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At least 649 records · Page 36Linked to original sources
PubMed1987

[The relationship between Ca++ ions and a protein specific to cromolyn in the degranulation of mast cells and basophils in the rat].

Previous research has shown that cromolyn (disodium cromoglycate) binds specifically to the membrane of rat mast and basophil leukemia (RBL) cells, forming a ternary complex with Ca++, blocking of the Ca++ results in inhibition of histamine release upon immunologic triggering. The specific cromolyn binding protein (CBP) has been isolated by using its high affinity form cromolyn. Specific monoclonal anti CBP antibodies have been obtained in mice and polyclonal anti-cromolyn antibodies in rabbits. These antibodies have been used for further purification and characterization of the CBP. Experiments on RBL cell lines have shown that CBP is essential for Ca++ influx and histamine liberation upon immunologic triggering by these cells. Variant CBP deficient RBL do not take up Ca++ and do not degranulate in response to immunologic triggering but their ability to respond normally can be induced by incorporating CBP into their membranes with help of Sendai virus carrier vesicles. This shows that CBP plays a crucial role for the RBL cells Ca++ influx and histamine release following IgE crosslinking.

Animals↗
PubMedDate not supplied

Pharmacological aspects of immune reactions.

"Immunopharmacology" evolved as a field of research in its own right when it was appreciated that pharmacological methods can contribute to the understanding of immune mechanisms on the one hand or can be used to influence or even control immune reactions at all stages and levels. The best studied subjects of immunopharmacology are release and effects of the chemical mediator substances which are responsible for the reactions of effector cells thus causing the clinical symptoms in allergic or inflammatory diseases. In the type I allergic (anaphylactic) reactions the primary target cells are tissue mast cells or basophil granulocytes which discharge their granular contents upon interaction of immunoglobulin E fixed to their surface with the specific antigen or--in the anaphylactoid reaction--upon stimulation with an appropriate chemical substance (so-called histamine-liberator). In both cases the stimulus leads to an influx or intracellular shift from one compartment to another of calcium ions, which in turn trigger membrane fusion and degranulation. This process can vary from a physiological secretion (in the case of IgE-antigen-interaction) to a pathological cytolysis (in the case of high concentrations of activated complement components or other chemical histamine releasers). As long as it is secretory it is subject to vegetative and hormonal modulation and regulation, mainly by catecholamines and other substances which increase cellular cAMP levels or inhibit calcium fluxes. Although cholinergic stimuli under certain circumstances induce mast cell degranulation and histamine release no definite role has yet been established for cholinergic mechanisms in type I allergies. Type II (Cytotoxic) and type III (immune complex mediated) allergies share the complement requirement. As far as mast cells and basophils are involved in such reactions their sensitivity towards pharmacological modulators is comparable to reactions induced by chemical histamine releasers. Otherwise these types of allergic reactions are dominated by phenomena of general inflammation. In those mainly cytotoxic effects of lipases and hydrolases are involved. cAMP active agents have, therefore, only limited modulating effects and steroid hormones are more effective in inhibiting the acute lesions in type II and III allergies. Only during the last decade the involvement of chemical mediators in type IV (cellular immunity) allergic reactions has been appreciated. 26 different factors called lymphokines have been discovered and classified as mediators of cellular immune reactions. However, rather little is yet known about their chemical nature and about the influence of drugs on their production or action.

Allergens↗
PubMedDate not supplied

Early increase in histamine concentration in the islets of Langerhans isolated from rats made diabetic with streptozotocin.

Sprague-Dawley rats were separated in 4 groups. G1 received streptozotocin (ST). G2 received nicotinamide (NC) followed by ST. G3 was a NC control and G4 was a citrate control. The rats were sacrificed after 28 h and the islets isolated. Histamine and histaminase were determined. In the islets there was an increase in histamine content in G1 and a smaller increase in G2. The first two groups differ significantly and also in relation to the control groups. A decrease in islet histaminase does not seem responsible for the increased histamine, since group 2 (NC + ST) which had no diabetes, had a lower activity than group 1 (ST). It is suggested that histamine liberation by ST may be related to the diabetogenic effect of this drug.

Amine Oxidase (Copper-Containing)↗
PubMed1988

[Low molecular weight peptides from the venom of the giant hornet Vespa orientalis. Structure and function].

