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At least 343 records · Page 19Linked to original sources
PubMed1992

Histamine leukocytosis. II. Source of histamine leukocytosis.

Leukocytes were labelled by intravenous injection of tritiated thymidine (3H-thymidine) in dogs to discover the source of the increased number of neutrophils in the circulating blood after injection of histamine in beeswax. Dogs with normal hemograms were given 1.0 mCi/kg of 3H-thymidine alone, and in different sequences, with histamine in beeswax. When 3H-thymidine was given during maintained histamine leukocytosis, labelled granulocytes appeared in and disappeared from the blood earlier than in control tests and the number of labelled cells was greater in the histamine-treated animals. Administration of histamine in beeswax 3 days after injection of 3H-thymidine also induced the premature appearance and disappearance of labelled neutrophils in the circulating blood. It was concluded that leukocytosis induced by the chronic action of histamine is due to 1) stimulated proliferation and differentiation of neutrophil precursor cells in the bone marrow and 2) the release of mature leukocytes from the bone marrow.

Animals↗
PubMed1992

[Effect of cetirizine, selective H1 antagonist of histamine on skin and bronchial reactivity and cellular histamine release in allergic diseases].

The study aimed at evaluating an effect of cetirizine--selective antagonist of histamine H1 receptor--on skin and bronchial reaction to histamine, and histamine release from the cells by pollen antigen and anti-IgE. Skin reactivity was tested thrice in 33 patients treated with Zyrtec (Polfa) for the chronic urticaria or allergic rhinitis. Reaction of the bronchi to histamine was tested with a technique described by Ryan et al in 10 asthmatic patients. As effect of cetirizine on histamine release from neutrophils was evaluated in patients with pollinosis before and on the fourth day of therapy. It was shown that the treatment with Zyrtec markedly decreases skin reaction to histamine. Single dose of drug administered 4 hours before the tests markedly restricts reactivity of the bronchi. Daily dose of 10 mg administered to patients with pollinosis stabilizes membranes of neutrophils.

Asthma↗
PubMed1988

[Histamine and lung cancer. II. Human lung cancer cell line and histamine].

Using tissue culture and biochemical technique, the effects of autacoid-histamine and histamine H-2 receptor's antagonist-cimetidine on human lung cancer cell line were studied. It was shown that histamine at the concentration of 1.8 x 10(-7) M stimulated proliferation of the lung cancer cells, but histamine at the concentration of 1.8 x 10(-4) M or cimetidine at 1.76 x 10(-7) M inhibited growth of the lung cancer cells. Relation between histamine, histidine decarboxylase, histamine formation capacity and tumor proliferation is discussed.

Adenocarcinoma↗
PubMed1982

Interaction of histamine with adrenergic smooth muscle neurotransmission. I. Effects of histamine on smooth muscle contractions induced by exogenous or by endogenous noradrenaline.

The effects of histamine on contractions in response to exogenous noradrenaline or to electrical stimulation were studied on two smooth muscle preparations with adrenergic neurotransmission--rat anococcygeal muscle and vas deferens. Histamine (1 X 10(-6)M-1 X 10(-4)M) did not affect significantly the contractions of vas deferens induced by noradrenaline (1 X 10(-8)M-1 X 10(-4)M), but decreased in a concentration-dependent manner the contractile effects of noradrenaline on anococcygeal muscle. The EC50 of noradrenaline on the latter preparation was increased 2.6-16.2 times by histamine but the antagonism was of a noncompetitive type. Histamine exerted a biphasic effect on the smooth muscle contractions in response to square wave electrical stimulation with supramaximal voltage (vas deferens--0.1 Hz, 1 sh or 10 Hz, 20 sh; anococcygeal muscle--5 Hz, 8 sh or 10 Hz 20 sh). The lower histamine concentrations (1 X 10(-12)M-1 X 10(-7)M) slightly potentiated the contractions and the higher concentrations (1 X 10(-6)M-1 X 10(-4)M) markedly inhibited the contractions in response to electrical stimulation. The results obtained are consistent with the hypothesis that the modulatory role of histamine for the adrenergic neurotransmission is mediated via presynaptic inhibitory H2--and postsynaptic excitatory H1--histaminergic receptors.

