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At least 613 records · Page 34Linked to original sources
PubMed1984

Histamine disposition in endothelial specific granules of the toad aorta.

High-performance liquid chromatography revealed that toad aorta delivered appreciable concentrations of histamine into the perfusate when perfused by Ringer's solution containing the histamine liberator. Electron micrographs of this vessel after the perfusion showed an expulsion of the endothelial specific granules into the vascular lumen. These results support to our previous hypothesis that the granules are a reservoir site of histamine and might take an important role in the regulation of vascular tone.

Animals↗
PubMed1989

The effect of gastrin-releasing peptide on acid secretion and the release of gastrin, somatostatin, and histamine in the totally isolated, vascularly perfused rat stomach.

We have studied the effect of gastrin-releasing peptide (GRP) on exocrine and endocrine secretion in the totally isolated, vascularly perfused rat stomach with or without concomitant infusion of a potent somatostatin antiserum. GRP (1 nM) showed a marginal acid-stimulatory effect (base line, 11.6 +/- 2.3 mumol/60 min, and after GRP, 20.0 +/- 2.2 mumol/60 min; p = 0.05). GRP significantly increased gastrin and somatostatin release to the venous effluent, and the venous gastrin concentration increased significantly during concomitant infusion of somatostatin antiserum. Furthermore, GRP inhibited histamine liberation, and somatostatin antiserum reversed this effect. The antiserum did not significantly stimulate acid secretion. Thus, the present study shows that GRP directly or indirectly affects both acid secretion and the release of gastrin, somatostatin, and histamine in the rat stomach.

Animals↗
PubMed1989

[Mast-cell mechanism of the pathogenesis of bronchial asthma and peroxidation of membrane lipids].

Examination of 155 patients with atopic, infection-dependent bronchial asthma (BA) and chronic asthmatic bronchitis in the phase of the disease exacerbation and remission has shown that hyperhistaminemia is common not only to atopic but also to infection-dependent BA. It is established that activation of lipid peroxidation of the membranes more pronounced during exacerbation and attacks of asthma is one of the most important alternative mechanisms of mast cell activation, that is supported by the data of experimental morphologic and biochemical studies of the effect exerted by peroxidized fatty acids on histamine liberation and mast cell degranulation.

Adult↗
PubMed1983

A comparison of histamine secretion from isolated peritoneal mast cells of the mouse and rat.

The effect of different histamine liberators on isolated peritoneal mast cells of the mouse and rat has been examined. Both cell types responded to the lectin, concanavalin A, and the release was in each case potentiated by phosphatidylserine. The rat cells released histamine on treatment with dextran but the mouse cells were essentially refractory to the polysaccharide. The mouse cells were significantly more responsive to the actions of the ionophore A23187 and adenosine 5'-triphosphate but much less reactive towards the polycations, compound 48/80 and peptide 401 (the MCD-peptide from bee venom). The reactivity of the mouse cells towards the latter two agents was enhanced in the absence of extracellular calcium. These results further emphasize the functional heterogeneity of mast cells from different sources.

Adenosine Triphosphate↗
PubMed1976

Induced tolerance in cold urticaria caused by cold-evoked histamine release.

The interrelations between cold sensitivity and release of histamine and other mediators in five patients with cold urticaria undergoing cold tolerance treatment were studied. Tolerance to cold was produced in all patients by repeated cold exposure. In four patients tolerance was maintained by once daily exposures. In the fifth patient 4-hourly exposures were necessary. Cold sensitivity was associated with histamine release in venous blood draining urticated skin. No prostaglandin activity was detected, and low concentrations of kinin activity were found in blood draining the normal and exposed skin of healthy subjects as well as in patients with cold urticaria. After induction of tolerance, no histamine release occurred on challenge by cold. Relapse of sensitivity was associated with reappearance of histamine release on challenge. The conclusion that tolerance is due to depletion of histamine stores in skin after repeated cold exposure was supported by diminished wealing in response to injection of a histamine liberator (compound 48/80) in cold-tolerant skin.