Three 14-member linear peptides (HR-1, HR-2 and HR-3) capable of degranulating mast cells and thus initiating histamine release were isolated from the venom of the giant hornet Vespa orientalis, using reverse phase high performance liquid chromatography. The complete amino acid sequence of the peptides HR-1 and HR-2 molecules and partial structure of peptide HR-3 were determined, using automatic degradation by the Edman method. It was shown that peptide HR-1 at relatively low concentrations (2-20 micrograms/ml) selectively liberated histamine from rat mast cells and, when taken at higher doses (50-100 micrograms/ml), exerted a non-selective cytotoxic action. Besides, this peptide caused erythrocyte hemolysis, inhibited Ca2+-ATPase with concomitant uncoupling of Ca2+ transport and ATP hydrolysis as well as induced the conductance of lipid bilayer membranes, predominantly for monovalent cations due to the formation of nonspecific single permeability channels.

Amino Acid Sequence↗
PubMed1985

Isolation and properties of cardiac and other mast cells from the rat and guinea-pig.

A method is described for the enzymic dispersion into their component cells of cardiac tissues from the rat and guinea-pig. The resulting suspensions contain ca. 1% free mast cells and exhibit a low spontaneous release of histamine. The reactivity of these cells towards a number of defined chemical histamine liberators is compared with that of other connective tissue mast cells from the same animals. The results obtained are discussed in terms of the general functional heterogeneity of mast cells from different locations.

Animals↗
PubMed1988

An electron microscopical observation of the endoneurial mast cells of the laboratory musk shrew: Suncus murinus).

Histochemical and ultrastructural properties of endoneurial mast cells of the normal and histamine liberator Compound 48/80 (48/80)--injected musk shrew, Suncus murinus (Suncus) were examined by light and electron microscopies. It was observed that the normal mast cells contained numerous cytoplasmic granules, with dense and irregular dense cores, covered at times with slender microvilli. The cells were diffusely located within the endoneurial sheath of the peripheral nerve fibers and in the intercellular spaces of the spinal ganglion cells. Histochemically, histamine, 5-hydroxytryptamine and heparin were observed in mast cell granules. Biochemical analysis also indicated a relatively high content of histamine in the suncus peripheral nerve. A single intradural-injection of 48/80 resulted in the degranulation of endoneurial mast cells and revealed peculiar axoplasmic changes make up of neurofilament-mitochondrial complexes in the peripheral nerve fibers. No remarkable histochemical and ultrastructural differences were observed between the endoneurial mast cells and the connective tissue mast cells in the suncus. The significance of these findings is discussed with regard to previous studies of the endoneurial mast cells in other laboratory animals.

Animals↗
PubMed1977

[Mechanisms of anaphylactoid reactions to drugs used in anesthesiology].

Anaphylactic reactions to drugs used in general anesthesia have a complex mechanism: true anaphylaxis by antigen antibody reaction (IgG our IgE) histamine liberation by certain substances with a special chemical structure, activation of the alternative route of complement. The authors recall the immunological stages in each case and give examples.

Adjuvants, Anesthesia↗
PubMed1957

Histamine release and pain production by xanthosine and related compounds.

Xanthosine (5 to 50 mug.) caused pain on intradermal injection in all human subjects tested: in about half the subjects it also gave a flare. Inosinic acid, uric acid, allantoin, alloxan and theophylline caused pain, but not a flare by intradermal injection in man. Xanthine caused both pain and flare. A number of related compounds in similar doses caused neither pain nor flare. Inosine, inosinic acid, and guanosine, but not xanthosine, were powerful histamine liberators in animals. The lowering of the cat blood pressure, depression of the activity of the guinea-pig ileum and stimulation of guinea-pig uterus by adenosine were confirmed.

Adenosine↗
PubMed1976

[Anaphylactoid complications due to the use of anesthetic products and adjuvants. Apropos of 18 cases].

Eighteen grave anaphylactic accidents arising during induction or during anaesthesia, are analysed. By order of frequency, the clinical signs are cutaneous manifestations (70 p. 100 of the cases), bronchospasm (65 p. 100), cardiovascular collapse (45 p. 100). In four cases, cardiac arrest occurred. The course was always favourable, with no after-effects. Immuno-allergic tests enabled one to make the diagnosis of true anaphylaxis in eight cases (seven shocks due to succinylcholine, one due to propanidide), of non specific histamine-liberation in five cases; in the other cases, it was impossible to express an opinion.

