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PubMed1986

Some studies on the release of histamine from mast cells treated with d-tubocurarine.

d-Tubocurarine (dTc) released histamine in non-cytotoxic fashion from peritoneal mast cells of the rat, mouse and hamster. The response was similar to that evoked by other cationic liberators such as compound 48/80 and polylysine in that it was extremely rapid and enhanced by calcium-deprivation at suboptimal concentrations of secretagogue. Tissue mast cells obtained by enzymic dissociation of the heart, lung and mesentery of the rat and guinea pig were unreactive or hyporesponsive to the effect of dTc. The compound liberated only very small amounts of histamine from isolated preparations of perfused guinea pig heart but significantly increased the rate and contractility of the heart. These results are discussed in terms of the general functional heterogeneity of mast cells from different locations.

Animals↗
PubMed1979

Effect of pylorus ligation on gastric mucosal mast cell population in normal and adrenalectomised albino rats.

Pylorus ligation in normal albino rats acts like a stressor leading to degranulation of mast cells in gastric mucosa, thereby decreasing their number. This decrease is less pronounced when pylorus ligation is done in adrenalectomized rats. This implies that action of a stressor on gastric function involves the adrenal steroids which liberate the powerful gastric stimulant histamine from gastric mucosal mast cells.

Adrenal Cortex↗
PubMed1985

Capillary permeability-increasing enzyme from the venom of Agkistrodon caliginosus (kankoku-mamushi): activity due to the release of peptide material from a protein in bovine plasma.

When a mixture of the purified capillary permeability-increasing enzyme from A. caliginosus venom and bovine plasma or heated bovine plasma was injected into the depilated skin of the back of a rabbit, the capillary permeability-increasing activity was much greater than that induced by injection of the enzyme alone. The substance which increases capillary permeability was extracted from the incubated mixture of bovine plasma and enzyme with 50-70% ethanol. Its activity was lost when treated with carboxypeptidase A. Thus, it is supposed that the increase in capillary permeability induced by the enzyme is due to a low molecular weight peptide released from a protein in bovine plasma by the action of the enzyme. No liberation by the enzyme of histamine or anaphylatoxins of the complement system was found.

Animals↗
PubMedDate not supplied

[On the hypotensive activity of carrageenan iota in the rat (author's transl)].

1. Carrageenan iota and dextran sulfate deplete the plasmatic stores of kininogens in the Rat. 2. A slow intravenous infusion of carrageenan iota in the anaesthetized Rat produces a lowering of blood pressure which is only transient because of the development of tachyphylaxy. At this stage the cardio-vascular system which fails to respond to carrageenan iota injection is also refractory to ellagic acid administration. After depletion of the plasmatic stores of kininogens by dextran sulfate, glandular kallikreins or ellagic acid, carrageenan iota has lost its hypotensive properties. It is concluded that the cardio-vascular effects of carrageenan iota are mainly due to activation of the kininogenskinins system. 3. Indomethacin curtails the hypotensive effects of kinins by inhibition of the release of prostaglandins by these polypeptides. It also reduces the duration of the hypotensive response to carrageenan. Carrageenan iota is neither a histamine nor a 5-hydroxytryptamine liberator.

Albinism↗
PubMed1985

Schistosoma mansoni: neurotransmitters and the mobility of cercariae and schistosomules.

The concentration-dependent action of alkyl-isothiouroniums on Schistosoma mansoni cercariae, ranging from partial to total abolition of locomotor and flame cell movements, and/or suppression of virulence, is due to H1-histamine receptor inhibition. Correspondingly, H1-receptor inhibitors of widely different chemical structure, such as clemizol, diphenhydramine, brompheniramine, and promethazine, in 0.03-0.06 nM concentrations, induced an analogous cercarial immobilization reversed by addition of excess histamine. In contrast, the H2-receptor inhibitors cimetidine and metiamide did not immobilize cercariae. Histamine, acetylcholine, and serotonin, added to cercarial suspensions, showed no direct activity. Their participation in the mechanism of cercarial mobility was shown by the dose-dependent effects of antagonists, such as the serotonin antagonist methysergide and the acetylcholinesterase inhibitor physostigmine. These effects were not reversible by addition of serotonin and acetylcholine, respectively. A histamine-irreversible cercarial immobilization induced by the H-liberator 48/80 suggested that, besides H1-receptor inhibition, H-liberation and/or depletion also participated in mobility and survival. The detection of histamine in the cercaria corroborated the participation of histaminergic mechanisms. S. mansoni schistosomules collected from the mouse lung reacted to H1 antihistamines like cercariae, with a dose-dependent reduction of mobility and somatic deformation, such as vacuolization, granulation, and caecal enlargement.

