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PubMed2001

Differential response of mast cells separated from various organs and basophils of dogs to the fluoroquinolone antimicrobial levofloxacin.

Histamine releases induced by the fluoroquinolone antimicrobial levofloxacin (LVFX) were investigated using mast cells separated from various organs and peripheral basophils of dogs, being the most susceptible species to quinolone derivatives, in both in vivo and in vitro systems. An intravenous infusion of LVFX at 30 mg/kg over a 30-min period produced endogenous histamine release from 5 min, and a maximum at 30 min, in which the plasma LVFX concentration was approximately 50 microM. A close correlation (r = 0.87, n = 20) between histamine and LVFX concentrations in plasma during the infusion was observed. In the in vitro study, LVFX at 30 microM or more caused histamine release from mast cells separated from the liver and skin, but not from the gastric mucosa, lung, and peripheral basophils. More exactly, the liver mast cells were most susceptible to LVFX among the organs tested. On the other hand, compound 48/80, a prototype histamine liberator, elicited the histamine release from the liver or skin mast cells at 10 microg/ml, and the calcium ionophore A23187 at 1 microM exhibited the histamine release from the mast cells derived from all organs examined. Histochemical analysis revealed that the liver and skin mast cells had positive reaction for both alcian blue and safranin staining, but the gastric mucosa and lung mast cells were only positive for alcian blue staining, indicating that LVFX preferably activated the connective tissue-type mast cells rather than the mucosal-type mast cells. The degranulation of the liver and skin mast cells brought about by either LVFX or compound 48/80, unlike the calcium ionophore A23187, was blocked by pretreatment with pertussis toxin, suggesting the involvement of pertussis toxin-sensitive G proteins. The results obtained from the canine experiments strongly suggest that LVFX induces histamine release from the connective tissue-type mast cells distributed mainly in the liver, somewhat in the cutaneous tissue, through the activation of pertussis toxin-sensitive G proteins.

Animals↗

PubMed1986

Modulation of histamine release from rat peritoneal mast cells by non-cytotoxic concentrations of the detergents Cremophor El (oxethylated castor oil) and Triton X100. A possible explanation for unexpected adverse drug reactions?

Clinically relevant histamine release caused by drugs and/or their solvents is a well known phenomenon. The mechanisms whereby these reactions occur are largely unknown. It was thought that the solubilizing agents potentiate the histamine release elicited by the drugs. Therefore the ability of the two detergents, Cremophor El and Triton X100, to modulate histamine release from rat peritoneal mast cells was examined. Both detergents were used in concentrations that did not themselves induce histamine release. The addition of the detergents to incubation media containing compound 48/80 (0.1 microgram/ml) elevated the release considerably (48/80 alone = 16.2 +/- 2.1% (n = 3); plus Cremophor El (5%) = 41.1 +/- 3.3% (n = 4); plus Triton X100 (0.02 microliter/ml) = 39.7 +/- 3.9% (n = 3); plus Triton X100 (0.01 microliter/ml) = 33.4 +/- 5.0% (n = 3)). In contrast, histamine release induced by Concanavalin A or the calcium ionophore A 23187 was inhibited by both detergents. Thus low concentrations of detergents appear to have a dual role, with both potentiation and inhibition of histamine release being observed. Surgical patients receive many drugs, some soluble in aqueous solutions, others only with the aid of solubilizing agents. 'Hangover effects' due to different plasma half lives, may therefore cause a seemingly harmless drug to act as a histamine liberator. It is therefore important to examine the action of clinically used solvents on histamine liberation caused by therapeutic agents, in order to gain a further understanding of the reaction mechanisms of adverse reactions to drugs.

Animals↗

PubMed1976

[In vivo blood histamine during anesthesia].

The authors studied the variations in histaminaemia in the plasma on the one hand, and in whole blood on the other hand: In volunteers:-after administration of histamine in an intravenous infusion ranging from 18 to 90 ng/min/kg;-after administration of thiopental, methohexital and propanidide. In volunteers, by means of the different parameters measured, the authors found that the mean plasma concentration was 0.69 +/- 0.26 ng/ml. In the whole blood, the histaminaemia was 54 +/- 18 ng/ml. The perfusion of histamine up to 45 ng/kg/min led to no symptomatology in 3 volunteers. Propanidide led to an average increase of 350 p. 100 in the initial normal figure of plasma histaminaemia approximately 5 minutes after the beginning of the injection. But there is no agreement between the figures obtained and the clinical signs (tachycardia, mild hypotension). The injection of thiopental led to an analagous symptomatology: i.e. tachycardia and mild hypotension, arising before the maximum increase in plasma histaminaemia. Methohexital, and althesin are also histamine-liberators. Only estomidate, a new pure hypnotic product as yet not commercialised, did not lead to histamine-liberation.