Adjuvants, Pharmaceutic↗
PubMed1988

Some studies on the isolation and properties of pulmonary mast cells from the pig.

Mast cells were isolated by the enzymic dissociation of lung tissue from the pig. The responses of these cells to a variety of histamine liberators and anti-allergic drugs were examined. On the basis of these findings, the possible use of porcine pulmonary mast cells in the study of immediate hypersensitivity reactions is discussed.

Animals↗
PubMed1986

Occurrence and release of histamine-containing granules in summer cells in adrenal glands of the frog Rana catesbeiana.

'Summer cells' of the adrenal gland in Rana catesbeiana were investigated by means of fluorescence microscopy and electron microscopy. Orthophthaldialdehyde treatment of freeze-dried tissues revealed that the summer cells possess histamine in the cytoplasmic granules. Based on the 'Faglu' technique, the summer cells were found to be free of monoamines. Ultrastructural examination showed that each summer cell was invariably surrounded by lipid cells and was segregated from other tissue components including neighbouring summer cells. Administration of compound 48/80 (a histamine liberator) evoked a rapid release of cytoplasmic granules. The envelope of the lipid cells became detached from the summer cells in the course of degranulation. Relationship between the summer cells and the mast cell family is discussed.

Adrenal Glands↗
PubMed1983

Modulation of the host response in human schistosomiasis. IV. Parasite antigen induces release of histamine that inhibits lymphocyte responsiveness in vitro.

Several mechanisms underlying the suppression of in vitro lymphocyte transformation responses to parasite antigens in human schistosomiasis have been previously described, but the role that immediate hypersensitivity reactions may have in regulating these lymphocyte transformation responses has been little explored. Using Hypaque-Ficoll-separated peripheral blood mononuclear cells (PBMC) from patients with schistosome infections, we found that histamine release could be demonstrated routinely in lymphocyte cultures challenged with adult worm, egg, or cercarial antigens. Release occurred within 1 hr of stimulation, and histamine persisted in the cultures for 6 days at levels of 10(-6) to 10(-7) M. That such concentrations were capable of suppressing LT responses in vitro was shown by the addition of exogenous histamine to modified PBMC culture systems from 10 normal individuals and eight patients with Schistosoma mansoni or Schistosoma mekongi infections. Responses to phytohemagglutinin, streptokinase-streptodornase, and tetanus were equivalently suppressed in both groups (50.8 +/- 6% in normals and 55.9 +/- 6.2% in patients), and the doses required for maximal suppression were similar. Passage of PBMC from infected patients over nylon wool, in addition to removing adherent suppressor cells, also markedly reduced the number of histamine-containing basophils (74 +/- 4.5% removed). The enhanced responsiveness to parasite antigen by PBMC depleted by nylon wool passage was abrogated by the addition of exogenous histamine to the cultures. These results indicate that in routine PBMC cultures 'nonspecific' lymphocyte suppression by histamine liberated from basophils in an antigen-specific fashion may help to account for the specific suppression of lymphocyte responses to parasite antigens so characteristic of patients with schistosome and other helminth infections.

Antigens↗
PubMed1997

[The clinical pharmacology of new benzylisoquinoline-diester compounds, with special consideration of cisatracurium and mivacurium].