Acetylcholine↗
PubMed1992

Cold urticaria as a model of mediator release: platelet factor 4, eosinophil cationic protein and histamine.

Platelet factor 4 (PF4) has previously been linked to precipitation of cold urticaria (CU). The aim of the study was to assess the liberation of PF4, eosinophil cationic protein (ECP) and histamine after cold challenge in patients with CU. Ten controls and 8 patients with CU verified by clinical data and cold challenge test were investigated. Assessment of histamine, ECP and PF4 were done using radioimmunoassays. In patients histamine increased after 10 min on the challenged arm (NS), PF4 increase was statistically significant (p less than 0.05) both in patients and controls. ECP release showed no significant changes. Treatment with doxepin results in clinical improvement, but no changes in mediator release were seen. Thus, in contrast to previous reports an increase of PF4 was seen both in controls as well as in patients. An involvement of ECP was not ascertained. Our data suggest that neither basophils, nor eosinophils or platelets are directly involved in cold urticaria and that mast cell-dependent mediators may be of greater relevance.

Adolescent↗
PubMed1987

Guanosine 5'-(gamma-thio)triphosphate stimulates arachidonic acid liberation in permeabilized rat peritoneal mast cells.

The exocytotic histamine secretion from ATP-permeabilized and Mg-resealed rat peritoneal mast cells is markedly enhanced by the addition of guanosine 5'-(gamma-thio)triphosphate (GTP gamma S) at a concentration of 100 uM. GTP gamma S also caused a great enhancement of arachidonic acid liberation from these cells. The level of released arachidonic acid in permeabilized cells enhanced by GTP gamma S in the absence of Ca2+ was nearly equal to the level of permeabilized cells incubated in the presence of Ca2+ but without GTP gamma S, suggesting the Ca2+ sparing effect of GTP gamma S. From the time sequential changes in the [3H]arachidonate radioactivities in various phospholipids, it is conceivable that nucleotide-dependent arachidonic acid release was mediated via phospholipase A2 pathway. The entrapment of a diacylglycerol (DG) lipase inhibitor, RHC 80267, caused suppression of both Ca2+- and guanine nucleotide-dependent arachidonic acid liberation in mast cells, indicating contribution of DG lipase pathway for arachidonic acid generation.

Adenosine Triphosphate↗
PubMedDate not supplied

[Evaluation of the combined action of muscarinic receptor antagonists and beta receptor agonists on reactivity of basophils isolated from blood of patients with atopic bronchial asthma].

The study aimed at evaluating effects of selective M1 receptors antagonist-pirenzepine-and selected beta-receptor-agonists-orciprenaline or salbutamol, given alone or in combination, on histamine release from basophils isolated from patients with atopic asthma. Histamine concentration in the cells was assayed with spectrofluorimetric technique described by Shor and modified by Scov and Norn, using anti-IgE and metacholine as liberators. It was showed, that pirenzepine inhibits histamine release caused by both anti-IgE and metacholine. In the latter case this inhibitory effect was more significant. Beta-sympathicomimetics acted conversely, significantly inhibiting immunological histamine release. This effect was weaker, if metacholine was used. Combination of these agents increased protective effect of pirenzepine on histamine release induced by metacholine.

Adult↗
PubMedDate not supplied

[Antihistaminics].

The antihistamines are drugs who compete for the histamine receptor H-1, blocking the liberation of autacoid mediators, that is the reason for their action in allergic diseases. It's important to know the pharmacodynamics and pharmacokinetics of these drugs in order to choose the best one for the patient, looking for the ones who have less side effects and work better. We show a summary of the principal antihistamines, their actions and side effects.

Eicosanoids↗
PubMed1976

Release of prostaglandins from healthy and sensitized guinea-pig lung and trachea by histamine.

