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At least 793 records · Page 44Linked to original sources
PubMed1975

[Storage of histamine in the blood following liberation from liver and antrum through trypsin: protective mechanism or a factor promoting pancreatic shock].

In dogs histamine was predominantly released from liver and antrum by intravenous injection of trypsin. The histamine content of the human liver was found to be high enough to allow the invasion of mg amounts of histamine into the circulation after histamine release. In blood histamine was rapidly taken up by corpuscular elements. At present it cannot be decided whether this mechanism leads to detoxification or to a more powerful action of histamine in the microcirculation.

Animals↗
PubMed1989

Free radicals induce ischemia-reperfusion injury and histamine release in the isolated guinea pig heart.

Free radicals are produced by perfusion of isolated guinea pig heart with FeCl3/ADP (10 microM/100 microM) and/or occlusion and opening of the left anterior descending coronary artery. Cardiac histopathology was correlated with histamine and lactate dehydrogenase release and with malondialdehyde production. A differential release of histamine and lactate dehydrogenase in the perfusate was detected, showing a preferential liberation of histamine in the reperfusion phase. The increase in lipid peroxidation product in left ventricular tissues after left coronary artery occlusion was maximal at the end of ischemia.

Adenosine Diphosphate↗
PubMed1981

[The histamine-release test, a new in-vitro method in the diagnosis of allergic diseases (author's transl)].

Liberation of histamine from autologous basophils after stimulation with antihuman IgE and various allergen solutions was measured, in part by autoanalyser, in 47 patients with allergic bronchial asthma or allergic rhinitis. Three patients were non-responders: there was no histamine release after stimulation. In the other patients, both antihuman IgE and the allergen solutions produced a definite histamine release, in such a way that at higher concentrations there occurred an inhibitory effect with both antihuman IgE and the antigen mixture. But this effect disappeared with increasing dilution, giving a bell-like dose-response curve. The test is thus of value also in the diagnosis of allergic conditions.

Antibodies, Anti-Idiotypic↗
PubMed1978

[Histamine and its role in peptic gastric diseases: the discovery of histamine-H2-receptor antagonists].

For the definition of histamine receptors the following prerequisites must be fulfilled: (1) Course of dose-response curves according to the mass-action law; (2) parallel displacement of these curves to the right in the presence of antagonists; (3) inhibition only by specific histamine antagonists; (4) slope of a Schild-plot not significantly different from unity. For H2-receptors these prerequisites could ideally be fulfilled, especially by the development of highly specific H2-receptor antagonists. However, this new class of compounds acts not only by mere competitive inhibition of histamine at its H2-receptor, but also by activating the metabolism of this secretagogue. A further explanation of the action of H2-receptor antagonists in the treatment of chronic duodenal ulcer may be given by studying the pathogenetic role played by histamine in the development of this disease: duodenal ulcer patients showed an increased liberation of histamine from mucosal mast cell stores as well as a decreased activity of histamine methyltransferase (i. e. longer action of histamine!). The rise in histamine content and histamine methyltransferase activity after vagotomy may be the basis for a biochemical explanation of the acid-reducing effect of this operation.

Animals↗
PubMed1988

Compound 48/80 elicits cholinergic contraction through histamine release in the chick oesophagus.

1. The effects of compound 48/80 on cholinergic nerve transmission and on the liberation of histamine in the isolated chick oesophagus were investigated. 2. Compound 48/80 (0.2-1 microgram ml-1) potentiated the cholinergic nerve-induced contraction and caused the contraction of the oesophagus itself. The latter response was prevented by atropine, tetrodotoxin and mepyramine but not by metiamide. 3. Compound 48/80 released dose-dependently endogenous histamine from the isolated chick oesophagus. 4. These results suggest that the action of compound 48/80 is mediated by the release of histamine from an endogenous pool and that histamine released endogenously facilitates the release of ACh from the intrinsic cholinergic nerve in the chick oesophagus.

Acetylcholine↗
PubMed1963

Rats resistant to the dextran anaphylactoid reaction.

In one colony of Wistar albino rats 23% were resistant to dextran and to egg-white, these animals (non-reactors) failing to show an anaphylactoid reaction after the intraperitoneal or intravenous injection of either of the two substances. Non-reactors were also found in a few other colonies of Wistar rats but not in colonies of other strains. Procedures which potentiated the anaphylactoid reaction in sensitive rats (reactors) did not alter the response of non-reactors. Dextran failed to release histamine from the perfused hind-quarters of non-reactors although other chemical liberators of histamine were effective. Lack of anaphylactoid reaction was not due to a deficiency of skin histamine or 5-hydroxytryptamine, and the blood sugar and serum protein levels of non-reactors were also normal. Non-reactors could be sensitized to antigens and their serum was antigenic to guinea-pigs. It is suggested that non-reactors lack a blood or tissue component with which dextran normally combines to produce an intermediate substance active in releasing amines.

