fluorescent dyes was performed. Intensity of fluorescence was expressed as relative fluorescence units (RFU). The data were analysed using ABI Prism 310 GeneScan collection software Version 3.1. Skin-prick test with histamine was evaluated after 10 min by measuring the diameter of the weal. The expression of H1R and H2R mRNA in healthy subjects was not significantly different in contrast to the lung cancer patients in which a significant prevalence of H2R mRNA expression was observed before surgery and only slightly decreased after (P < 0.001). Skin-prick test--negative in one patient before surgery, after treatment was positive in all patients and the diameter of histamine weal was significantly increased (P < 0.001). One may assume that the prevalence of the expression of H2R mRNA in patients reflects the status of immunosuppression caused by cancer. Since histamine exerts its suppressive activity trough H2R it seems reasonably to include the antagonists of this receptor to the cancer therapy which may restore a relative balance between accessibility of both types of histamine receptors.
Aged↗
Effect of histamine and histamine blockers on the ovulatory process in the vitro perfused rabbit ovary.
An increase in the content of histamine in the ovary following luteinizing hormone (LH) release and the inhibition of ovulation in the rabbit by antihistamines suggest that histamine may be involved in the ovulatory process. The effects of various doses of histamine and antihistamines on ovulation were investigated using the in vitro perfused rabbit ovary system. Histamine (100 ng/ml) added to the perfusate at hourly intervals induced ovulation, although at a rate below that observed following human chorionic gonadotropin (hCG) administration. Cimetidine (10 micrograms/ml), an H2 blocker, inhibited histamine-induced ovulation, while the H1 blocker, chlorpheniramine (66.7 micrograms/ml), failed to do so. Neither cimetidine nor chlorpheniramine was able to block ovulation following hCG (50 IU). In all experimental groups in which histamine was used to induce ovulation, both extruded ova and follicular oocytes remained in an immature stage and displayed little evidence of degeneration. In contrast, a high percentage of ova exposed to hCG were mature. Ovarian edema was increased in ovaries in which ovulation occurred, regardless of treatment. A linear correlation was noted between ovulatory efficiency and degree of ovarian edema. Histamine may be an intermediary in the mechanism of follicular rupture, but does not support ovum maturation. However, the inability of H1 and H2 antagonists to block hCG-induced ovulation raises questions regarding the role of histamine in the physiologic process of ovulation.
Animals↗
Histamine and duodenal ulcer: effect of omeprazole on gastric histamine in patients with duodenal ulcer.
Gastric mucosal concentrations of histamine and of its metabolic enzyme, histamine methyltransferase activity, were measured in patients with duodenal ulcer disease and patients with an apparently normal stomach and duodenum. Patients with duodenal ulcer had significantly less (p less than 0.05) mucosal histamine (median 204 nmol/g) than control subjects (median 252 nmol/g). There was no significant difference between the two groups in their histamine methyltransferase activity values. Omeprazole therapy did not significantly change mucosal histamine (+23%), histamine methyltransferase activity (+5%), histamine release before (+5%) or during (+7%) pentagastrin infusion. It significantly decreased acid secretion during pentagastrin stimulation (median -73%, p less than 0.001). Omeprazole, like cimetidine, does not stop histamine release during pentagastrin stimulation.
Anti-Ulcer Agents↗
Role of histamine in the aetiology of byssinosis. I Blood histamine concentrations in workers exposed to cotton and flax dusts.
The formation or the accumulation, or both, of histamine in the lungs may be potentiated by agent(s) present in cotton dust at higher level(s) than in flax dust and negligible in cottonseed dust. It has been suggested that such potentiation may be due to the activation of the ability of the lung to produce histamine and/or produce or recruit mast cells; this may present an acceptable explanation of the mechanism by which the propagation of the chronic effect of the dust proceeds in cotton and flax workers. Histamine accumulated in the lung over the weekend is released on exposure to dust causing the symptoms of byssinosis. The difference in the rate of histamine metabolism relative to the rate of histamine formation in byssinotic subjects leads to a more prolonged histamine accumulation than in symptom free subjects, with the consequent appearance of the symptoms of byssinosis. Continuous exposure to dust, without weekend interruption, leads to equivalent rates of histamine formation and metabolism with non-considerable histamine accumulation in the lungs and consequent absence of the symptoms of byssinosis.
Bronchitis↗
Effect of intravenous histamine, allergen (Ascaris suum Extract) and compound 48/80 and inhaled allergen-aerosol on bronchoconstriction and histamine release.
The effect of a histamine releaser (48/80), an antigen (Ascaris suum extract) and of exogenous histamine infusion on antigen aerosol-induced bronchoconstriction was investigated in 24 mongrel dogs. During these substance infusions, the high values of arterial plasma histamine did not correlate with the degree of bronchoconstriction. Further, a severe bronchoconstriction with a relatively low arterial plasma histamine concentration was observed during antigen inhalation. During substance inhalation, a high local concentration of histamine is assumed to explain the increased bronchial "sensitivity" to actual plasma levels of histamine. Also, the responsiveness of the bronchial tree to antigen aerosol was observed to be reduced 90 min after induction of a strong histamine release. The importance of histamine in the first phase of immediate hypersensitivity is discussed.
Allergens↗