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PubMed1994

Effect of isolation stress on brain mast cells and brain histamine levels in rats.

The effects of the chronic social stress of isolation on changes in brain mast cells (MC), the hypothalamic histamine content and the activity of the hypothalamic-pituitary adrenal (HPA) axis were investigated in rats. Social stress of isolation markedly reduced the total number of brain mast cells, most significantly by 90% in the first day. The extent of MC degranulation, 36-67%, in stressed rats did not significantly differ from that in control animals, 45-58%. Isolation stress substantially, though not significantly, increased the hypothalamic histamine content. The serum corticosterone levels in isolated rats did not significantly differ from the control levels. These results indicate that social stress of isolation considerably diminishes the number of brain MC and suggest that histamine which might be liberated from these cells does not significantly influence the HPA activity.

Animals↗
PubMed1999

Decreased arachidonic acid liberation participates in the anti-aggregatory effect of the histamine H(1)-receptor antagonist Bromadryl.

The in vitro effect of the histamine H(1)-receptor antagonist Bromadryl on aggregation of human blood platelets was studied. Bromadryl inhibited stimulated platelet aggregation in a dose-dependent way. Depending on the aggregation stimulus used, its mean inhibitory concentrations were 16 micromol/litre (thrombin), 18 micro mol/litre (A23187), 92 micromol/litre (adrenaline) and 395 micromol/litre (adenosine diphosphate). The inhibitory effect was most pronounced in aggregation stimulated with phorbol 12-myristate 13-acetate (IC(50) = 3 micromol/litre), suggesting interference of Bromadryl with protein kinase C activity. In Bromadryl-treated platelets, a very good correlation was found between aggregation and liberation of arachidonic acid; the correlation coefficients calculated for thrombin- and A23187-stimulated platelets were 0.94123 and 0.98611, respectively. This indicates that interaction of Bromadryl with phospholipase A(2) (an enzyme liberating arachidonic acid) may be involved in the anti-aggregatory effect. However, in platelets stimulated with thrombin, thromboxane formation was decreased at a lower mean inhibitory concentration of Bromadryl (6 micromol/litre) than arachidonic acid liberation (72 micromol/litre); thus, phospholipase A(2) does not seem to be the only site in the arachidonate metabolism cascade affected by Bromadryl. Although specific interference of Bromadryl with histamine receptors could not be excluded, alterations in platelet membrane structure and functions are supposed to be principal in the anti-aggregatory effect of Bromadryl.

Journal Article↗
PubMed1989

Antiallergic activity of picumast dihydrochloride in several animal species.

Picumast dihydrochloride (3,4-dimethyl-7-[4-(4-chlorobenzyl)piperazine-1-yl]propoxycoumarin dihydrochloride) was compared with cromoglycate, ketotifen and mepyramine as an inhibitor of allergic and anaphylactoid reactions. 1. In guinea-pigs, pretreatment with picumast dihydrochloride given intravenously, orally or by inhalation prevented bronchospasm induced by antigen or histamine. The fraction of the bronchospasm remaining after mepyramine pretreatment was further reduced by picumast dihydrochloride. 2. Systemic administration of picumast dihydrochloride inhibited antigen-induced conjunctivitis, whereas mepyramine and ketotifen were inactive. 3. Intravenous and oral pretreatment with picumast dihydrochloride inhibited the antigen-induced mast cell degranulation in rat mesentery. The effective doses of cromoglycate given intravenously were twice as high as those of picumast dihydrochloride. Picumast dihydrochloride did not inhibit antigen-induced bronchoconstriction in rats. 4. The cutaneous reaction induced with Ascaris antigen in atopic monkeys was insensitive to the antihistaminic action of ketotifen, whereas it was inhibited by low doses of picumast dihydrochloride. Both compounds suppressed skin reactions induced by histamine. 5. Picumast dihydrochloride decreased IgE production in atopic high responder mice. It did not prevent autoimmune nephritis in NZB/W mice. 6. In rats, picumast dihydrochloride did not reduce cotton pellet granuloma, nor adjuvant arthritis. The inhibition of carrageenin oedema is presumably due to its anti-oedematous properties rather than to an antiproliferative activity. In conclusion, the inhibition of allergic and anaphylactoid reactions by picumast dihydrochloride can be attributed to a combined inhibition of liberation and action of histamine and other mediators.

Airway Resistance↗
PubMed1992

Biscoclaurine alkaloids inhibit receptor-mediated phospholipase A2 activation probably through uncoupling of a GTP-binding protein from the enzyme in rat peritoneal mast cells.