Basophils↗

PubMed1981

Studies on pruritogenic and histamine-releasing effects of some putative peptide neurotransmitters.

Pruritus, whealing and axon-reflex erythema appeared in human skin after intradermal injection of (i) several peptides with a putative transmitter function, i.e. vasoactive intestinal polypeptide (VIP) (10(-7)--10(-4) M), [Gln4]-neurotensin (10(-7)--10(-4) M), neurotensin (10(-5)--10(-4) M) and secretin (10(-5)--10(-4) M), which were compared with substance P (10(-7)--10(-5) M) previously shown to be one of the most potent histamine liberators when administered intradermally in humans; (ii) the basic polypeptide protamine (10(-7)--10(-4) M); and (iii) histamine (0.3-10 micrograms/ml) and the histamine liberator compound 48/80 (0.3-10 micrograms/ml). The reactions were inhibited in a dose-related manner by the antihistamine mepyramine, indicating that the peptide-induced responses were mediated by released histamine. This was further confirmed by the histamine release observed when the peptides were incubated with rat peritoneal mast cells. In human skin, VIP was more potent than the other neuropeptides and had roughly the same potency as substance P. The two adjacent basic amino-acid residues and the amide substitution of the terminal C-group of VIP, in addition to its strong net basic charge, may explain its potency as a histamine releaser.

Adolescent↗

PubMed1985

The effect of compound 48/80 on the carbachol-evoked acid secretion of the isolated mouse stomach.

The aim of the present work was to determine in the isolated mouse stomach whether the depletion of mast cell histamine by compound 48/80 influences the acid secretion, evoked by carbachol. Each effect of carbachol was compared to the effect of histamine (10(-6) M), applied after each carbachol application. After carbachol and histamine, compound 48/80 was applied twice or three times successively; the second and the third application were not able to evoke any secretion. After 48/80, the applications of carbachol and histamine were repeated and their effects compared to those before the applications of compound 48/80. Three concentrations of the compound were used: 20, 100 and 500 micrograms/ml. The lowest concentration of the histamine liberator did not significantly change the response to carbachol, The highest one reduced it but the effect of histamine was reduced, too. Compound 48/80 in concentration 100 micrograms/ml significantly augmented the secretory effect of carbachol. The possible explanation for this effect is that histamine, liberated from mast cells, is taken up by some other cells in the tissue from where it is liberated by carbachol stimulation.

Animals↗

PubMed1989

The role of membrane bound sialic acid of rat mast cells in histamine release induced by compound 48/80 and derivatives as well as calcium.

Histamine release induced by compound 48/80 from rat mast cells is not dependent on extracellular Ca2+. Preincubation of mast cells with trypsin has only little effects on histamine release induced by this polycation. This work also demonstrates that histamine release induced by compound 48/80 and its analogues in the absence of extracellular Ca2+ depends on membrane bound sialic acid of the mast cell. Neuraminidase treatment of the cells in the presence of extracellular Ca2+ leads to histamine liberation. These findings suggest that sialic acid residues of the mast cell membrane constitute the site at which polycations exert their stimulatory actions of histamine liberation.

Animals↗

PubMed1981

The effect of concentration on the binding of compound 48/80 to rat mast cells: a fluorescence microscopy study.

A fluorescent analog of the chemical histamine liberator, compound 48/80, has been synthesized by the covalent attachment of rhodamine to the 48/80 polymer (R-48/80). The histamine liberating characteristics of this analog were similar to those of the parent compound. The binding characteristics of R-48/80 to rat peritoneal mast cells were then studied using fluorescence microscopy. At concentrations that caused minimal secretory stimulation (less than 1.0 microgram/ml), R-48/80 bound to the mast cell surface in a diffuse manner, with no indication of patching or capping. When the cells were incubated at higher concentrations, where non-cytotoxic histamine secretion was stimulated, the drug bound heavily to the exposed granules, but not to unexposed granules or other cell organelles. At cytotoxic concentrations, R-48/80 caused extensive cell clumping, with the drug bound to masses of cell debris and released granules. Therefore, although R-48/80 binds initially to the cell membrane, its primary binding site at concentrations that induce secretion becomes the mast cell granule. The properties of these granules should thus be considered when studying the binding of compound 48/80 or other cationic drugs to rat peritoneal mast cells.