Amines↗
PubMed1993

Neurohormonal regulation of histamine release from isolated rabbit fundic mucosal cells.

Histamine-containing cells isolated from rabbit fundic mucosa were found in a small cell elutriation fraction (cells with diameter about 9-12 microns) enriched in mucus and endocrine cells and containing less than 1% mast cells (F1 cells). Gastrin (HG-17), pentagastrin and CCK-8 (C-terminal octapeptide of cholecystokinin) dose-dependently stimulated histamine release (EC50, respectively, 0.126 +/- 0.03, 0.92 +/- 0.15 and 0.211 +/- 0.025 nM) and somatostatin inhibited this release. PGE1, PGE2 and PGD2 alone were unable to enhance histamine release even at high concentrations but, when used in combination with gastrin of CCK-8, the release of histamine caused by these peptides was potentiated (about 1.5- to 2-fold). Carbachol also enhanced the liberation of histamine but with a weaker potency and efficacy than the gastrointestinal peptides (EC50: 1.50 +/- 0.06 microM). The use of specific muscarinic antagonists for M1-, M2- and M3-type receptors led us to conclude that an M1 receptor might be involved in the muscarinic-induced stimulation of histamine release. Activators of protein kinase C, 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1-oleyl-2-acetyl-glycerol (OAG) as well as the calcium ionophore, A23187, induced histamine release, whereas agents which increased intracellular cAMP content were devoid of effect.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1995

Refilling state of internal Ca2+ stores is not the only intracellular signal stimulating Ca2+ influx in human endothelial cells.

To further analyse the role of the refilling state of internal Ca2+ pools in the stimulation of Ca2+ influx in human endothelial cells, we investigated the combined effect of thapsigargin (TG) and histamine on cytosolic Ca2+ concentration ([Ca2+]i) and inositol polyphosphate production. At normal extracellular Ca2+ levels, TG induced a progressive and sustained elevation in [Ca2+]i which was dose-dependently prevented by pretreatment with 1-10 microM histamine. Similarly, pretreatment with 0.1 and 1 microM TG suppressed histamine-induced Ca2+ transients partially and totally, respectively. TG pretreatment did not alter the inositol triphosphate (IP3) level liberated by histamine, but modified IP3 metabolism by decreasing inositol biphosphate (IP2) and increasing inositol monophosphate (IP1) contents. In the absence of Ca2+ influx, 1 microM TG only induced a small transient increase in [Ca2+]i whereas the Ca2+ mobilization evoked by 10 microM histamine was unchanged. In both cases, the absence of any additional effect of either TG, histamine or 2 microM ionomycin indicated the complete depletion of Ca2+ stores. The re-establishment of the transmembrane Ca2+ gradient induced a transient rise in [Ca2+]i. Its amplitude differed between histamine- and TG-treated cells. It was imposed by cell pretreatment and was selectively affected by changes in the membrane potential. At 5 mM external K+, the transient rise in [Ca2+]i was more marked in histamine- than in TG-stimulated cells; this difference was suppressed by TG pretreatment. The presence of 130 mM external K+ increased Ca2+ entry in TG-treated cells but reduced it in histamine-stimulated cells. These results indicate that the refilling state of internal Ca2+ stores does not constitute the single regulator of Ca2+ influx. TG and histamine seem to activate Ca2+ influx through distinct but interdependent pathways regulated by membrane potential.

Calcium↗
PubMed1991

Aspects of the role of prostaglandins in gastrin histamine regulation of gastric acid secretion.

There is convincing evidence from in vitro studies that prostaglandins interfere with the gastrin histamine regulation of gastric acid secretion in an opposing manner. They can inhibit the action of histamine on the parietal cell when given as single-dose treatment. Conversely, when given at high doses, they liberate endogenous histamine, probably from nonparietal cells. In in vivo experiments prostaglandins are potent inhibitors of acid secretion when studied with single-dose treatment but are capable of stimulating basal acid secretion when chronically applied to rats. Studies performed in whole animal preparations on the effect of cyclooxygenase inhibitors have not fully clarified which of these two histamine-modulating effects of prostaglandins is of prime physiologic significance but favour suppression of histamine activity with subsequent acid inhibition. It appears that somatostatin release is the mechanism through which prostaglandin can simultaneously inhibit acid secretion and release plasma gastrin. At least in the rat, the pattern of plasma gastrin and somatostatin release is, similarly to acid secretion, partly reversed during prolonged prostaglandin treatment.

Animals↗
PubMed1984

Histamine-releasing activity (HRA). III. HRA induces human basophil histamine release by provoking noncytotoxic granule exocytosis.