Animals↗
PubMed1982

Interaction of histamine with adrenergic smooth-muscle neurotransmission. III. Significance of magnesium ions for the effects of histamine on contractions induced by endogenous noradrenaline.

The significance of Mg2+ for the effects of histamine on smooth-muscle contractions in response to electrostimulation with different frequency has been studied in organs with adrenergic neurotransmission (prostatic part of vas deferens and anococcygeal muscle of rats). Reduction of the concentration of Mg-ions below 1.05 mM usually markedly potentiates the electrostimulation-induced contractions, whereas high Mg2+-concentrations (above 1.05 mM) sharply reduce their magnitude. The changes in the concentration of the Mg-ions in the nutrient medium do not influence essentially the inhibitory effects of histamine on smooth-muscle contractions in response to electrostimulation. In the presence of lower concentrations muscle contractions in response to electrostimulation. In the presence of lower concentrations of Mg-ions, the potentiating effect of histamine on electrostimulation does not change substantially. The rise in Mg2+-concentration above 1.05 mM considerably increases the potentiating action of the low histamine concentrations on the electrostimulation-induced contractions. This effect was more pronounced in smooth-muscle preparations stimulated with a lower frequency. The data obtained suggest that histamine counteracts the contractile response to electrostimulation induced by high concentrations of Mg-ions. It may be assumed that Ca-ions also participate in the realization of this histamine effect.

Animals↗
PubMed1982

Histamine-receptor bearing lymphocytes. II. The use of flow cytofluorometric analysis of histamine-receptors on mouse lymphocytes of different organs.

The histamine binding capacity of cells in various lymphoid organs has been determined by flow cytofluorometric (FCF) analysis of histamine receptors. Using fluoresceinated bovine serum albumin conjugated to histamine (HIS-BSA-FITC) as a staining reagent two distinct lymphocyte subpopulations of differing fluorescence intensity have been identified in each organ investigated. The thymus has a low number of histamine-receptor bearing cells, while bone marrow, lymph nodes and spleen reveal increasing binding capacities to the histamine conjugate. It is suggested that there exists a different susceptibility of distinct lymphocyte subpopulations for histamine, thereby enabling its controlled immunoregulatory activity.

Animals↗
PubMed1986

Histamine H2 receptor activity and histamine metabolism in human U-937 monocyte-like cells and human peripheral monocytes.

Functional and specific histamine H2 receptors were characterized in human peripheral monocytes and in U-937 cells, before and after retinoic acid--induced differentiation into monocyte/macrophage-like cells. The relative potencies of histamine and the H1, H2 receptor agonists and antagonists studied are remarkably similar in U-937 cells and U-937 monocytes. There is no change in histamine concentration and activity of the enzymes forming and degrading histamine during monocytic-like differentiation. The results raise the possibility that histamine H2 receptors might be involved in pathophysiological regulations (proliferation/differentiation and biological function) of normal and leukemic monocytes.

Adult↗
PubMed2005

Histamine, histamine receptors (H1 and H2), and histidine decarboxylase expression by chondrocytes of osteoarthritic cartilage: an immunohistochemical study.

Degeneration and loss of articular cartilage are the characteristic features of osteoarthritis (OA), with the appearance of fibrillations, cell clusters, matrix depletion, and changes in matrix composition all apparent. Histamine has a recognised role in allergic and inflammatory reactions, and is reported to affect several aspects of chondrocyte behaviour. The immunohistochemical (IHC) studies reported here have demonstrated histamine (H), both H1 and H2 receptors, and the histamine-producing enzyme histidine decarboxylase (HDC) in a variable proportion of human articular chondrocytes in OA cartilage specimens. Such observations were especially evident within the degenerative, superficial zone, and more so in late-stage disease. By contrast, "normal" age-matched cartilage specimens showed relatively little immunopositive staining for histamine and HDC. These findings strongly suggest that histamine and H-receptor expression by HAC in OA cartilage is potentially an important contributor to the atypical, aberrant phenotype of OA chondrocytes.

Biomarkers↗
PubMed1985

H2 histaminic receptors in rat cerebral cortex. 1. Binding of [3H]histamine.