Animals↗

PubMed1980

Thermographic analysis of skin test reaction using AGA thermovision.

The course of infrared thermography including isothermograms on the skin surface was investigated considering blood flow, redness of the skin and permeability of blood vessel, in the following skin reactions: 1. Intracutaneous injection of histamine and histamine liberator compound 48/80 increased the heat radiation. Local application of antihistamine externa which decreased the development of the urticarial histamine reaction, increased the infrared radiation of the skin surface. Combined injection of histamine or histamine liberators with antihistamines in a sufficient dosis (1:1 respectively 4:1) diminished also the heat radiation in addition to the urticarial reaction. 2. The Pyrexal reaction of the skin with early erythema and later papule development shows an equivalent picture in the AGA Thermovision. The pretreatment shows an equivalent picture in the AGA Thermovision. The pretreatment of the skin with corticosteroid ointments shows a corresponding lowering of the erythema, of papule development as well as of heat radiation. The blanching of corticosteroids after occlusive dressing is difficult to recognize by the isotherms of AGA Thermovision. 3. Allergic reactions of the immediate type show, corresponding to the wheal eruption, a marked increased of heat radiation combined with a projection of the enlarged veins on the skin surface. 4. Allergic reactions of the delayed type are combined with a definite elevation of heat radiation of the skin. The area of a positive skin test with allergic eczematous reaction shows a distinct elevation of ann infrared radiation. Although the allergic skin area which was substantiated by a positive skin test was no longer visible, a distinct infrared radiation could be detected. Preventive treatment of the test area of skin patch-testing with corticosteroids inhibits the heat radiation even if the allergic eczematous reaction occurs faintly. The thermographic analysis of the different skin test reactions complied with the morphological aspects of the reaction.

Dermatitis, Atopic↗

PubMed1974

The release of histamine during gastric acid secretion in conscious rats.

1. Conscious gastric-cannulated rats were given [(3)H]histidine and aminoguanidine by dosage procedures intended to build up fast-turnover and slow-turnover pools of tissue [(3)H]histamine. Acid secretion was stimulated by I.V. infusion of pentagastrin, and the [(3)H]histamine content of gastric juice and excretion in urine were determined at 30 min intervals.2. The amount of [(3)H]histamine in gastric juice derived from either a slow-turnover or fast-turnover pool was very low in unstimulated animals, and was not altered during pentagastrin-stimulated acid secretion.3. From a slow-turnover pool pentagastrin caused increased urinary excretion of [(3)H]histamine. This was abolished by gastrectomy, so that the [(3)H]histamine liberated by pentagastrin from this pool appears to have been derived from the stomach. Evidence was not found for the existence of a slow-turnover histamine pool in the glandular mucosa of the stomach, and the source within the stomach of this pentagastrin-liberated histamine is thus uncertain.4. From a fast-turnover pool pentagastrin did not cause an increased urinary excretion of [(3)H]histamine. The amount of [(3)H]histamine excreted by gastrectomized rats was not different from that produced by gastric-cannulated animals. This suggests that a high proportion of urinary histamine derived from a fast-turnover pool was non-gastric in origin.5. Differences in the time scale of [(3)H]histamine release and acid secretion were not found. In some experiments the urinary output of [(3)H]histamine was prolonged beyond the end of pentagastrin administration and gastric acid secretion. However, the overall data do not suggest that urinary histamine output and gastric acid secretion take different time courses.

Animals↗

PubMed1975

The effect of specific brain phospholipid on the rat's allergic encephalomyelitis.

A new preparation which contains specific brain phospholipids (Gricertine) acts as a histamine liberator in CNS and protects rats from allergic encephalomyelitis. It is supposed that the protective effect of Gricertine on the allergic encephalomyelitis is based on its histamine-liberator properties which can occur during the first days of therapy: this would explain the large decrease of the brain histamine after 3 weeks of treatment. Gricertine is also able to remove clinical symptoms of allergic encephalomyelitis in rats. It is presumed that Gricertine may also be acting independently of that mechanism, in the way that it replaces phospholipids that disappeared in the cases where demyelinisation had taken place.