The mechanism underlying the inhibitory effect of biscoclaurine (bisbenzylisoquinoline) alkaloids on phospholipase A2 activation in the signalling system of stimulated rat peritoneal mast cells was studied. Cepharanthine, berbamine and isotetrandrine inhibited antigen- and compound 48/80-induced arachidonic acid liberation, but not diacylglycerol formation or histamine release. They had no effect on A23187-induced arachidonic acid liberation, which was prevented by p-bromophenacyl bromide, a known phospholipase A2 inhibitor, and also did not affect phospholipase A2 activity in a cell-free system including an exogenous phospholipid substrate. Each alkaloid also inhibited arachidonic acid liberation induced by guanosine 5'-O-(3-thiotriphosphate) in saponin-permeabilized mast cells, and by mastoparan or NaF plus AlCl3 intact cells. Furthermore, each alkaloid abolished the inhibitory effect of islet-activating protein on the compound 48/80-induced arachidonic acid liberation. These data suggest that these alkaloids suppress the receptor-mediated phospholipase A2 activation through, at least in part, uncoupling of a GTP-binding protein from the enzyme, rather than by affecting the enzyme directly.

Alkaloids↗
PubMed1988

Immunologic dysfunction in scleroderma: evidence for increased mast cell releasability and HLA-DR positivity in the dermis.

To investigate the role of mast cells and cell-mediated immunity in the pathogenesis of scleroderma, we studied wheal size after skin testing with compound 48/80, a liberator of mast cell histamine, and demonstrated increased mast cell releasability in skin that appeared normal, adjacent to involved skin. Immunofluorescent staining for HLA-DR showed dermal positivity in 12 of 13 involved- and 9 of 13 uninvolved-skin biopsy specimens from scleroderma patients, compared with only 1 of 10 controls. By immunoperoxidase staining, most of the DR positivity was found in fibroblast-like cells. These findings further support the notion of immunologic dysfunction in scleroderma.

Adolescent↗
PubMed2003

Something fishy: six patients with an unusual cause of food poisoning!

Scombroid fish poisoning is a clinical syndrome attributed to the ingestion of contaminated fish. A toxin or toxins, known as scombrotoxin, result from decomposition by endogenous flora of the amino acid histidine liberating bioactive amines, predominantly histamine. The presentation has features of histamine toxicity, typically with urticaria, flushing, headache, abdominal cramps, diarrhoea and vomiting. The course is usually mild and self-limiting. The author describes six cases of scombroid poisoning after ingestion of fish from the same Canberra restaurant. One case resulted in significant hypotension necessitating a prolonged stay in the ED.

Adult↗
PubMedDate not supplied

Pharmacological actions of APP 201-533, a novel cardiotonic agent.

APP 201-533 [3-amino-6-methyl-5-phenyl-2(1H)-pyridinone] was investigated in vivo in anesthetized and unanesthetized dogs and pithed open-chest cats and in vitro in guinea pig atria and papillary muscles, skinned muscle fibers from pig hearts, and rat myocardium. Left ventricular dP/dt was increased in anesthetized dogs after intravenous injection of 0.2 and 2 mg/kg APP 201-533 (34 +/- 3 and 132 +/- 28%, respectively) and in unanesthetized dogs after oral doses of 1.5-7.5 mg/kg (34 +/- 11-138 +/- 43%). The substance induced moderate tachycardia. Large intraduodenal doses of APP 201-533 reduced afterload in anesthetized dogs. The compound does not seem to act either by stimulation of alpha- or beta-adrenoceptors or histamine receptors or by liberation of catecholamines. APP 201-533 up to 10(-5) M had no electrophysiological effect on normal action potentials in guinea pig papillary muscles. A phosphodiesterase-inhibiting activity (IC50 = 1.6 X 10(-4) M) may be responsible for the positive inotropic action. Another key to the mechanism of action may be based on our observation of a shift of the relationship between cardiac force and intracellular Ca2+ concentration. In contrast to amrinone and ouabain, APP 201-533 increases Ca2+ sensitivity of the myocardial contractile structures.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1993

Comparative effect of antiinflammatory drugs on rat paw edema induced by human sterile dental plaque extract, carrageenan or dextran.