Saturable binding of [3H]histamine in equilibrium with homogenates of rat cerebral cortex reveals Hill coefficients between 0.4 and 1.0, depending upon the conditions. Data from individual experiments are well described assuming one or two classes of sites. Only the sites of higher affinity (KP1 = 3.9 +/- 0.5 nM) are observed when binding is measured by isotopic dilution at a low concentration of the radioligand (less than 1.5 nM) in the presence of magnesium or by varying the concentration of the radioligand. The sites of lower affinity (KP2 = 221 +/- 26 nM) appear during isotopic dilution at higher concentrations of the radioligand or at lower concentrations either upon the addition of guanylyl imidodiphosphate (GMP-PNP) or upon the removal of magnesium. Estimates of the second- and first-order rate constants for association and dissociation of [3H]histamine agree well with KP1. Apparent capacities corresponding to KP1 and KP2 are of the order of 100 ([R1]t) and 1300 pmol/g of protein ([R2]t), respectively. Simple interconversion cannot account for the changes in binding that occur upon adding GMP-PNP or removing magnesium, since the increase in [R2]t exceeds the decrease in [R1]t. Moreover, the apparent amount of high-affinity complex exhibits a biphasic dependence on the concentration of [3H]histamine; an increase at low concentrations is offset by a decrease that occurs at higher concentrations. The latter appears to be positively cooperative and concomitant with formation of the low-affinity complex. These and other observations indicate that the binding of histamine is inconsistent with models commonly invoked to rationalize the binding of agonists to neurohumoral receptors. GMP-PNP and magnesium reciprocally alter capacity at the sites of higher affinity, however, and the reduction caused by GMP-PNP reflects a substantial increase in the rate constant for dissociation at the sites that appear to be lost. The sites labeled by [3H]histamine thus reveal the properties of neurohumoral receptors linked to a nucleotide-specific G/F protein.

Animals↗
PubMed1983

Histamine H1 receptors and prostaglandin-histamine interactions modulating contractility of rabbit and rat testicular capsules in vitro.

The stimulatory effect of histamine on rabbit and rat testicular capsule was blocked by the H1 blocker, diphenhydramine, but not by the H2 blocker, cimetidine, suggesting the presence of H1 histamine receptors in both rabbit and rat testicular capsules. In the rabbit, both anti-prostaglandin F (PGF) and anti-prostaglandin E (PGE) effaced spontaneous autorhythmic contractions. They markedly inhibited PGF 2 alpha, PGE1 and histamine-stimulated contractions of the rabbit testicular capsule. In the rat, anti-PGF or anti-PGE had no inhibitory effects on the capsular tone, but they both inhibited the stimulatory effects of histamine. These data suggest that the action of histamine on the rabbit and rat testicular capsules could be due partly to a secondary release of the PG's, PGE2 and PGF2 alpha.

Animals↗
PubMed1989

SK&F 93574, a histamine H2-receptor antagonist, releases histamine in the dog.

This study was designed to establish whether SK&F 93574 releases histamine in dogs. Three female beagle dogs each received single infusions (on separate days) of each of SK&F 93574 (2.5 mg kg-1), polyvinylpyrrolidone (PVP, 20 mg kg-1) and sterile saline. The treatments were given at 14 day intervals by rapid intravenous infusion at 0.5 mL kg-1 min-1 for 2 minutes. Dogs showed clinical signs of histamine release such as vasodilation, licking lips, head drooping and increased gut movement after treatment with the known histamine releaser PVP or the test compound SK&F 93574. These signs were of similar severity and duration for the two compounds. No such changes were observed when the dogs received vehicle alone. Treatment with PVP or SK&F 93574 also resulted in markedly elevated plasma histamine concentrations (greater than 10-fold increase over control). It is concluded that intravenous administration of SK&F 93574 to dogs is associated with histamine release.

Animals↗
PubMed1984

Effects of histamine and histamine receptor antagonists on ion transport in rabbit descending colon.