Histamine-releasing activity (HRA) is an approximately 10,000-15,000 dalton, protease-sensitive factor that induces the rapid liberation of histamine from human basophils. Production of HRA by human peripheral blood mononuclear cells in vitro is augmented by concanavalin A or antigen, suggesting a mechanism whereby lymphocytes may regulate basophil mediator release in vivo. In order to determine whether HRA provokes conventional exocytosis of basophil granules or, alternatively, results in mediator release by some other mechanism such as vesicular transport or cytotoxicity, we investigated the ultrastructural features of human blood basophils purified over Percoll and exposed to HRA in vitro. HRA preparations induced a noncytotoxic pattern of basophil degranulation very similar to that previously observed in basophils triggered to release histamine in response to specific antigen, C5a, or mannitol. Thus, cytoplasmic granules were extruded singly through multiple separate points of fusion between perigranular membranes and the plasma membrane. Degranulating basophils exhibited plasma membrane activation but lacked a polarized configuration. By contrast, those basophils exposed to HRA that did not exhibit evidence of degranulation displayed a single elongated cellular process. The development of this polarized cellular configuration, similar in some respects to that of uropod-bearing motile guinea pig basophils, may have reflected chemokinetic or chemotactic effects of preparations containing HRA activity.

Antigens↗
PubMed2002

IL-6 enhances IgE-dependent histamine release from human peripheral blood-derived cultured mast cells.

We examined whether interleukin (IL)-6 exerts the stimulatory effects on the secretion of histamine from human mast cells triggered by crosslinking of the high affinity IgE receptor (FcepsilonRI) with IgE and anti-IgE. As target cells, we used peripheral blood-derived cultured mast cells grown with SCF, because they were superior in FcepsilonRIalpha expression to cord blood-derived mast cells. Incubation with SCF+IL-6 for 1 week increased the IgE-dependent release as well as intracellular content of histamine in the cultured mast cells, as compared with the values obtained by incubation with SCF alone. The magnitude of these increases was higher than that for priming with SCF+IL-4. A striking difference was also found in the expression of FcepsilonRIalpha between the two-factor combinations. The addition of IL-6 during FcepsilonRI crosslinking with IgE/anti-IgE in the presence of SCF did not influence histamine secretion. When SCF, IL-6 and IL-4 were used together, a further increase was observed in the anti-IgE-dependent liberation of histamine from the cultured mast cells, compared with the two-factor combinations. These results suggest that IL-6 functions as a secretagogue for the inflammatory mediator of human mast cells in the presence of SCF.

Histamine↗
PubMed2005

Effect of combined histamine H1 and H3 receptor blockade on cutaneous microvascular permeability elicited by compound 48/80.

The pharmacological consequences of combining a histamine H1 receptor antagonist with a H3 antagonist on cutaneous microvascular permeability due to intradermal (i.d.) injections of compound 48/80, a mast cell liberator of histamine, was studied in the anesthetized guinea pig. Compound 48/80 (0.0003, 0.001, 0.003 and 0.01%) induced permeability responses were attenuated, as determined by Evans blue extravasation, in animals pretreated with the H1 antagonist, chlorpheniramine (CTM; 1.0 mg/kg, i.v.) by 17 +/- 4, 31 +/- 4, 32 +/- 4 and 37 +/- 4%, respectively. Combination treatment with an H1 and H3 antagonist displayed greater inhibitory efficacy against the effects elicited by compound 48/80. Specifically, combined treatment with CTM (1.0 mg/kg, i.v.) and the H3 antagonist, thioperamide (THIO 1.0 mg/kg,i.v.) inhibited the skin responses of i.d. compound 48/80 (0.0003, 0.001, 0.003 and 0.01%) by 36 +/- 4, 45 +/- 4, 49 +/- 4 and 54 +/- 4%. A second H3 antagonist, clobenpropit (CLOB; 0.3 mg/kg, i.v.) plus CTM (1.0 mg/kg, i.v.) also inhibited Evans blue extravasation. Treatment with THIO (1.0 mg/kg, i.v.) and CLOB (0.3 mg/kg, i.v.) administered alone had no effect on compound 48/80-induced skin responses. We conclude that combination administration of a H1 and a H3 histamine receptor antagonist produces greater inhibitory effect on cutaneous microvascular permeability produced by released mast cell-derived histamine than either a H1 or H3 antagonist administered separately. In addition, the antiallergy activity of combining a H3 antihistamine with a H3 antagonist activity might provide a novel approach for the treatment of allergic skin diseases such as urticaria.

Animals↗
PubMed1982

Histamine and epidermal proliferation.

Histamine is liberated in the inflammatory reaction and has been reported to inhibit epidermal cell division in vitro. This study has investigated the effects of histamine and HI and H2 antagonists on epidermopoiesis in vivo in man. No direct stimulatory effect of histamine was detected for normal epidermis. A combination of HI antagonist (chlorpheniramine) and H2 antagonist (cimetidine) led to further increases in epidermal labelling indices in mitotically stimulated epidermis. The administration of HI antagonist alone led to a decrease in mean epidermal thickness. These data suggest that histamine release is unlikely to play a major role in the hyperplasia of inflammatory dermatoses, but that it may be possible to influence epidermal reactions via the HI and H2 receptors.