The effect of antihistamine (diphenhydramine) or antihistamine and antiserotonin (cyproheptadine) or aspirin-like (acetylsalicylic acid and indomethacin) or corticosteroid (dexamethasone) drugs on the edema induced by various doses of carrageenan, dextran or human sterile dental plaque extract, injected intraplantarily in the rat paw were comparatively studied. The results showed that: (a) human dental plaque extract injected into the rat paw induces a dose-dependent inflammatory response, confirming that it is a potent phlogistic agent; (b) the edema induced by the plaque extract though closer to the pattern of carrageenan-induced edema, was different to both the carrageenan- and the dextran-induced edema in its time course and the response to antiedema drugs; (c) histamine and serotonin are liberated in the plaque-induced edema but they play no essential role; (d) the inhibitors of arachidonic acid metabolite formation (ASA, indomethacin and dexamethasone) inhibit this inflammation suggesting the presence of prostaglandin-like substances since its first phase.

Analysis of Variance↗
PubMed1992

[Pharmacological properties of salmeterol].

Salmeterol is an original molecule characterized by its long duration of action (greater than 12 hrs in humans). Salmeterol is a highly selective beta-2 agonist that is from 2 to 15 times more potent than salbutamol on beta-2 receptors of bronchial smooth muscle and 10,000 times more potent than isoprenaline on beta-1 receptors. The duration of action of salmeterol on bronchial smooth muscle has been shown to be much superior than all other beta-2 sympathomimetics that have been studied, including formoterol. Salmeterol has two side chains that are linked by a long hydroxycarbon chain. Its long duration of action could be explained by the link to the cell membrane through an exo-site which is distinct from the beta-2 receptor. In vitro and in the animal model, salmeterol has a triple effect: inhibition of the liberation of inflammatory mediators (histamine, prostaglandins, leukotrienes), inhibition of cell influx and of protein extravasation. The relevance of this effect remains to be establish in humans.

Adrenergic beta-Agonists↗
PubMed1975

Role of the eosinophil in the allergic reactions. II. Release of prostaglandins from human eosinophilic leukocytes.

Human eosinophilic leukocytes respond to a variety of stimuli by liberating an inhibitor of histamine release. The active principle(s) in this eosinophil-derived inhibitor (EDI) was found to be a mixture of acidic lipids of similar physiocochemical behavior and biologic activity to prostaglandins E1 and E2. Indomethacin, an inhibitor or prostaglandin synthesis, specifically blocked the immune release of EDI. The results indicate that stimulation of human eosinophilic leukocytes results in synthesis and release of prostaglandins E1 and E2 from these cells. These findings strongly support the hypothesis that the eosinophil assumes a modulatory role in the allergic inflammatory reaction. The ways by which, under specific antigenic (allergenic) stimulation, human eosinophils could modulate the events asssociated with the allergic response, through the released prostaglandins, are discussed.

Adenosine Diphosphate↗
PubMed1994

Immediate hypersensitivity. A brief, personal history.

The discovery of anaphylaxis by Portier and Richet that reinjection of a substance caused disease instead of immunity was sensational as it was against the prevailing DOGMA. Passive transmission of hypersensitivity with human antibody by Prausnitz (the P-K reaction, 1921) was an important step in the study of human hypersensitivity. Anaphylaxis was shown to be the consequence of liberation of vasoactive substances (histamine and SRS-A) from mast cells when the allergen crosslinks two IgE molecules fixed to mast cell Ig receptors (Ovary, 1961). The use of smooth muscle contraction (Dale, 1913) and vascular permeability increase (PCA, Ovary, 1948) became important for experimental studies. The clonal selection of antibody formation (Burnet, 1929) opened a new era in immunological concepts. The demonstration of the Fc receptor on mast cells (Ovary, 1961) called attention to the importance of cellular receptors. The carrier effect (Ovary & Benacerraf, 1963) was explained by recognition by T cell receptors of a processed carrier fragment complexed to Ia molecules (Unanue, Grey, 1981). Human IgE responsible for allergies was discovered in 1965 by K. & T. Ishizaka. Tonegawa in 1973 destroyed the "one gene-one protein" DOGMA, showing that the immunoglobulin, germline gene is discontinuous: i.e., composed of exons (which will form the Ig molecule) separated by introns. The CD4 cells were subdivided into Th1 and Th2 cells (Mosmann & Coffman, late 1980's). The Th2 secretes IL-4 necessary for IgE production (Paul, Vitetta, & others, early 1980's). B cells multiply before antibody production or become memory B cells, but what causes a B cell to become a memory cell is not known. The B cell does not change specificity but can switch the isotype using "switch recombinase" and the s segment of the Ig molecules (Honjo, early 1980's). IgE production was shown to be suppressed by lymphokines, such as IFN-gamma and IL-2. A great progress in understanding the mechanism of allergic reaction has been the result of intense investigations by many scientists. A more complete understanding, better prophylaxis and an improved treatment are the goals of the near future.