Adolescent↗
PubMed1976

Effect of bilateral adrenalectomy and parenteral betamethasone on gastric mucosal mast cell population in albino rats.

The histamine-laden mast cells of gastric mucosa in albino rats are shown to degranulate on administration of Betamethasone, but they increase in number in adrenalectomized rats. It is concluded that Betamethasone, and also adrenal glucocorticoids increase gastric secretion by liberating histamine from mast cells and histamine in turn acts on the gastric glands.

Adrenalectomy↗
PubMed1993

Antarelix (EP 24332) a novel water soluble LHRH antagonist.

A novel water soluble LHRH antagonist (EP 24332-Antarelix) is described. Its activity in vitro and in vivo in several animal models is given. Antarelix (Ac-D-Nal, D-Cpa, D-Pal, Ser, Tyr, D-Hci, Leu, Lys-(iPr), Pro, D-Ala-NH2) in view of its potency, modest histamine-liberating activity and high water solubility has been selected for further development.

Animals↗
PubMed2000

Morphine-induced cardiovascular stimulation: the effects of two doses on healthy subjects.

UNLABELLED: In humans, morphine induces hypotension, probably because of histamine liberation. Earlier animal studies have, however, suggested that morphine can induce immediate cardiovascular stimulation when given as a sole medication. The aim of this study was to evaluate the initial effects of morphine on circulation, oxygen consumption, and plasma histamine and catecholamine concentrations. Oxycodone was used as a reference drug. Eight healthy volunteers received, in a random, cross-over, double-blinded fashion: 0.07 mg/kg morphine (M1); 0.14 mg/kg morphine (M2); 0.14 mg/kg oxycodone (O); and placebo (P) as a 2-min IV injection for pain. Mean arterial blood pressure (MAP), heart rate (HR), and oxygen consumption (VO(2)) were recorded. Plasma histamine and catecholamine concentrations were determined. Both M1 and M2 elicited an initial, but transient, increase in MAP from 84 +/- 5 to 96 +/- 9 mm Hg (P < 0.05) and from 83 +/- 8 to 100 +/- 10 mm Hg (P < 0.05), respectively. A parallel increase in HR was also seen after M1 (from 62 +/- 12 to 70 +/- 10 bpm, P < 0.05) and M2 (from 67 +/- 9 to 78 +/- 8 bpm, P < 0.05). After M2, this was accompanied by a simultaneous increase in VO(2) from 295 +/- 39 mL/min to 322 +/- 61 mL/min (P < 0.05). After O, as well as P, no increase in MAP or HR was detected. Plasma histamine and catecholamine concentrations were not clearly affected by any of the treatments. We conclude that the immediate effect of morphine on the hemodynamics of healthy volunteers was stimulation, not hypotension. This effect was not seen in conjunction with oxycodone, a morphine-like mu-receptor agonist. IMPLICATIONS: In this double-blinded, randomized study, we evaluated whether morphine could induce immediate cardiovascular stimulation, as seen previously in animal studies. In healthy volunteers, during a painful stimulus, morphine caused an initial, transient hemodynamic stimulation, accompanied by increased oxygen consumption, without detectable release of histamine or catecholamines into the plasma. Oxycodone caused only minor hemodynamic alterations.

Adult↗
PubMed1979

Histamine release and complement changes following injection of contrast media in humans.

Mechanisms responsible for allergic-like reactions following administration of radiographic contrast media (RCM) are unclear. Aortic root blood specimens were obtained sequentially in 6 subjects following injection of RCM into the pulmonary artery during cardiac catheterization. In 5 subjects, elevated plasma histamine levels (up to 80 ng/ml) occurred within minutes. Levels of C3, C4, factor B, and total hemolytic complement activity were decreased in the same specimens. No hemodynamic or clinical abnormalities were noted. These findings support the concept that RCM can liberate histamine in vivo in humans. Complement alterations may be related to localized RCM-protein interaction. It is unclear whether complement changes are related to the RCM-induced allergic mediator release.