Adult↗
PubMed2004

Opioid-induced mast cell activation and vascular responses is not mediated by mu-opioid receptors: an in vivo microdialysis study in human skin.

UNLABELLED: Activation of mast cells and the systemic release of histamine is a common side effect of opioids. Nevertheless, fentanyl and its derivatives show only a slight activation of mast cells with a subsequent liberation of histamine and tryptase. In this study, we used intradermal microdialysis to assess whether this stimulatory effect of opioids on mast cells depends on the activation of opioid receptors. This new approach allowed us to measure the dose-dependent release of histamine and tryptase from mast cells and the subsequent vascular and sensory effect without systemic side effects in volunteers. The opiate codeine and the synthetic opioids meperidine, fentanyl, alfentanil, sufentanil, remifentanil, buprenorphine, and the opioid antagonist naloxone were tested. Only codeine and meperidine induced mast cell activation with the release of tryptase and histamine, leading to protein extravasation, flare reactions, and itch sensations. Because naloxone did not attenuate these effects, it is unlikely that mu-opioid receptors are involved in the activation of mast cells. IMPLICATIONS: Opioid effects on mast cells were assessed using intradermal microdialysis. Mast cell activation was seen with codeine and meperidine; no other opioid induced degranulation. Therefore, histamine release seen at large concentrations of potent micro agonists is caused by an unspecific effect rather than an activation of opioid receptors.

Adult↗
PubMed1994

Staurosporine inhibits the anaphylactic reaction of the isolated guinea-pig heart.

Isolated hearts from ovalbumin sensitized guinea-pigs were perfused according to Langendorff. Ovalbumin injection decreased coronary flow. Left ventricular pressure amplitude and heart rate increased initially and decreased thereafter. Concomitantly, the liberation of histamine, prostaglandin F2 alpha, as well as the sum of leukotrienes C4/D4/E4/F4, measured in the perfusate by radioimmunoassay, was augmented. Staurosporine (1 microM), an inhibitor of protein kinases, did not influence the liberation of mediators in response to antigen challenge, but inhibited all mechanical responses. Infusion of phorbol myristate acetate, an activator of protein kinase C, into non-sensitized hearts decreased coronary flow and left ventricular pressure amplitude, but did not liberate mediators. Staurosporine (1 microM) abolished these mechanical responses. The results indicate that staurosporine suppresses cardiac anaphylaxis by blockage of mediator effects rather than by inhibition of liberation or formation of mediators.

Alkaloids↗
PubMed1979

Vagus nerves and the gastric tissue histamine concentration in pylorus ligated albino rats.

Gastric tissue histamine concentration was determined, 6 and 16 hours after pylorus ligation in vagus intact and vagotomized albino rats and the results were compared with those of respective control animals, sacrificed, 6 and 16 hours after ether anaesthesia alone. The gastric tissue histamine concentration of rats subjected to none of the experimental situations was also determined and taken into comparison. The results show that the stress of pylorus ligation reduced the gastric tissue histamine concentration, the reduction being more with increased duration of stress. On the other hand, subdiaphragmatic vagtomy preserved the histamine concentration of gastric tissue irrespective of the duration to which the animals were exposed following pylorus ligation. It appears that increase in vagal discharges during stress leads to increased liberation of histamine from the gastric wall, thereby, reducing the gastric tissue histamine concentration; the reduction being proportional to the duration of stress and increase in vagal discharges, whereas, in the absence of vagal impulses following subdiaphragmatic vagotomy, the gastric tissue histamine concentration is preserved in spite of the stress to which the animals were exposed.

Animals↗
PubMedDate not supplied

Antianaphylactic and antiasthmatic properties of new piperazinyl 7-(beta-hydroxypropyl)-theophylline derivatives in guinea pigs.

The present studies have demonstrated that new piperazinyl 7-(beta-hydroxypropyl)-theophylline derivatives (R3, R6, R7) possess antihistamine, antianaphylactic and antiasthmatic properties. The compound R6 exerted especially pronounced selective protective action in experimental histamine asthma and provided effective prevention against anaphylactic shock in guinea pigs. The evidence was also presented that compound R6 inhibited in vitro mast cell degranulation induced by the preparation 48/80 liberating endogenous histamine. It was shown that the compound R6, i.e. 7-beta-hydroxy-gamma-[N1-(N4-benzyl)-piperazinyl)-theophylline efficiently competed with histamine of both endo- and exogenous origin and inhibited the mediator release from the mast cells.

Anaphylaxis↗