History, 20th Century↗
PubMed1980

[Contribution of biological tests in the evaluation of professional asthma (author's transl)].

The eventual difficulties of diagnosing professional asthma sometimes need the help of methods of complementary diagnosis. The histamine-release test and that of basophils granules liberation are studied in this work, concerning 12 substances with a suspected allergenic action (saw-dust, textile fibres, chemicals, products of plant origin). The histamine-release and granules liberation tests were performed according to the techniques described respectively by Lichtenstein and Benveniste. Both examinations were positive in a concording manner in 8 cases out of 12, but this positivity was difficult to interprete for etiopathogenic reasons. The study of the curve of histamine-release in relation with the dose of allergen used in the test nevertheless enables to differentiate two types of answers, one related to an allergic mechanism, the other to an irritative one. These observations led to the deduction that a positive granules liberation test could be due to a non allergic mechanism. Negativity in both tests does not allow the rejection of the part played by these substances into the genesis of respiratory signs. Indeed these tests only investigate one part of the mechanisms which can be involved: direct stimulation of vagal irritant receptors and the plain pharmacological reactions escape from this type of biological investigations. The biological tests studied in this work can be used in a complementary fashion in the etiological survey of professional asthma but they cannot replace the realistic tests, more reliable because they react whatever the etiopathogenic mechanism involved.

Adult↗
PubMed1987

Energy metabolism in rat mast cells in relation to histamine secretion.

1. The relation between the energy metabolism and the secretory activity of rat peritoneal mast cells has been studied by determination of the cellular content of ATP and the rate of lactate production reflecting the rate of ATP synthesis under various experimental conditions. Secretion of histamine was induced by the antigen-antibody reaction, the polymeric amine compound 48/80, and the divalent ionophore A23187. 2. In presence of low concentrations of metabolic inhibitors (oligomycin or antimycin A) a linear relation between the secretion of histamine induced by all three liberators and the cellular ATP content at the time of cell activation was demonstrated. This may indicate a direct link between ATP and the secretory mechanism. 3. The possibility of an increased utilization of ATP during histamine secretion was explored in mast cells exposed to metabolic inhibitors. Incubation of mast cells with 2-deoxyglucose (2-DG) decreased the ATP content of the cells, and a long-lasting and stable level of mast cell ATP was observed. This is explained by a small decrease in the rate of ATP-synthesis by 2-DG. In 2-DG-treated cells secretion of histamine in response to compound 48/80 or the antigen-antibody reaction could still occur, and the secretion is shown to be associated with a decrease of the cellular ATP level. This ATP decrease indicates that secretion occurs by an ATP-requiring mechanism, that causes an increased cellular utilization of ATP in association with the secretory response. 4. The possibility has been considered that increased cytosol concentration of calcium in association with secretion may decrease the rate of ATP-synthesis due to accumulation of calcium by the mitochondria. This possibility can be excluded by the observation that in presence of respiratory inhibitors an identical ATP decrease was found during the secretion as in the case of the glycolytic inhibitor alone. This indicates that increased utilization of ATP by the cells was related directly to the secretory response. This observation was made with all three secretagogues. 5. A quantitative evaluation of the increased amount of ATP utilized by the cells in relation to the secretory response was performed by use of metabolic inhibitors. The ATP requirement of compound 48/80-induced secretion was 0.15 pmol/10(3) cells. This was observed when the ATP-synthesis was decreased to a negligible value.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

Release of gastric histamine in patients with urticaria and food allergy.

In a clinical study the participation of histamine in the allergenic response of patients with food allergy was investigated. The resting levels of gastric tissue and plasma histamines of 10 patients were slightly higher than the respective values of normal volunteers. 5 minutes after local intragastral allergenic provocation a decline of the mucosal histamine content of the allergen-treated area was noticed. Parallel investigations on the mast cell content of the stomach mucosa revealed a parallel decrease of the o-phthaldialdehyde stained cells, whereas the number of toluidine blue stained cells remained unchanged. These data are in accordance with an antigen-induced IgE-dependent liberation of the mast cell histamine stores.

Adult↗
PubMed1976

[Anaphylactic shock in anesthesia].