The effects of histamine and its antagonists on the release of prostaglandin E and F2alpha (PGE and PGF2alpha) and the 15-keto-13,14-dihydro PGF2alpha/E (metabolites) were examined in minced and whole perfused guinea pig lung. Lung fragments released considerable amounts of prostaglandins into the incubation media with time alone: parenchyma more PGF2alpha than PGE, trachea more PGE than PGF2alpha. The levels of PGF2alpha found in the filtrates of both tissues on per gram basis were about the same, whereas the concentrations of PGE were several fold higher in the media of incubated trachea. In contrast to lung, trachea released only trace amounts of metabolites. These differences in synthesis and turnover are probably of importance for maintenance of the adequate ventilation-perfusion ratios. The process of sensitization caused a significant increase in the outflows of PGF2alpha and metabolites from the lung fragments. The PGE to PGF2alpha ratio was decreased in both parenchymal and tracheal tissues. Increased spontaneous release of prostaglandins was also found in whole perfused sensitized lung. This was consistent with the hypothesis that sensitization with antigen alters the biochemical properties of the organism. Incubation of lung fragments with histamine had only a small additional effect on the liberation of prostaglandins, since the baseline release was high due to the trauma of mincing. However, histamine perfusion of whole lung caused severalfold increase in the outflows of prostaglandins. Pretreatment with pyrilamine (histamine receptor 1 antagonist) decreased the subsequent release of PGF2alpha by histamine. On the other hand, pretreatment with metiamide (histamine receptor 2 antagonist) diminished the subsequent release of PGE. It is suggested that stimulation of histamine receptor 1 is predominantly (but not solely) related to the synthesis of PGF2alpha, and stimulation of the receptor 2 is related to the synthesis of PGE.

Animals↗
PubMed1985

Simultaneous inhibitions of inositol phospholipid breakdown, arachidonic acid release, and histamine secretion in mast cells by islet-activating protein, pertussis toxin. A possible involvement of the toxin-specific substrate in the Ca2+-mobilizing receptor-mediated biosignaling system.

Incubation of rat mast cells with compound 48/80 resulted in transient breakdown of phosphatidylinositol 4,5-bisphosphate, rapid generation of inositol polyphosphates, 45Ca inflow, and the arachidonic acid liberation mainly from phosphatidylcholine, eventually leading to histamine secretion. All of these processes of signaling from Ca-mobilizing receptors to degranulation were markedly inhibited by prior 2-h exposure of cells to islet-activating protein (IAP), pertussis toxin. A23187 caused 45Ca inflow and releases of arachidonic acid and histamine without inducing breakdown of inositol phospholipids. The effects of A23187, in contrast to those of compound 48/80, were not altered by the exposure of cells to IAP. Incubation of the supernatant fraction of mast cell homogenates with the active component of IAP caused the transfer of the ADP-ribosyl moiety of added [alpha-32P]NAD to a protein with Mr = 41,000. The IAP-catalyzed ADP-ribosylation of this protein was prevented by guanosine 5'-(3-O-thio)triphosphate, indicating that this IAP substrate resembles, in character, the alpha-subunit of the guanine nucleotide regulatory protein (Ni) involved in inhibition of adenylate cyclase. The degree of ADP-ribosylation of this IAP substrate was prevented progressively by pre-exposure of the homogenate-donor cells to increasing concentrations of IAP. The half-maximally effective concentrations of the toxin were 0.2 to 0.6 ng/ml for all the IAP-sensitive processes studied. Thus, the ADP-ribosylation of the Mr = 41,000 protein occurring during exposure of cells to IAP appears to be responsible for the inhibition of signaling observed. It is proposed that the alpha-subunit of Ni, or a like protein, mediates signal transduction arising from Ca-mobilizing receptors, probably prior to Ca2+ gating.

Adenosine Diphosphate Ribose↗
PubMed1987

Interference with the distribution and release of arachidonic acid in human keratinocytes by bradykinin, histamine and phosphatidic acid.

The effects of bradykinin, histamine, phosphatidic acid and leukotrienes B4 and C4 on the distribution and release of 14C-arachidonic acid in human keratinocytes in culture were investigated. Bradykinin, histamine, and phosphatidic acid were found to liberate 14C-arachidonic acid from membrane phospholipids, whereas leukotrienes B4 and C4 were ineffective in this respect. The decrease in the labeling of phospholipids was accompanied by increased labeling of the non-phosphorus lipids. The present study suggests that bradykinin, histamine, and phosphatidic acid may interfere with the distribution and release of arachidonic acid in human keratinocytes in culture.

