SEARCH · PubMed Health

Results for “HISTAMINE LIBERATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources

PubMed1986

Inhibition of complement dependent experimental inflammation in human skin by different heparin fractions.

The anticoagulant activity of heparin is dependent on its affinity for antithrombin III (AT III) and on its molecular weight. In contrast, heparin fractions differing in these respects are equally effective inhibitors of the human complement system in vitro. In this study we designed and evaluated a model to investigate the effects of different heparin fractions on a complement dependent inflammation. Locally administered heparin, in a dose-dependent manner, inhibited the flare, itch and wheal responses induced by intradermal injection of heat-aggregated human IgG (HAGG). These reactions were also inhibited by the antihistamine mepyramine, favouring the view that HAGG activates complement and that the observed inflammatory response is mediated by anaphylatoxin liberation of histamine. Similar cutaneous reactions induced by trypsin, which can generate C3a and C5a by proteolysis of C3 and C5, the histamine liberator compound 48/80 or histamine were inhibited by mepyramine but not by heparin. Thus it is strongly suggested that heparin inhibits the HAGG induced reactions by modulating the early pre-C3 steps of complement activation. On a weight basis heparin fractions differing in AT III-affinity or in average molecular weight (5,000 and 16,000 D) were equally potent modulators of the HAGG-induced inflammation. We conclude that heparin can inhibit an apparently complement-dependent inflammation irrespective of its AT III-affinity or of its size, and suggest that a heparin with low anticoagulant activity could be of value as a modulator of inflammation and should be useful in investigating the consequences of complement inhibition in inflammation.

Animals↗

PubMedDate not supplied

[System of pharmacologic control of histamine release by mast cells on exposure to different agents].

A scheme has been devised that makes it possible to assess a specific mechanism of action of any histamine-releasing agent. The scheme suggests a switch off of different stages of histamine secretion--interaction of a histamine liberator with surface cell receptors, entry of Ca2+ into the cell, temperature- and energy-dependent stages of histamine liberation, a stage that depends on microtubules, a system regulating histamine liberation with cyclic nucleotides. The scheme was made use of in clarification of the mechanism of histamine liberation on exposure of the mast cell to a specific antigen, to different doses of heavy metal salts, prednisolone and alkylating cross-binding agents.

Alkylating Agents↗

PubMed1988

[The amount of histamine released in vivo by hypnotics (thiopental, methohexital, propofol) studied by assays of plasma histamine].

Accidents observed during induction of anaesthesia are most often linked to non-specific histamine liberation. The sale of new hypnotics (Methohexital and Propofol), has brought the hope that their histamine-liberation potential would be lower. The study was done in patients who were at risk of histamine-liberation (atopics, drug allergies etc.). Two series of patients were studied after anti H1 and tranquilizer premedication. Histamine liberation by Propofol versus Thiopental as the inducer was studied in the first group. In the second, the combination was Methohexital versus Thiopental. In both series studied the new hypnotics Propofol and Methohexital did not release histamine non-specifically in atopics at risk. Neither clinical reactions non increase of histamineamia were seen. It is concluded that these two new drugs are safe.

Drug Hypersensitivity↗

PubMed1995

Substance P-induced histamine release in tracheally perfused guinea pig lungs.

The capacity of substance P (SP) and endogenously released tachykinins to liberate histamine was examined in isolated tracheally perfused guinea pig lungs. Increasing doses of tracheally injected SP were associated with the recovery of increasing amounts of histamine from lung effluent. The mechanism of SP-induced histamine liberation was explored in studies with neurokinin-(NK) receptor agonists and antagonists. Tracheal injection of either the NK1 agonist [Sar9,Met(O2)11]SP or the NK2 agonist [beta-Ala8]-neurokinin A-(4-10) was associated with a significant increase in histamine recovery from lung effluent. In addition, both the NK1 antagonist CP-99994 and the NK2 antagonist SR-48968 significantly inhibited SP-induced histamine release. These findings support the hypothesis that SP can liberate histamine from guinea pigs lungs by a mechanism that depends predominantly on NK1- and NK2-receptor activation. The liberation of endogenous tachykinins by acute tracheal injection of capsaicin was also associated with augmented histamine recovery, which was inhibited by combined NK1- and NK2-receptor blockade. Tracheal injection of SP was associated with an increase in the percentage of airway mast cells exhibiting histological evidence of degranulation. This study demonstrates that exogenous SP, as well as endogenous tachykinins released from capsaicin-sensitive neurons, can liberate histamine, most likely from airway mast cells, by a mechanism that depends predominantly on the activation of NK1 and NK2 receptors.