Adult↗
PubMed1983

Histamine release into tracheal lumen and bronchial reactivity. Effect of compound 48/80 administered by different routes in various doses on histamine release and bronchial reactivity.

The influence of tracheal lavage with compound 48/80 on the bronchial response to challenge with ACH and AE was studied in 24 animals. Furthermore, the effect of i.v. administration of 48/80 was compared to its administration into the tracheal lumen. No increased histamine liberation was detected in the tracheal fluid after lavage with 48/80, nor was an influence on the bronchial response observed. These observations were the same as those described for tracheal lavage with water. The same amounts of this secretagogue induced, after i.v. administration, a high histamine release which correlates significantly with blood pressure decrease.

Acetylcholine↗
PubMed1979

Synthetic peptides comprising sequences of the human immunoglobulin E heavy chain capable of releasing histamine.

On the basis of previous studies on the structure-activity relationship of model polypeptide histamine liberators, a site within the Fc region of immunoglobulin E antibody molecules has been proposed as that responsible for the direct triggering of target mast cells after antigen challenge. Peptides comprising this region of the epsilon-chain have now been synthesized and shown to induce histamine release from normal rat peritoneal mast cells in a selective manner essentially similar to that mediated by anaphylactic antibody-antigen interaction.

Animals↗
PubMed1999

The antipruritic effect of a 5-HT3 receptor antagonist (tropisetron) is dependent on mast cell depletion--an experimental study.

The background of this study is that 5-HT3 receptor antagonists are reported to have an antipruritic effect in uremic and cholestatic pruritus. Recently, we could not confirm such an effect in healthy subjects under experimental conditions. Therefore, it was the aim of the present study to further evaluate a possible antipruritic effect of a 5-HT3 receptor antagonist (tropisetron) on serotonin- and histamine-induced itch before and after skin mast cell depletion in 10 healthy subjects. The results were compared to serotonin and histamine iontophoresis in non-pretreated and pretreated skin with an orally applied antihistamine (cetirizine). Skin mast cell depletion was performed by iontophoretical application of compound 48/80. Wheals and flares were planimetrically evaluated. Itching and burning sensations were rated on an analog scale over a 24-min period. The test protocol also comprised alloknesis, defined as induction of perifocal itch sensations by a mechanical stimulus. When serotonin was iontophoretically applied after mast cells had been depleted before, oral tropisetron resulted not only in significantly lower whealing, itching and alloknesis but also reduced flares. In contrast, after oral pretreatment with tropisetron histamine-induced reactions before and after mast cell depletion did not significantly change. Our study demonstrates that in this model, tropisetron as a 5-HT3 receptor antagonist does not effect histamine-induced itch but has a measurable effect in serotonin-induced reactions when mast cells were depleted before. From these data evidence now exists why tropisetron is to some extent effective in certain types of pruritus such as uremic pruritus, known for increased histamine liberation and increased serotonin levels as well as degranulated and diffusely spread mast cells in the skin.

Adult↗
PubMed1992

Influence of nitrovasodilators on bovine pulmonary histamine release.

The organic nitrates and related nitrovasodilators are relaxants of vascular and airway smooth muscle. Very little information is currently available regarding the influence of nitrates and related nitrovasodilators on pulmonary autacoid release. This study examined the influence of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside on histamine release from bovine lung mince. Spontaneous histamine release from bovine lung mince was not altered by 0.1 nM to 1 microM glyceryl trinitrate, isosorbide dinitrate or sodium nitroprusside. Glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside produced a concentration-dependent decrease in A23187 (10 microM) stimulated histamine release. Glyceryl trinitrate also inhibited histamine liberation following the addition of compound 48/80. Further studies indicated that the inhibitory action of glyceryl trinitrate was reversed by coincubation with the guanylate cyclase inhibitor, methylene blue (10 microM). These findings indicate that glyceryl trinitrate, sodium nitroprusside and isosorbide dinitrate inhibit non-immunologically stimulated pulmonary histamine release and suggest that alterations in guanylate cyclase activity may influence pulmonary histamine release.

