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PubMed1960

The inhibition of mast cell damage and histamine release in anaphylaxis by pyridine and diphosphopyridine nucleotidase inhibitors. Comparison with compound 48/80.

In rats and guinea-pigs both mast cell damage and histamine release in anaphylaxis were inhibited by pyridine, nicotinamide, diethylnicotinamide, nicotinic acid, isonicotinic acid and isonicotinic acid hydrazide, which are known to be inhibitors of diphosphopyridine nucleotidases. On the other hand these compounds potentiated histamine release and mast cell damage by compound 48/80 in guinea-pigs although inhibiting the same phenomena in rats. The relationship of these findings with the mechanism of histamine liberation in anaphylaxis is discussed.

Anaphylaxis↗
PubMed1985

[Physiology of nodal tissue and effect of products used in anesthesia].

The three fundamental properties of the nodal tissue, i.e.: excitability, automaticity and conduction of the depolarisation wave, are directly dependent on ionic transmembrane currents. These currents, either active or passive, determine the characteristics of the membrane action potential. Passive ionic movements cross gated transmembrane channels which activation is voltage-dependent, sometimes time-dependent and, for Ca2+ channels, dependent on intra-cellular cyclic AMP content. Both intra and extra-cellular ionic concentrations (K+, Ca2+, Mg2+) alter these passive movements. Active ionic movements require ATP hydrolysis and depend only on cellular metabolism. The neurovegetative system and its transmitters modulate the nodal tissue function altering passive ionic currents. Drugs employed during anesthesia change this function either by direct action on the ionic currents or by indirect action on the neurovegetative system or on histamine liberation. Thus: local anesthetics block selectively fast sodium channels; halogenated volatile anesthetics inhibit slow calcium channels: and narcotics are quite always vagomimetics, sometimes sympathicolytics, they often release histamine. Nevertheless, mechanism of action of various drugs remain unclear.

Action Potentials↗
PubMedDate not supplied

Effect of alcohol-feeding on gastric mucosal mast cell population and gastric tissue histamine concentration in albino rats.

Albino rats fed on 30% ethyl alcohol for 60 days demonstrated significant reduction in the histamine concentration of the gastric wall, estimated by bio-assay, as well as in the gastric mucosal mast cell population. It can, therefore be concluded that alcohol liberates histamine from the gastric mast cells even in the presence of alcohol-induced gastritis.

Animals↗
PubMed1982

Peripheral hypotensive and central hypertensive effects of cimetidine.

Rapid intravenous (i.v.) injections of high doses (16-128 mumol/kg) of cimetidine induced a short-lasting (5-15 min) hypotension in anaesthetized rats. Diastolic pressure was reduced more than systolic pressure, suggesting vasodilatation. Heart rate was not affected. Diphenhydramine pretreatment (100 mumol/kg i.v.) did not antagonize the hypotensive effect of cimetidine. However, in the presence of diphenhydramine, cimetidine induced bradycardia. Intracerebroventricular administration of cimetidine or metiamide (2 mumol/rat) increased the blood pressure and heart rate. It is concluded that the hypotension after i.v. cimetidine is mediated by peripheral mechanisms. Since diphenhydramine pretreatment had no antagonistic effect cimetidine-induced hypotension could not be due to indirect H1-receptor stimulation caused by histamine liberation.

Animals↗
PubMed1957

Action of anaphylactic shock and anaphylatoxin on mast cells and histamine in rats.

Anaphylactic shock in rats produces disruption of mast cells. These cells are also disrupted when rat mesentery is incubated with antigen in vitro. The plasma histamine reaches a maximum about 5 min. after injection of the antigen. Though antihistamines protect rats against anaphylactic shock, they do not prevent mast cell disruption. Previous depletion by compound 48/80 of the histamine bound to the mast cells prevents anaphylactic shock and the increase in plasma histamine. Anaphylatoxin produces no mast cell alterations or plasma histamine increase, and thus does not seem to act as a histamine-releasing agent in rats. Probably nearly all the histamine liberated in anaphylaxis in rats comes from the mast cells.

Anaphylatoxins↗
PubMed1990

Biphasic blood pressure response to neuropeptide Y in anesthetized rats.