Animals↗

PubMed1989

Occurrence of histamine-production-increasing factor in the postanaphylactic phase of allergic inflammation.

Experimental study on histamine liberation in a postanaphylactic phase of allergy was carried out employing an air pouch model of allergic inflammation in rats. The antigen used was azobenzenearsonate-conjugated acetyl bovine serum albumin. Synthesis and liberation of histamine took place in the inflammatory pouch in the dorsum of the allergic rats, and brought about a gradual rise in the histamine level in the pouch fluid with a peak at 24 h after the antigen challenge. The time course of the histamine level in the pouch fluid was quite similar to that of histidine decarboxylase activities in the inflammatory tissues. alpha-Fluoromethylhistidine reduced the histamine level in the postanaphylactic phase, although it had been ineffective in the anaphylactic phase. A substance capable of increasing histamine production by bone marrow cells was found in the pouch fluid of allergic rats, while it was absent in the normal rat serum and pouch fluid of nonsensitized rats. The histamine-production-increasing activity rose until 24 h after the antigen challenge, but fell at 48 h in parallel with changes both of histamine levels in the pouch fluid and histidine decarboxylase activity in inflammatory tissues. The histamine-production-increasing factor is thought to be a protein, since it was inactivated by treatment with heat (70 degrees C for 30 min) or trypsin. Its molecular weight was estimated to be between 25,000 and 40,000.

Anaphylaxis↗

PubMed1987

Histamine release induced by Arg-Pro-Lys-Pro(CH2)11CH3 from rat peritoneal mast cells.

The substance Arg-Pro-Lys-Pro-(CH2)11CH3 [SP1-4C12] was synthesized by forming a peptide bond between Arg-Pro-Lys-Pro, the N-terminal sequence of substance P and dodecylamine. The aim was to examine the roles of the N- and C-terminal sequences of substance P in stimulating histamine release from mast cells of the rat peritoneal cavity. SP1-4 C12 induces concentration-dependent histamine release in the range 8 to 200 nM. SP1-4C12 was 50 times more potent than substance P and 300 times more potent than dodecylamine. Unlike dodecylamine itself, SP1-4C12 induced noncytolytic histamine release which was inhibited by benzalkonium chloride and by the substance P antagonist [D-Pro4,D-Trp7,9,10]SP4-11. Histamine release induced by SP1-4C12 was inhibited at temperatures below 16 degrees C and did not require the presence of extracellular calcium ions. It is suggested that substance P and some other basic histamine liberators initiate histamine secretion by a mechanism that involves the insertion of a hydrophobic region into the membrane lipid which is necessary to present positively charged moieties to a receptor site involved in activating the secretory mechanism.

Animals↗

PubMed1984

[Animal experiment studies on the role of inflammation mediators in corneal neovascularization].

Natural and synthetic inflammatory compounds were implanted in the corneas of rabbits to clarify the question whether corneal neovascularization is induced by stromal edema alone, or by neovascular mediators. It could be demonstrated that prostaglandin E1 and E2 have an angiogenetic capacity, whereas their precursor (arachidonic acid) as well as PGA1, A2, B2, I2 and Thromboxan A2 were inactive in this regard. Histology showed that corneal neovascularization is always accompanied by the invasion of polymorphonuclear leukocytes. Corneal edema in the beginning of vascularization can be explained by the activities of PGE (vasodilation, increase of vascular permeability, liberation of histamine). The implantation of lipoxygenase-dependent arachidonic acid compounds (5-HETE, Leukotriene B4) demonstrated that these mediators share in the process of neovascularization by inducing the chemotaxis. The above mentioned activities of prostaglandins and leukotrienes could also be demonstrated following penetrating keratoplasty and alkali burns of the anterior segment inducing extensive corneal neovascularization. An analysis of the prostaglandin- and leukotriene-dependent mechanisms could be achieved by selective PG- and LT-inhibitors. Radioimmunoassays showed a definite correlation between the concentrations of PGE and the amount of neovascularization following alkali burns. The results of our research lead to the following scheme of pathophysiology of corneal neovascularization: hypoxic, chemical, thermic and mechanical alterations of the cornea induce an activation of corneal cytomembranes, thus initiating the cyclooxygenase-dependent synthesis of prostaglandins with consecutive vasodilation and increase of vascular permeability as well as histamine liberation resulting in corneal edema; on the other hand, prostaglandins proved to have a minimal chemotactic activity; the lipoxygenase-dependent synthesis of leukotrienes inducing chemotaxis and diapedesis of polymorphonuclear leukocytes into the corneal stroma. These inflammatory cells are then the main source of newly synthesized leukotrienes maintaining the chemotaxis, and prostaglandins with angiogenetic activity. Cyclooxygenase- and lipoxygenase-inhibitors can inhibit these activities at two different levels, leading to an approach of successful therapy of corneal diseases inducing neovascularization.