The effects of histamine on colonic ion transport were examined in in vitro preparations of rabbit descending colon. Serosal addition of histamine (10(-5) M) produced a transient increase in short-circuit current (Isc) and transepithelial conductance. The Isc response to histamine could be blocked by removing Cl from both bathing solutions, adding furosemide (10(-3) M) to the serosal bathing solution, adding indomethacin to the serosal and mucosal bathing solutions (10(-5) M), or removing Ca from the serosal bathing solution. In addition, the histamine-induced increase in Isc was inhibited in a dose-dependent manner by the H1-receptor antagonist diphenhydramine, with a maximal inhibition at 10(-4) M and a half-maximal inhibition at 3 X 10(-7) M. The H2-receptor antagonist cimetidine (10(-3) M) was without effect on the histamine response. Measurement of unidirectional Na, K, and Cl fluxes revealed that serosal addition of diphenhydramine (10(-3) M) reduced basal Isc due to a decrease in mucosal-to-serosal Na flux. Serosal addition of diphenhydramine (10(-3) M) also inhibited the increase in Isc produced by serosal addition of prostaglandin E1, 8-bromo-cAMP, cholera toxin, or the ionophore A23187. Measurement of unidirectional K and Cl fluxes revealed that prostaglandin E1 alone increased serosal-to-mucosal K and Cl fluxes and reduced the mucosal-to-serosal K flux, thereby increasing net K and Cl secretion. Serosal diphenhydramine (10(-3) M) abolished the changes in Cl fluxes produced by prostaglandin E1 and reduced the magnitude of the changes in K fluxes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Histamine-releasing properties of T-3762, a novel fluoroquinolone antimicrobial agent in intravenous use. I. Effects of doses and infusion rate on blood pressure, heart rate and plasma histamine concentration.

T-3762, a newly developed fluoroquinolone antimicrobial agent, ciprofloxacin (CPFX) and ofloxacin (OFLX) were administered intravenously to anesthetized dogs by intravenous infusion, and blood pressure, heart rate and plasma histamine concentrations were monitored. T-3762 decreased blood pressure by 12.0%, without alterations in heart rate and plasma histamine concentration, only when infused at 150 mg/min. CPFX and OFLX both produced a rapid decrease in blood pressure in a dose-related manner, with an accompanying decrease in heart rate, but to a lesser extent. After infusion at 150 mg/min, CPFX caused death in 2 animals within a few minutes, while OFLX produced maximum decreases in blood pressure and heart rate, by 69.0% and 26.4%, respectively. The infusion of these 2 agents resulted in dose-related increases in plasma histamine concentrations parallel to the decreases in blood pressure: the maximum, attained with CPFX at 50 mg/min and OFLX at 150 mg/min, were 379.2 and 167.8 ng/ml, respectively. For CPFX and OFLX, the relationship between the maximum levels of decreased blood pressure and increased histamine concentration in plasma was highly significant. The hypotension induced by CPFX was efficiently reduced by the pretreatment of animals with antihistamines. The results from this study suggest that hypotension induced in dogs following the intravenous infusion of fluoroquinolone antimicrobial agents may be dependent on their ability to cause histamine release from cells and tissues, and indicates that T-3762 is devoid of this ability in comparison to CPFX and OFLX.

Animals↗
PubMed1993

Histamine H2-receptor plays only a minor role in histamine-induced wheal response in the squirrel monkey and guinea pig.

We examined the contribution of the histamine H2-receptor to the histamine-induced wheal response in squirrel monkeys and guinea pigs. Intradermal injection of histamine, 2-pyridylethylamine (a selective H1-agonist), and dimaprit (a selective H2-agonist) dose-dependently induced the wheal response in squirrel monkeys and guinea pigs, although the reaction to dimaprit was much weaker than that to the other agonists. Chlorpheniramine dose-dependently depressed the wheal response in squirrel monkeys and guinea pigs at doses of 0.03-1 mg/kg and 0.03-3 mg/kg, p.o., respectively. However, famotidine, ranitidine and cimetidine had no effect at doses up to 30, 100 and 300 mg/kg, p.o. in guinea pigs and up to 1, 10 and 400 mg/kg, p.o. in squirrel monkeys, respectively. Cimetidine (3-300 mg/kg, p.o.) dose-dependently potentiated the inhibitory effects of chlorpheniramine (0.1 mg/kg, p.o.) in guinea pigs, but had no effects in squirrel monkeys. Famotidine and ranitidine did not alter the response to chlorpheniramine in either animal. These results suggest that the histamine H2-receptor plays only a minor role in the histamine-induced wheal response in squirrel monkeys and guinea pigs.