The effects of neuropeptide Y (NPY) on systemic arterial blood pressure and heart rate were studied in anesthetized intact and pithed rats. I.v. doses of NPY (0.3-30 nmol/kg) raised the mean arterial blood pressure dose dependently. At doses of greater than or equal to 3.0 nmol/kg, the initial pressor response was followed by a dose-dependent fall in blood pressure in intact and pithed rats. The depressor response was accompanied 1-2 min after the NPY injection by a slight increase in heart rate in pithed rats but not in intact rats, and 10 min after the injection by a decrease in heart rate in intact rats. After repeated injections of NPY, the depressor effect vanished, whereas the integrated pressor response over time was markedly enhanced. After pretreatment with the histamine H1-receptor antagonist, mepyramine, or with the histamine liberator, compound 48/80, the pressor response to NPY remained but the depressor response disappeared. We suggest that the marked fall in blood pressure can be attributed to NPY-evoked histamine release from mast cells.

Anesthesia↗
PubMed1999

[Level of histamine in supernatants from the basophil activation test: applications to hymenoptera allergy and drug allergy--preliminary study].

Histamine Release technic consists in calculating histamine liberated by blood cells in touch with an allergen. To this day, this method is only used in Hymenoptera venom allergy diagnosis. The principle of this study is to measure histamine released by activated basophils in surnageons of Basophil Activation Test (BAT) for different allergens: Hymenoptera venoms: Bee, White Faced Hornet, Vespula Wasp. Drugs: Cefaperos, Clamoxyl, Alfatil, Rapifen, Diprivan, Nesdonal, Mivacron. A threshold of positivity (amplification factor in comparison with the control) is determined for these two classes of allergens: 45 for Hymenoptera venoms and 9 for drugs. These results, compared to the other diagnosis technics (Histamine Release, Basophil Activation Test, Prick Tests) discloses very high correlation rates in each case. This method seems to be a reliable method for Hymenoptera venom allergy diagnosis and for drugs allergy diagnosis too. However, this study is based on a few number of patients, so a significant statistic conclusion can't be expressed but it opens an interesting way of research.

Basophil Degranulation Test↗
PubMed1982

Potentiation of histamine-induced itch and flare responses in human skin by the enkephalin analogue FK-33-824, beta-endorphin and morphine.

The effect of various opioid or putative neurotransmitter peptides on histamine-induced itch and flare responses was studied in humans after intradermal injection. Significant enhancement of the histamine responses was induced by the stable methionine-enkephalin analogue FK 33-824, beta-endorphin and morphine. The putative neurotransmitters substance P and vasoactive intestinal polypeptide (VIP)--which moreover are potent histamine liberators--had no enhancing effect. The potentiation induced by FK 33-824 was induced neither by local pretreatment with Compound 48/80 to deplete the local stores of mast-cell-bound histamine, nor by oral pretreatment with indomethacin to inhibit prostaglandin formation in the skin. Thus, the enhancement did not seem to be due to histamine release or to prostaglandin formation and the mechanism of the effect remains to be shown. The specific morphine antagonist naloxone did not inhibit the potentiation by FK 33-824, which might indicate that ordinary opiate receptors were not involved. The results support the idea that pain and itch are qualitatively separate processes and suggest possible mechanisms of morphine-induced pruritus. The findings are of particular interest in view of recent reports on the presence of methionine-enkephalin in Merkel cells.

Adolescent↗
PubMed1984

Calcium dependency of inhibition by arachidonic acid of compound 48/80-induced histamine release from mast cells.

Compound 48/80 ( compd 48/80)-induced histamine secretion from rat mast cells was inhibited almost completely by pretreatment of the cells at 37 degrees with 25 microM arachidonic acid in the presence of 1.8 mM Ca2+. As the Ca2+ concentration was reduced below 1.8 mM, 25 microM arachidonic acid became less inhibitory and, then, progressively more stimulatory for histamine release with or without compd 48/80. No additive effect on histamine release was obtained by combining compd 48/80 and arachidonic acid. Pretreatment of mast cells with lidocaine, an inhibitor of Ca2+ binding to phospholipid, or with nordihydroguaiaretic acid, an inhibitor of Ca2+ flux and lipoxygenase, stimulated arachidonic acid-induced histamine release. Arachidonic acid also inhibited a compd 48/80-induced spike increment of intracellular 45Ca2+ uptake and a decrease of total 45Ca2+ uptake by 45Ca2+-preloaded mast cells. Arachidonic acid and Ca2+ also suppressed melittin-induced histamine release and compd 48/80-induced release of radioactivity from mast cells preloaded with [3H]arachidonic acid. These results suggest that exogenous arachidonic acid or its metabolite(s) may interact with membrane-associated Ca2+, disturbing Ca2+ availability for the trigger mechanism of compd 48/80-induced histamine release or inhibiting the subsequent metabolism of arachidonic acid via the lipoxygenase pathway to form active metabolites involved in the histamine liberating mechanism.