Animals↗

PubMed1996

Release of histamine in whole blood by oxygen radicals: division between specific and unspecific processes.

Oxygen derived free radicals are involved in many pathological processes such as postischemic reperfusion injuries, hepatotoxicity of drugs and inflammatory processes. Thereby these oxygen radicals induce lipid peroxidation and perturbation of cellular membranes. The aim of our present study was to determine whether oxygen radicals generated by the xanthine oxidase/ hypoxanthine system cause a release of histamine in human blood cell cultures. Stimulation of blood cell cultures with oxygen radicals induced a histamine liberation which was mainly due to calcium independent processes during the first 30 min, whereas then calcium requiring processes took part in the release of histamine. The regulation of the leukocyte selection LECAM-1 was altered by oxygen radicals whereas histamine, which is known to modulate vascular selectin expression, did not affect the expression of LECAM-1. Our data indicate that oxygen radicals induce a direct calcium independent release of histamine which is due to membrane pertubating processes during the first phase but also induce a specific reaction leading to a further indirect histamine liberation which is probably mediated by PAF.

Cell Adhesion Molecules↗

PubMed1979

Gastrin-histamine as a normal sequence in gastric acid stimulation in the rabbit.

In a suspension of isolated gastric glands the effect of secretagogues on the oxyntic cells can only be detected by direct stimulation. An indirect stimulus like gastrin inducing one type of cell to liberate histamine which then acts on the oxyntic cells will not be detectable because of the very high dilution of the liberated substance. Thus the isolated gland preparation presents a means by which two steps in a sequential stimulation can be separated. There is no evidence that gastrin acts directly on the oxyntic cells but it does liberate histamine in a dose-effect relationship, which would in an intact stomach give histamine concentrations sufficient to effectively stimulate the acid secretion. Thus in the rabbit histamine seems to be a normal physiological mediator for gastrin stimulation.

Animals↗

PubMed1988

Inhibitory effect of anti-allergic agent NCO-650 on histamine release induced by various secretagogues.

Histamine release from rat peritoneal mast cells induced by antigen and anti-IgE was essentially complete within 2 min and 3 min, respectively, but that due to Concanavalin A (Con A) was complete only within 9 min. An anti-allergic agent NCO-650 [trans-4-Guanidinomethylcyclohexanecarboxylic acid p-tert-butylphenyl ester hydrochloride], which is a strong inhibitor of trypsin, dose-dependently inhibited anti-IgE-induced histamine release from rat peritoneal mast cells. Moreover, the rate and extent of histamine release from rat peritoneal mast cells induced by various histamine liberators such as antigen, concanavalin A, ionophore A 23187 and compound 48/80 are significantly diminished in samples incubated with NCO-650. The IC50 values of NCO-650 on histamine release induced by antigen, anti-IgE, Concanavalin A, A23187 and compound 48/80 were in the order of micromolar range, i.e. 1.9, 3.6, 4.6, 2.9 and 6.1 microM, respectively. On a molecular basis, NCO-650 is 1000-fold more potent than DSCG, an anti-allergic drug, in inhibiting the antigen-induced histamine release. The present results suggest that the effect of NCO-650 might be due to the inhibition of a common process underlying the release of histamine by various histamine liberators.

Animals↗

PubMed1975

Induction of histamine release and densensitization in human leukocytes.

Protein A from Staphylococcus aureus has been found to react with all human leukocyte preparations tested. In 70 percent of the experiments the reaction leads to histamine release. Furthermore, protein A treatment of cells at 37 degrees C, both in complete and Ca-2+-free medium, results in the inhibition of anti-IgE-induced histamine release in all cell preparations, indicating that protein A and anti-IgE antibodies release histamine from the same cells. This inhibition seems to be due to the blocking or exhaustion of a step in the biochemical pathway, leading to histamine release activated by both protein A and anti-IgE. In some cell preparations desensitization but no histamine liberation is induced by protein A. No inhibition occurs if the protein A treatment is performed at 4 degrees C. It is concluded that protein A elicits histamine liberation and desensitization by acting on IgG present on the surface of the basophil granulocytes. Treatment of leukocytes at 37 degrees C with anti-IgE antibodies, or F(ab)2 fragments from such antibodies, also results in an inhibition of a subsequent anti-IgE-induced histamine release. Desensitization with low doses of anti-IgE results in an inhibition of the same type as that obtained with protein A. Supraoptimum amounts of anti-IgE or high amounts of monovalent Fab fragments from anti-IgE immunoglobulin G give an inhibition that could be due to a competition between the sensitizing and the challenging agents for combining with cell fixed IgE molecules. This inhibition is independent of temperature and calcium concentration.