Animals↗

PubMed1982

Carrageenan-induced oedema in the rat paw - histamine participation.

Participation of histamine in the inflammatory reaction produced by carrageenan was studied. Mepyramine did not influence the course of the inflammatory reaction. In contrast to when mepyramine was used, there was a significant inhibition of carrageenan oedema when cimetidine was used. Pretreatment of animals with compound 48/80 significantly reduced the oedema formation. Neither mepyramine nor cimetidine reversed the inhibition of rat paw swelling produced by histamine liberators. It is concluded that histamine participates in carrageenan oedema via its H2-receptors and that the anti-inflammatory effect of compound 48/80 is not connected with the 'anti-inflammatory' action of liberated histamine.

Animals↗

PubMed1991

Effect of chloroquine on isolated mast cells.

Chloroquine liberated a relatively low amount of histamine from isolated rat mast cells. In a dose-dependent way, this drug inhibited histamine liberation from mast cells stimulated with compound 48/80, A23187, concanavalin A plus phosphatidylserine (Con A + PS) and abolished histamine liberation induced by exaprolol. The degranulation was decreased in cells stimulated with 48/80, Con A + PS and exaprolol. Chloroquine significantly inhibited the formation of thromboxane B2 in mast cells stimulated with 48/80, Con A + PS and A23187. We assume that chloroquine interferes with mast cells at a plasmic membrane site as well as intracellularly.

Adrenergic beta-Antagonists↗

PubMed1989

[Histamine-related reactions in patients with byssinosis].

The purpose of the study was to analyze the mechanism of histamine action in histamine-dependent reactions of neutrophils and lymphocytes in patients with byssinosis and chronic asthmatic bronchitis under cotton and flax dust effect. The appraisal of histamine content in blood serum, receptor/histamine distribution of lymphocyte and neutrophil subpopulations (rosette-forming double and triple reactions), determination of histamine modeling effect on lymphocyte-neutrophil cooperation in the inhibition reaction of leukocyte migration revealed that under cotton dust effect neutrophils and the complement system were involved into the histamine liberation process in byssinosis patients, lymphocytes were most likely not involved into the process. Flax dust-affected histamine reactions were not so distinct: lymphocyte and neutrophil reactivity in byssinosis patients did not exceed the standards. Patients with chronic asthmatic bronchitis had high blood concentration of histamine and experienced some changes in cells' migration characteristics. It was assumed that primarily nonimmune mechanisms of histamine liberation and activation of the complement system were involved into byssinosis pathological process in patients exposed to cotton and flax dust effect. In patients with chronic asthmatic bronchitis there occurred all 3 activation mechanisms of biologically active substances, i.e., allergic and nonantigenic ways of histamine liberation and activation of the complement system.

Adult↗

PubMed1977

Response of skin to ammonium persulphate.

In order to investigate the histamine liberating actions of ammonium persulphate, skin slices from three species (guinea pig, rat and monkey) were incubated in vitro with concentrations of ammonium persulphate ranging from 1 to 1000 microgram/ml. None of these concentrations released significant amounts of histamine in guinea pig or monkey skin. In the rat the highest concentration (1000 microgram/ml) released 20-24% of the histamine content of the skin, but the intensitivity of this response to cooling indicates a non-specific "toxic" action on mast cells. By contrast a known chemical histamine liberator, compound 48/80, released significant amounts of histamine from skin at much lower concentrations in all three species. Ammonium persulphate is clearly not a potent histamine liberator. Ammonium persulphate dermatitis is presumably a result of increased sensitivity of skin mast cells, due to immunological or other factors, in susceptible individuals.

Ammonium Sulfate↗

PubMed1976

[2 cases of anaphylactic-type reaction to alphadione (Alfatesine, Althesin, CT 13.41)].