Animals↗
PubMed1983

Anaphylaxis after Hymenoptera stings in three patients with urticaria pigmentosa.

Three patients with urticaria pigmentosa are reported who developed symptoms of anaphylaxis after Hymenoptera stings. Serum IgE antibodies to various Hymenoptera venoms could not be detected in any of the patients. Skin tests were completely negative in one patient, and borderline reactions with honeybee and yellow jacket venom, respectively, were found in the other two. Peripheral blood leukocytes of these latter two patients did not release significant amounts of histamine after exposure to the respective venoms. In patients with mastocytosis, anaphylaxis after insect stings may not be IgE-mediated but due to mediator release by the pharmacologic action of histamine liberators normally present in Hymenoptera venoms.

Adult↗
PubMed2002

ReN 1869, a novel tricyclic antihistamine, is active against neurogenic pain and inflammation.

The tricyclic compound (R)-1-(3-(10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5-ylidene)-1-propyl)-3-piperidine carboxylic acid (ReN 1869) is a novel, selective histamine H(1) receptor antagonist. It is orally available, well tolerated, easily enters the central nervous system (CNS) but no adverse effects are seen in mice at 300 mg/kg. ReN 1869 at 0.01-10 mg/kg is antinociceptive in tests of chemical nociception in rodents (formalin, capsaicin, phenyl quinone writhing) but not in thermal tests (hot plate and tail flick). ReN 1869 amplifies the analgesic action of morphine but does not show tolerance after chronic dosing. Moreover, the compound is effective against inflammation of neurogenic origin (antidromic nerve stimulation, histamine-evoked edema) but not in carrageenan-induced inflammation. We suggest that ReN 1869, via H(1) blockade, counteracts the effect of histamine liberated from activated mast cells and inhibits pain transmission in the dorsal spinal cord. ReN 1869 represents a new class of antihistamines with pain-relieving properties that probably is mediated centrally through histamine H(1) receptors but alternative mechanisms of action cannot be excluded.

Animals↗
PubMed1979

Effect of terbutaline, a beta 2-adrenergic receptor stimulating compound, on cutaneous reponses to histamine, allergen, compound 48/80, and trypsin.

The beta-adrenoceptor stimulating agent terbutaline (2 ng-2 microgram) injected intradermally in eight atopic subjects produced a dose-dependent inhibition of the skin reactions induced by subsequently injected allergen. After injection of 0.5 microgram terbutaline inhibition of the flare and weal responses was demonstrable throughout the observation period of 90 min. The flare response induced by histamine, the histamine liberator compound 48/80 and the proteolytic enzyme trypsin was not inhibited by terbutaline in the doses used, suggesting a selective action of terbutaline on the allergen-induced response. The weal response elicited by histamine and compound 48/80 was slightly reduced by 2 microgram terbutaline. It is suggested that pretreatment of the skin with terbutaline interferes with the ability of the cutaneous mast cells to respond to challenge with allergen and that terbutaline produces this effect in doses lower than those needed to counteract the permeability increasing effect of released mediator substances.

Adolescent↗
PubMed1990

[Analysis of the adverse effects of drugs at the cellular and subcellular levels].

A release of histamine after the lipophilic betablockers exaprolol and propranolol correlates with their capability of displacing the bound membrane Ca2+ and increasing the disorder of phospholipidic membranes of the isolated mast cells. Electron microscopy confirmed intracellular displacement of histamine from granules of mast cells after exaprolol without marked structural changes on the plasmatic membrane. Hydrophilic and selective atenolol, which does not possess a histamine-liberating effect, decreases spontaneous transfer of the intracellular calcium, decreases the disorder of the mast-cell membranes, and together with exaprolol and propranolol inhibits, in dose-dependence way, the gain of extracellular histamine in cells. The inhibitory effect of EDTA, tetrodotoxine and suramine on histamine release after exaprolol explains the non-receptor mechanism of exaprolol effect, which confirms a possibility of induction of adverse effects of blockers of the beta-adrenergic receptor in the development of a bronchospasm.

Adrenergic beta-Antagonists↗
PubMed1992

Influence of CGS 9343B, an inhibitor of calmodulin activity, on histamine release from isolated rat mast cells.