Animals↗
PubMed1982

Effect of ketotifen and oxatomide on histamine secretion from mast cells.

The anti-histaminic drugs ketotifen and oxatomide have a dual effect on rat peritoneal mast cells. At high concentrations they induce histamine release, whereas at low concentrations they inhibit secretion evoked by IgE-directed ligands. The latter effect is observed in the presence and absence of exogenous calcium. The significance of this result for the general mode of action of anti-anaphylactic drugs is discussed. Neither compound liberates histamine from isolated mesenteric cells from the rat or guinea pig, further emphasizing the functional heterogeneity of mast cells from different sources.

Animals↗
PubMed1983

[Current data of occupational asthma].

The problem of occupational asthma is in state of change as evidenced by the official reports: The official Journal of the 23 January 1982 contains important alterations in the lists of occupational asthma, changing some and creating others, as with table 66 in which numerous occupational allergies are listed. The authors discuss current diagnostic methods in which realistic provocation tests play an important part; current causes are considered and are duly allocated between natural animal or vegetable products or chemicals produced by industry. The authors strive to define which aetiologies are declining and which remain every day problems. Occupational asthma should be treated at source though the offending agent is not always apparent. The mechanism may be allergic, or often non allergic histamine-liberation or other pharmacodynamic mechanisms. Finally, the understanding of occupational asthmas throws light on the mechanism of asthma itself.

Adult↗
PubMed1984

Effects of topically applied clobetasol-17-propionate on histamine release in human skin.

The effects of topical glucocorticoid treatment on histamine responses and histamine release induced by the histamine liberating agent compound 48/80 were studied in 17 healthy volunteers. The potent glucocorticoid ointment clobetasol-17-propionate was applied on one upper arm of each individual 14, 4 and 2 hours before testing. The other arm was treated in the same way with the corresponding vehicle. Solutions of histamine and compound 48/80 were injected intradermally in both arms. The size of the flare reaction and the duration of the itch response were recorded. It was found that the flare reactions evoked by histamine were slightly (p less than 0.05) reduced on the steroid-pretreated arm whereas the responses to compound 48/80 were much more suppressed (p less than 0.01). Glucocorticoid treatment did not influence the itch responses to histamine while the itch duration following injection of compound 48/80 was significantly reduced in steroid-treated skin compared to control skin. Our results indicate that topical glucocorticoid treatment can suppress histamine release from dermal mast cells in man.

Adult↗
PubMed1984

Effect of neonatal treatment with capsaicin on carrageenan-induced paw oedema in the rat.

The time course of the paw oedema induced by the subplantar injection of carrageenan was studied in rats treated neonatally with capsaicin and in their vehicle-treated controls. In the capsaicin-treated rats, which show a permanent deficit of unmyelinated primary sensory neurones, carrageenan produced an oedema which was larger and lasted longer than in the vehicle-treated rats. Pretreatment with the histamine liberator compound 48/80 reduced the carrageenan-induced paw oedema only in the capsaicin-treated rats whereas pretreatment with indomethacin reduced it in both groups of rats. The increased and prolonged inflammatory response to carrageenan in capsaicin-treated rats may be explained by an enhanced release of histamine from mast cells and may also reflect a 'trophic disorder of the denervated skin'.

Animals↗
PubMed1989

Comparison of histamine assay methods in measuring in vitro-induced histamine release in patients with allergic rhinitis.

histamine release tests using whole blood were applied in testing in vitro Type I birch allergic reaction in two patients with allergic rhinitis. Heparinized blood was incubated with varying dilutions of allergen for 30 min at +37 degrees C. After centrifugation of the blood, plasma was separated and the liberated histamine was analysed by histamine radio enzyme assay (REA), high performance liquid chromatography (HPLC) with post-column derivatization system or radio immuno assay (RIA), and the results obtained by these methods were compared. REA and HPLC gave similar results, while RIA gave somewhat higher values, but was less sensitive.

Adolescent↗