Arachidonic Acid↗
PubMed2007

Chronic urticaria--which clinical parameters are pathogenetically relevant? A retrospective investigation of 339 patients.

BACKGROUND: Urticaria is a clinical reaction pattern triggered by many factors causing liberation of vasoactive substances such as histamine, prostaglandins and kinins. It presents as transient itching wheals which are either limited to the local stimulus area or more widespread. Urticaria is classified according to its duration into acute (duration > or = 6 weeks) and chronic (duration 6 weeks) forms. Various clinical investigations may be initiated to diagnose the cause. This study critically evaluates the relevance of frequently performed laboratory investigations and searches for infectious foci, as well as the results of physical provocation testing and oral provocation with food additives. PATIENTS AND METHODS: The laboratory and clinical data of 339 patients who had been treated for urticaria at the Christian-Albrechts-University in Kiel over a period of four years were collected in a data entry form and statistically evaluated. Nominal values were analyzed by their relative and absolute quantities, quantitative parameters with the help of statistical data such as minimum, maximum, median and 25th and 75th percentiles. RESULTS: Chronic recurrent urticaria was most common, accounting for 52% of cases. Women were affected 1.8 times more often than men. One-third of the patients also had angioedema. The medians of all laboratory parameters evaluated were within normal values. Only rarely were elevated antinuclear antibody titers, abnormal thyroid function tests or active infections such as hepatitis B or borreliosis detected. The search for infectious foci identified tonsillitis or sinusitis in almost 50% of analyzed patients. Positive reactions to physical testing occurred in 30% of patients and in 11% to oral provocation with various food additives. CONCLUSIONS: This study of a large patient group stresses the relevance of individually-tailored evaluations in patients affected with urticaria rather than an expensive initial broad diagnostic testing. More specific searches should be based on individual clues.

Female↗
PubMed1981

Effect of pharmacologic agents on antigen-induced decreases in specific lung conductance in sheep.

The purpose of this investigation was to determine the primary mediators responsible for the decrease in specific lung conductance (SGL) after airway challenge with Ascaris suum antigen in allergic sheep. On different occasions, separated by 10 to 14 days, pulmonary resistance and thoracic gas volume were measured in 5 sheep with Ascaris suum hypersensitivity before and for 2 h after a standard inhalation challenge with this antigen. Initially and at the end of the study, inhalation challenge decreased mean SGL to 38 and 44% of baseline, respectively. Pretreatment by intravenous injection of the H1 receptor antagonist chlorpheniramine (2 mg/kg) completely prevented the antigen-induced decrease in SGL. Similar results were obtained with inhalation of the mediator release blocking agent, disodium cromoglycate (1 mg/kg), prior to antigen challenge. The decrease in SGL after inhalation challenge was not modified by pretreatment with the H2 receptor antagonist, metiamide (3 mg/kg), the anticholinergic agent, atropine (0.2 mg/kg), the prostaglandin synthetase inhibitor, indomethacin (2 mg/kg) by intravenous injection, or with inhalation of FPL-55712 (1% solution), an antagonist of slow-reacting substance of anaphylaxis (SRS-A). We concluded that during allergic bronchoconstriction in sheep (1) the decrease in SGL is mediated by histamine via H1 receptors, (2) other liberated or activated mediators including SRS-A do not decrease SGL, and (3) cholinergic reflex mechanisms are not involved in this response.

Airway Resistance↗
PubMedDate not supplied

Disturbance of myocardial energy liberation in experimental charcoal embolism of canine pulmonary artery.

Experimental charcoal embolism of the pulmonary artery was produced in dogs. Changes in hemodynamics, electrophysiology, and cardiac energy liberation were observed. The effects of histaminic and antihistaminic drugs on these changes were also studied. After two infusions of charcoal suspension, acute right ventricular overloading was recognized hemodynamically and electrophysiologically. Mitochondria isolated from both ventricles exhibited uncoupling of oxidative phosphorylation polarographically. These changes were enhanced with histamine injection and reduced with diphenhydramine injection. Histamine was seen to have some uncoupling effects on the heart mitochondria and a slight effect on cardiac dynamics. It is concluded that oxidative phosphorylation of the heart mitochondria was uncoupled in the acute stage of experimental pulmonary embolism, and that histamine might emphasize this change directly or indirectly or both, that is, directly affecting the myocardial cell metabolism, and indirectly aggravating myocardial hypoxia through pulmonary vasoconstrictive action.