Investigations of calmodulin involvement in cell responses has been complicated by the lack of selective calmodulin antagonists. A novel inhibitor, CGS 9343B, reportedly without influence on protein kinase C, is used in the present study of mast cell responses. The histamine release induced by antigen and compound 48/80 in the presence of calcium was enhanced by 10-20 microM CGS 9343B and inhibited by higher concentrations. Only inhibitory effects on the response to compound 48/80 in the absence of calcium and to the ionophore A23187 were observed, the latter being inhibited by 20 microM CGS 9343B. The influence on responses to combinations of the phorbol ester TPA and the ionophore A23187 was more complex, giving rise to enhancement at lower and inhibition at higher concentrations of CGS 9343B in a manner which depended on the experimental conditions. Unlike previously used calmodulin antagonists, CGS 9343B is devoid of detergent effects and without serious metabolic interference. The inhibitor seems useful to reveal differences in the mechanisms involved in responses to various histamine liberators. Our results conform with an inhibition of calmodulin by CGS 9343B but are at present inconclusive.

Animals↗
PubMed2000

Topical ophthalmic beta blockers may cause release of histamine through cytotoxic effects on inflammatory cells.

AIM: To evaluate the effects of beta blockers used in ophthalmology on the release of histamine from mixed cell preparations containing human leucocytes and basophils. METHODS: A mixed leucocyte and basophil preparation was obtained from venous blood of healthy non-atopic volunteers. Cell preparations were then incubated with betaxolol, metipranolol, timolol, or carteolol. After incubation for 1 hour the histamine content of the supernatant was analysed by automated fluorometric analysis. Cell viability was tested by measuring lactate dehydrogenase (LDH) concentrations. RESULTS: Betaxolol and metipranolol in concentrations between 10(-2) M and 10(-3) M liberated histamine from human blood cells in a dose dependent manner. Carteolol and timolol had no effect on histamine at these concentrations. At the same concentrations LDH was also detected in the supernatants of cell suspensions incubated with metipranolol or betaxolol. CONCLUSIONS: Betaxolol and metipranolol induce substantial histamine release from human leucocytes, probably as a result of their cytotoxic effect.

Administration, Topical↗
PubMed1979

Histamine release from platelets for assay of byssinogenic substances in cotton mill dust and related materials.

Previous reports suggest that byssinosis, an asthma-like condition among textile workers, may be mediated in part by histamine liberated following inhalation of dust. A simple, sensitive, and reliable procedure using pig platelets which contain the unusually high concentration of 0.8-1.6 microgram histamine/10(9) cells has been devised for the assay of histamine-releasing factors in cotton mill dust and related materials, and has yielded results generally in accordance with earlier assays using chopped lung tissue. As little as 50--100 microgram of total extractable substances from cotton mill dust can be measured. The activity of the extract is associated with the non-dialysable high molecular weight portion. However, conditions of acid hydrolysis do not destroy the activity. Extracts of leaves from different varieties of plant are highly potent, which suggests that the factors responsible for byssinosis are widely distributed plant components, present in textile fibre plants and converted to a respirable form by handling processes. Ellagic acid and sodium metasilicate release histamine from pig platelets, and represent new classes of compounds with possible roles in the aetiology of byssinosis.

Allergens↗
PubMed1982

Histamine synthesis, imidazole dipeptides, and wound healing.

The relationships among anserine (beta-alanyl-1-methyl-L-histidine), carnosine (beta-alanyl-L-histidine), free histidine, and histamine metabolism were examined in rats wounded by dorsal skin incision. Following wounding, rats were treated with either a histamine liberator (compound 48/80) or a histidine decarboxylase inhibitor (4-imidazolyl-3-amino-2-butanone). The liberator greatly enhanced wounded skin-breaking strength and collagen deposition at the wound site, while the histidine decarboxylase inhibitor reduced skin-breaking strength and collagen deposition. In the second experiment of this study, histamine or histidine treatment was shown to prevent trauma-induced reductions of tissue carnosine but was less effective in ameliorating tissue anserine loss. The results illustrate an interaction between imidazole dipeptides and stress and suggest that carnosine acts as a histidine reserve in relation to histamine synthesis during trauma.

Animals↗
PubMed1982

Degranulation of endothelial specific granules of the toad aorta after treatment with compound 48/80.

Incubation of isolated toad aortas in Ringer solution containing compound 48/80, a histamine liberator, resulted in marked degranulation of endothelial specific granules. Since incubation of these vessels in Ringer solution only did not show significant morphologic changes in these granules, these findings suggest that the degranulation was induced by histamine release from the granules, as in the case for mast cell degranulation, and that endothelial specific granules are a storage site of histamine in the toad aorta. The present morphologic data were supported by preliminary chromatography, which showed appreciable concentrations of histamine in the granule-containing pellets of subcellular fractions of homogenized toad aortas.

Animals↗