Animals↗
PubMed1986

Theoretical studies on the activation mechanism of the histamine H2-receptor: the proton transfer between histamine and a receptor model.

A proposed molecular mechanism for the activation of the H2-receptor of histamine was simulated with ab initio calculations including geometry optimization with several basis sets. The system is modeled by a proton-relay chain produced by the binding of a histamine molecule to a receptor model consisting of an anionic anchoring site, and proton donor and acceptor sites. The anchoring of histamine cation at a negative receptor site is simulated by the interaction with a hydroxyl anion or by calculations on neutral histamine; the proton donor and acceptor sites are modeled by ammonium and ammonia groups, respectively. Results of the calculations reveal that a significant decrease in the barrier for the movement of the proton from the donor site to the N1 nitrogen in the imidazole portion of histamine occurs as a consequence of the neutralization of the side chain and the simultaneous interaction of the N3 nitrogen with the proton acceptor. An increase of the driving force for the proton transfer process is produced by these interactions, as observed from the relative energies of the initial and final steps of the charge relay. The barrier and the driving force depend on the nature of the proton acceptor site. This simulation of the receptor activation mechanism provides the basis for exploration of the partial receptor activation by molecules characterized as partial agonists and the lack of activation by molecules that act as antagonists on this receptor.

Binding Sites↗
PubMed1980

Lack of influence of histamine H1-, and H2-receptor antagonists on histamine level in rat brain.

The intraperitoneal administration of three antihistaminic drugs of H1 type: mepyramine, diphenyhydramine (each 5 and 30 mg/kg) and danitracen (2 and 10 mg/kg) did not modify histamine level in the rat brain after 2 h. Histamine H2-receptor antagonists: cimetidine (25-250 microgram) and metiamide (100 microgram) given directly into the brain had no significant effect on histamine content after 1.5 h. L-histidine (0.5 g/kg i.p.) increased after 1.5 h histamine level in various experiments by 50-75% above control. All antihistaminic drugs did not change significantly histamine level in the brains of L-histidine-treated rats though a slight but consistent tendency to decrease the L-histidine effect in the group of H2-receptor blocking drugs was observed.

Animals↗
PubMed1980

Effect of histamine on the spontaneous E rosette formation after blockade of histamine H2 receptors with cimetidine.

Thirteen patients with clinical diagnosis of hay fever, were examined. T lymphocytes subpopulation was determined by the E rosette test. The present study is concerned with the effect of histamine on the ability of T lymphocytes for E rosette formation after blockade of the histamine H2 receptor with its inhibitor cimetidine. It has been found that histamine effect is expressed by the histamine H2 receptor, as its blockade with cimetidine leads to the failure of histamine to inhibit rosette formation by T lymphocytes.

Adolescent↗
PubMed1995

Homologs of histamine as histamine H3 receptor antagonists: a new potent and selective H3 antagonist, 4(5)-(5-aminopentyl)-1H-imidazole.

The influence of alkyl chain length variation on the histamine H3 receptor activity of histamine homologs 1 was investigated. A series of 4(5)-(omega-aminoalkyl)-1H-imidazoles 1 was prepared with an alkyl chain length varying from one methylene group to 10 methylene groups. Besides the H3 activity, the affinities of these compounds for the H1 and H2 receptors were determined. The ethylene chain of histamine is optimal for agonistic activity on all three histamine receptor subtypes. For the H3 receptor, elongation of the alkyl chain from three methylene groups on leads to compounds with antagonistic properties. 4(5)-(5-Aminopentyl)-1H-imidazole (impentamine, 1e) is the most potent and selective H3 antagonist from this series of 4(5)-(omega-aminoalkyl)-1H-imidazoles 1, with a pA2 value of 8.4 (on guinea pig jejunum). A specific antagonistic binding site for this compound is proposed.

Animals↗