Animals↗
PubMed1986

[Present physiopathological concepts of asthma in adults].

Curiously enough, a kind of curse combined with therapeutic fatalism still hovers over bronchial asthma and a sense of hopelessness may be encountered when faced with this illness. This pessimism is totally unfounded. However, our therapeutic possibilities depend partly on a better understanding of the asthma syndrome. In the past, this condition may not have been recognised for what it is, that is to say a multi factorial syndrome resulting from the innate and the acquired, from specific (allergic) and/or non-specific factors. Undoubtedly, too much responsibility has been placed on the allergic factor in asthma. Although important, it has made us overlook the fact that, allergic or not, asthma is an inflammatory illness of the bronchi provoked by the liberation of mediators. The role of histamine has been well known for a long time and we now realise the importance of the actions of the metabolites of arachidonic acid (prostaglandins and thromboxanes on the one hand, leukotrienes on the other). The characteristics bronchial hyperreactivity observed in asthma may certainly be congenital but this factor may also be acquired as in professional and post-viral asthma. If bronchial asthma remains under-diagnosed and under-treated in France and in Europe it is due to the fact that the artificial distinction between paroxysmal (bronchitis called "asthmatic"), and persistent (that is to say a so-called asthmatic illness), is is often maintained. There is no real ground for maintaining this distinction. Every child with wheezy dyspnea must therefore be the object of a thorough, initial medical examination, including in particular a respiratory function exploration followed by the institution of a long-term, coherent therapeutic strategy.

Adult↗
PubMed1982

[Chronic urticaria. Treatment with ketotifen].

Ketotifen inhibits the Ca++ pass through the mastocyte and basophil membrane. So inhibit histamine and S. R. S. A. liberation. Results in the treatment with Ketotifen of 36 cases of chronic Urticaria are exposed. Patients between ten and fifty years old, and with symptoms chronicity during from two until ten years, were studied. Chronic cases of unknown etiology, cholinergic urticaria, salicylates urticaria, urticaria by pressure, local heat urticaria and chronic dermographism were treated. Results were hopeful. Especially in patients with cholinergic urticaria, urticaria by heat, salicylates urticaria and strong idiopathic dermographism.

Administration, Oral↗
PubMed1984

Differential activation of membrane phospholipid turnover by compound 48/80 and ionophore A23187 in rat mast cells.

Membrane phospholipid turnover was investigated during histamine release from rat mast cells. Addition of calcium ionophore A23187 (0.5 microgram/ml) to mast cells prelabeled with [3H]glycerol induced the rapid and progressive increase in phosphatidic acid (PA) and 1,2-diacylglycerol (DG), which was concomitant with the small rise in phosphatidylinositol (PI). Loss of the level in triacylglycerol (TG) was very marked. Polyamine compound 48/80 (5 micrograms/ml) was shown to cause rises in PA, 1,2-DG, and PI without any significant changes in TG. Both stimuli increased incorporation of exogenous [3H]glycerol into phospholipids, indicating the involvement of de novo synthesis in phospholipid metabolism. Studies with [3H]arachidonic acid-labeled mast cells showed an enhanced liberation of radioactive arachidonate and metabolites upon histamine release. There were associated decreases of radioactivity in phosphatidylcholine (PC) and TG when exposed to A23187, while phosphatidylethanolamine (PE) was degraded as a result of 48/80 activation. The transient increases of [3H]arachidonoyl-1,2-DG and PA were caused by 48/80, while A23187 showed a gradual rise in the radioactivity in these two lipid fractions. These findings reflect activation of phospholipase C. When mast cells were activated by low concentrations of A23187 (0.1 microgram/ml) and 48/80 (0.5 microgram/ml), different behaviors of PI metabolism were observed. An early degradation of PI and a subsequent formation of 1,2-DG and PA suggest that the lower concentrations of these agents stimulate the PI cycle initiated by PI breakdown rather than de novo synthesis. These results demonstrate that marked and selective changes in membrane phospholipid metabolism occur during histamine release from mast cells, and that these reactions seem to be controlled by the coordination of degradation and biosynthesis, depending on the type and the concentration of stimulants. A23187 stimulates arachidonate release perhaps via the cleavages of PC and TG, whereas 48/80 liberates arachidonate from PE.

Animals↗