Two cases of anaphylactic-type reaction to alfadione were referred to our Department for immuno-allergic enquiry. From the clinical standpoint, the pictures obtained were rather similar, dominated by dramatic collapse of abrupt onset associated with an erythemato-oedematous cervico-facial rash, however with a favourable course under respiratory and circulatory emergency resuscitation. The immunological enquiry carried out in both cases did not enable one to attribute the responsibility for the accident to alfadione or to cremophor EL nor to be able to put it down to a direct pharmacological histamine-liberation, or to a specific histamine-liberation due to an antigen-antibody reaction.

Adult↗

PubMed1978

Histamine release in rats after administration of five neuromuscular blocking agents.

The effect of five neuromuscular blocking agents on histamine levels of various tissues was studied. Blood and tissue samples were taken from male rats previously treated intravenously with neuromuscular blocking agents. d-Tubocurarine proved to be the most potent histamine liberator. Alcuronium, gallamine and succinylcholine were only moderate histamine liberators, whereas pancuronium released practically no histamine. The results from the individual tissues suggest that the possible sources of increased blood histamine concentrations are tongue and skin with high histamine content. No release of histamine was found from the lung.

Animals↗

PubMed1996

Histamine release in skin monitored with the microdialysis technique does not correlate with the weal size induced by cow allergen.

The purpose of this study was to monitor histamine release in immediate-type hypersensitivity reactions in the skin of 10 atopic patients, sensitive to cow, by using the microdialysis technique. Three healthy subjects, without any atopic features or background, served as the control group. The probe inserted into the forearm dermal skin was perfused with isotonic saline solution. Samples were collected at 15-min intervals. After the first allergen challenge of four prick tests close to the probe with cow allergen extract, the skin was similarly repricked again in five patients and three healthy subjects, and in five other patients, 25 microliters of 10 mumol/l substance P (SP) was injected intracutaneously. The samples were analysed for histamine by radioenzyme assay. The patients were clinically evaluated for allergic symptoms, prick- and scratch-patch test reactivity and for serum cow-specific, and total, IgE levels. The baseline histamine concentration was 7.5 +/- 4.0 nmol/l (mean +/- standard deviation: SD; n = 10). After the allergen challenge, the histamine concentration in the consecutive samples was 11.9 +/- 11.0 nmol/l, 91.1 +/- 127.3 nmol/l, 61.0 +/- 94.2 nmol/l and 33.7 +/- 53.7 nmol/l. The peak concentration was detected in the 15-30 min fraction, and it varied between 0 and 406 nmol/l regardless of the weal size. The second allergen challenge was unable to induce marked additional histamine release, but SP induced extensive histamine liberation in those patients who did not exhibit histamine release during the preceding prick tests. In three healthy subjects, the baseline histamine concentration was 6.2 +/- 3.9 nmol/l. After the allergen challenge, no additional histamine liberation could be measured. Surprisingly, the histamine release was not related to the size of the cow-induced weal nor was it related to any specific allergic symptoms or IgE levels. The results suggest that, in some patients, mast cell mediators other than histamine play a significant part in immediate-type allergic reactions of skin.

Adult↗

PubMed1975

Blood histamine levels and arteriovenous concentration differences after the intravenous administration of the basic compounds l-3 and 48/80 in the anaesthetized dog.

The effects of the i.v. administration of inulin trinicotinate-monomethochloride (L-3) on haemodynamics, airway pressure and blood histamine levels were studied in chloralose-anaesthetized dogs and compared with the effects of compound 48/80. The control arterial histamine level was 0.041 plus or minus 0.002 mug/ml (mean plus or minus SEM) as determined by a fluorometric assay. L-3 (0.15 mg/kg) released high amounts of histamine, as indicated by a peak level in arterial histamine of 0.212 plus or minus 0.027 mug/ml within 3 min, which was not futher enhanced on increasing the dosage of L-3 to 1 mg/kg. After the i.v. injection of 0.15 mg/kg of 48/80 the peak level in arterial histamine was 0.146 plus or minus 0.008 mug/ml, and the level was further markedly elevated to 0.918 plus or minus 0.068 mug/ml after the administration of 1 mg/kg of 48/80. The concomitant fall in systemic blood pressure and the rise in airway pressure can be satisfactorily explained on the basis of histamine liberation. Whereas these parameters as well as the blood histamine concentration gradually returned to control values, the heart rate remained elevated during the observation period of 2 h. The arteriovenous differences in blood histamine across various tissues and organs following L-3 and 48/80 administration indicated histamine release mainly from skin and muscle and histamine uptake by the kidney, the digestive tract and to a lesser extent the lungs. The portal-hepatic vein differences revealed no consistent changes in liver histamine balance. As regards the lungs and liver, the present results suggest a dynamic equilibrium between histamine release and uptake in these organs in the intact animal. Both, L-3 and 48/80 elicited a similar pattern of histamine release and uptake. The extreme histamine releasing capacity of 1 mg/kg of 48/80 may be explained by an additional non-selective mechanism of histamine liberation.