The notion of anaphylactic shock under anaesthesia implies sensitization, with a minimum delay of 1 week, on the occasion either of a previous anaesthesia with the responsible product, or with taking a drug with common antigenic determinants. Clinically this is reflected by the rapid and explosive appearance of symptoms which are always comparable: tendency to vascular collapse, respiratory bronchospastic distress, erythematous rash and Quincke's edema, gastrointestinal disorders, etc. These signs and symptoms of anaphylactic shock are closely related to the pharmacological actions of substances liberated during the reaction, of reaginic orgin (histamine, S.R.S.A.). It is reproduced by the direct effects of numerous anaesthetics on the liberation of theses very substances without the intermediary of an immunological mechanism. In consequence, the clinical argument alone is not sufficient to assert the true anaphylactic nature of a shock. Consequently, the elements of the history must be strongly borne in mind: notion ofsensitization during a previous anaesthesia, to the responsible product or to a drug which could have a crossed antigenicity with it.

Adolescent↗
PubMed1985

The effects of the dihydropyridine Bay K 8644 in guinea-pig isolated trachealis.

In trachea bathed by Krebs solution containing indomethacin 0.8 mumol l-1, Bay K 8644 (0.01-1 mumol l-1) evoked mild spasm. Peak tension was achieved after 10 min and was generally less than 20% of an acetylcholine (ACh) maximum. The effect of Bay K 8644 was not potentiated by addition of 2.5 mmol l-1 potassium chloride (KCl) to the Krebs solution. Bay K 8644 (1 mumol l-1) caused a small potentiation of KCl and tetraethylammonium (TEA). In contrast it did not modify the actions of ACh or histamine. Bay K 8644 (1 mumol l-1) caused a small potentiation of the effect of calcium chloride (CaCl2) tested in trachea bathed by a K+-rich, Ca2+-free, MOPS-buffered physiological salt solution. Organic inhibitors of calcium influx such as nifedipine (0.1 mumol l-1), verapamil (1 mumol l-1) or diltiazem (10 mumol l-1) each caused marked depression of concentration-effect curves to KCl. Bay K 8644 (0.01-1 mumol l-1) provided concentration-dependent protection against this effect in all three cases. Estimation of calcium influx by the lanthanum technique revealed that Bay K 8644 (1 mumol l-1) was able to promote the cellular influx of Ca2+. Intracellular electrophysiological recording showed that Bay K 8644 (1 mumol l-1) caused no change in the resting membrane potential of trachealis cells and no change in the properties of the spontaneous electrical slow waves. However, Bay K 8644 was able to delay the slow wave suppression evoked by 1 mumol l-1 nifedipine. The ability of Bay K 8644 to promote Ca2+ influx and its ability to protect against the effects of several structurally-unrelated inhibitors of Ca2+ influx are consistent with Bay K 8644 acting as an agonist at the dihydropyridine receptor associated with the voltage-operated Ca2+ channel (VOC) of trachealis muscle. By this action it potentiates those spasmogens (KCl, TEA) which act by permitting Ca2+ influx through VOCs. In contrast it has no effect on those spasmogens (ACh, histamine) which principally act to liberate Ca2+ from intracellular sites of sequestration.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1984

Production and antagonism of cutaneous vascular permeability in the guinea pig in response to histamine, leukotrienes and A23187.

The method of Katayama et al. (Microbiol. Immunol. 22:89-101, 1978) for assessing cutaneous vascular permeability was modified and used to evaluate responses of the dermal vasculature to histamine, leukotriene (LT)C4, LTD4 and the ionophore A23187. These agonists were given intradermally, whereas antagonists and other types of inhibitors were administered i.v. Histamine was shown to cause vascular leakage via an H1 receptor. No evidence for H2 receptor activation or involvement of cyclooxygenase products was found. The results also suggested that a portion of the response to histamine was due to the liberation of LTD4. LTC4 produced a mixed response comprised of vasoconstriction and increased vascular permeability, the latter possibly due to its conversion to LTD4. FPL 55712 antagonized LTD4-induced permeability in a dose-dependent manner, whereas indomethacin had no effect. Neither pyrilamine nor FPL 55712 reduced the response to A23187. A dose of indomethacin that did not affect the response to A23187 when given alone markedly reduced the ability of ionophore to cause vascular leakage when combined with either pyrilamine or FPL 55712. Thus, histamine and LTD4, in combination with one or more of the cyclooxygenase products, may be involved in A23187-induced cutaneous vascular permeability. Finally, two calcium channel blocking agents, nifedipine and diltiazem, did not block the vascular leakage caused by A23187.

Animals↗