Animals↗

PubMed1980

[Ultrastructure of liver cells during experimental histamine shock (author's transl)].

An light and electronmicroscopic study of the rabbit hepatocytes during shock after experimental histamine release by Polymyxin-B-sulphate was made. As soon as five minutes after the histamine liberation the endoplasmatic reticulum becomes dissociated and the mitochondria show a spherical transformation. When the shock lasts up to one hour the changes are more intensive. The rest of deteriorated mitochondria and the endoplasmic membranes are expelled from the cells into the sinusoid lumina in form of myelinic figures. The hepatocyte microvilli swell up at first, and later, from the fifteenth minute after the beginning of shock they disappear which results in the flattening of the plasma membrane or its complete dissapearance in some places. Endothelial cells suffer similar alterations and they also acquire cytoplasmic protrusions. The findings lead to the conclusion that the changes of hepatocytes during shock after histamine liberation are primarily due to the direct influence of released histamine, and secondarily to the influence of hypoxia produced during the shock state.

Animals↗

PubMed1975

Prostaglandin, slow-reacting substance, and histamine release from anaphylactic guinea-pig hearts, and its pharmacological modification.

Prostaglandins (Pgs), slow-reacting substance of anaphylaxis (SRS-A), and histamine were released from anaphylactic isolated perfused guinea pig hearts. Pgs were to the greatest part of the F2alpha-type. PgE2 was found in traces only. Neither PgA2, nor the metabolites 13,14-dihydro-15-keto-PgF2alpha and 13,14-dihydro-15-keto-PgE2 were detected in the perfusates. Isoproterenol reduced the PgF2alpha output significantly. This effect was increased by the addition of theophylline. Propranolol did not reverse the effect of isoproterenol, but in a high concentration (5 mug/ml) reduced the PgF2alpha output for its own. Indomethacin completely abolished the anaphylactic prostaglandin release. The histamine liberation was significantly decreased only by the combination of isoproterenol and theophylline, and also by a high concentration of propranolol (5 mug/ml). In contrast to the Pg release, the anaphylactic SRS-A and histamine liberation was not abolished by indomethacin, but rather increased. The results are discussed in view of the possible role of the released substances in the functional events of cardiac anaphylaxis.

Anaphylaxis↗

PubMed1978

Flare and itch induced by substance P in human skin.

Intradermal injection of synthetic substance P (10(-7)--10(-5) M in humans produced flare, wheal and itching. These responses were inhibited by oral pretreatment of the subjects with an antihistaminic drug (chlorcyclizine) or by local pretreatment with Compound 48/80 administered to deplete the local stores of mast-cell bound histamine. The findings indicate that the responses induced by substance P were mainly mediated by histamine released from the dermal mast cells. In contrast to previously studied histamine liberators, substance P was less potent when acting on rat mast cells in vitro than on human skin mast cells in vivo. When incubated with rat peritoneal mast cells, about 100 times higher concentrations (10(-5) M) were required to induce histamine release than in the in vivo studies on humans. It was concluded that substance P is a potent histamine liberator in human skin.

Adult↗

PubMed1976

[In vivo blood histamine during anesthesia].

Assays of overal histaminaemia were carried out, in 150 patients anaesthetised according to three different techniques, apart from any surgical act. 119 anaesthesias took place without any incident, 33 were disturbed by the appearance of rashes or of bronchospasm. The overall histaminaemia varied according to three types of graphs (a flat graph, an ascending graph, or a descending graph) without it being possible to evoke any relationship between this course and the clinical signs. It seems that the presence of a background predisposing to histamine-liberation is however responsible for greater frequency of the descending graphs, and that the method of administration of the anaesthetic product is a factor which can intervene in the genesis of the phenomena of histamine-liberation during anaesthesia. An interpretation of the variations in the graphs of histaminaemia is attempted by the authors.

Adolescent↗