Airway Resistance↗

PubMed1980

Inhibition of histamine release from human lung in vitro by antihistamines and related drugs.

1 A series of cationic, lipophilic histamine H1-receptor antagonists, neuroleptics, antidepressants and monoamine oxidase inhibitors were tested for their effects on anti-IgE-induced histamine release from human lung fragments in vitro. 2 They had a biphasic effect: at low concentrations a dose-related inhibition of histamine release was observed whereas, at higher concentrations, the drugs liberated histamine even in the absence of antigen. 3 Mepyramine, a much less lipophilic drug than the others tested, was only weakly active on mast cells at pharmacological concentrations. 4 The potency of the drugs as release inhibitors was not related quantitatively to their histamine liberating potency. 5 There was no; correlation between activity on mast cells and histamine H1-receptor antagonism. 6 Mast cell stabilization may play a part in the activity of these drugs as anti-allergic agents.

Chlorpheniramine↗

PubMed2002

tan and ebony genes regulate a novel pathway for transmitter metabolism at fly photoreceptor terminals.

In Drosophila melanogaster, ebony and tan, two cuticle melanizing mutants, regulate the conjugation (ebony) of beta-alanine to dopamine or hydrolysis (tan) of the beta-alanyl conjugate to liberate dopamine. beta-alanine biosynthesis is regulated by black. ebony and tan also exert unexplained reciprocal defects in the electroretinogram, at ON and OFF transients attributable to impaired transmission at photoreceptor synapses, which liberate histamine. Compatible with this impairment, we show that both mutants have reduced histamine contents in the head, as measured by HPLC, and have correspondingly reduced numbers of synaptic vesicles in their photoreceptor terminals. Thus, the histamine phenotype is associated with sites of synaptic transmission at photoreceptors. We demonstrate that when they receive microinjections into the head, wild-type Sarcophaga bullata (in whose larger head such injections are routinely possible) rapidly (<5 sec) convert exogenous [3H]histamine into its beta-alanine conjugate, carcinine, a novel metabolite. Drosophila tan has an increased quantity of [3H]carcinine, the hydrolysis of which is blocked; ebony lacks [3H]carcinine, which it cannot synthesize. Confirming these actions, carcinine rescues the histamine phenotype of ebony, whereas beta-alanine rescues the carcinine phenotype of black;tan double mutants. The equilibrium ratio between [3H]carcinine and [3H]histamine after microinjecting wild-type Sarcophaga favors carcinine hydrolysis, increasing to only 0.5 after 30 min. Our findings help resolve a longstanding conundrum of the involvement of tan and ebony in photoreceptor function. We suggest that reversible synthesis of carcinine occurs in surrounding glia, serving to trap histamine after its release at photoreceptor synapses; subsequent hydrolysis liberates histamine for reuptake.

Animals↗

PubMed1982

Histamine release from rat peritoneal mast cells exposed to ultraviolet light.

After irradiation with ultraviolet light, rat peritoneal mast cells incubated with the histamine liberator compound 48/80 were found to have reduced capacity to release histamine. The action spectrum for histamine release inhibition seemed to be in the wavelength region of UVB. UV-light per se did not induce histamine liberation other than for dosages greater than or equal to 1.45 J/cm2. No such release was observed with the doses of UVA studied (3.4-20.5 J/cm2). The metabolic inhibitor 2.4-dinitrophenol (DNP), which almost completely inhibited compound 48/80-elicited histamine release, did not influence the UV-induced histamine release, indicating that the latter was not a secretory process but due to cytotoxic leakage of histamine from the cells. These results suggest that inhibition of histamine-releasing capacity or reduction of skin histamine due to photolysis of mast cells may explain the beneficial effect of UV in pruritic disorders where histamine release from mast cells is involved.

Animals↗