The benzylisochinoline muscle relaxants have a highly selective affinity to the motor endplate which is associated with an absence of autonomic side effects such as ganglionic and vagus block. The requirement of only low clinical doses also reduces histamine liberation. Muscle relaxants with high neuromuscular blocking potency have a slow onset. Both atracurium and cisatracurium undergo Hofmann-Elimination in the plasma whereas mivacurium is hydrolyzed by pseudocholinesterase. The difference in kinetics between these pathways render atracurium and cisatracurium muscle relaxants of intermediate duration of action while mivacurium is short acting. Cisatracurium, one of the ten stereoisomeres of atracurium, is 3 to 4 times as potent as atracurium, does not release histamine, has no cardiovascular side effects and, due to the small clinical doses resulting from its high neuromuscular blocking potency, produces only negligible quantities of laudanosine. Its ED95 is 0.05 mg/kg. Good intubation conditions can be expected within 1.5 to 2 min following 3- to 4-times the ED95. Thereafter is takes about 65 min for T1 to recover to 25% of control. Maintenance doses of 0.02 to 0.04 mg/kg have a duration of action of 15 to 20 min. An infusion of cisatracurium of 1.0 to 2.0 mcg/kg/min, is adequate to maintain a 90 to 95% neuromuscular block. The time of recovery is largely independent on the total dose of cisatracurium administered by either repeated injection or infusion. Mivacurium is a racemate of 3 stereoisomeres of which the trans-trans- and the cis-trans-compound account for 95% of the neuromuscular blocking effect. In adults the ED95 is 0.08 mg/kg. The ensuing recovery of T1 to 25% of control is about 15 min. Rapid injection of 3xED95 may transiently lower the arterial blood pressure and may produce skin flushing in an incidence of 30 to 40%. Larger doses should be injected slowly with 30 to 60 s. The onset of mivacurium neuromuscular block following 3xED95 is relatively slow (2 min). Maintenance doses of 0.05 to 0.1 mg/kg have a duration of action of 5 to 10 min. A 95% neuromuscular block may be maintained by an infusion of 3 to 12 micrograms/kg/min. The time of recovery does not depend on the total cumulative dose given by either repeated injection or by infusion. The duration of mivacurium neuromuscular block may be drastically prolonged in the presence of low or atypical plasmacholinesterase. Both neostigmine and edrophonium are suitable reversal agents. None of the presently available benzylisochinoline muscle relaxants has the potential to completely replace succinylcholine.

Anesthesia↗
PubMed1995

The role of gastric mast cells, enterochromaffin-like cells and parietal cells in the regulation of acid secretion.

The idea presented here is that, in gastric mucosa, two independent regulatory systems use the same transmitter: histamine molecules. The IgE/mast cell system is dispersed throughout the body, while the other regulates the gastric acid secretion. IgE molecules in gastric mucosa are attached to the mast cells. Mast cells release histamine molecules after the antigen has been recognized by IgE. These molecules normally act on vascular H1 receptors to promote extravasation and chemotaxy. Gastrin molecules are released from antral G cells to stimulate gastric acid secretion. Their influence on parietal cells is indirectly augmented by gastrin governed release of histamine molecules from enterochromaffin-like cells. These histamine molecules normally act on H2 receptors of parietal cells to promote gastric acid secretion. Chronic infection of gastric mucosa (i.e. with Helicobacter pylori), autoimmune disorders or repetitive mucosal exposure to the same antigen, can develop chronic inflammation of gastric mucosa. Gastric acid secretion is diminished with secondary hypergastrinemia and increased release of histamine from enterochromaffin-like cells in an attempt to stimulate the few remaining parietal cells. Hypothetically, increased concentrations of released histamine in gastric mucosa might activate the vascular H1 receptors with extravasation and aggravated inflammation. This can further decrease the number of active parietal cells, reduce gastric acid secretion and potentiate hypergastrinemia. In this hypothetical setting, H1 blockers might reduce the damage by abolishing the vascular reactions. The prolonged antigen load on gastric mucosa can promote production of specific IgE antibodies. Further exposures to the same antigen degranulate sensitized mucosal mast cells. Liberated histamine can produce extravasation through the vascular H1 receptor and, hypothetically, local hyperacidity through the parietal cell H2 receptors. The result would be hyperacidity and hypogastrinemia with possible ulcer disease. Some individuals are more predisposed to IgE production or have increased numbers of mast cells that might explain why only some people develop ulcer disease after H. pylori infection.

Animals↗
PubMed1981

The effects of nonidet P40 on the function of rat peritoneal mast cells in vitro.

1 Treatment of purified rat peritoneal mast cells at 37 degrees C with concentrations of the non-ionic detergent nonidet P40 (NP40) up to 0.005% (v/v) failed to reduce their viability. 2 There was a marked reduction in the histamine releasing capacity of NP40-treated mast cells upon challenge with a variety of selective (adrenocorticotrophic hormone 1-24 (Synacthen), rabbit anti-rat IgE antiserum, adenosine triphosphate (ATP) and the calcium ionophore, A 23187) and non-selective (rabbit anti-rat mast cell antiserum plus complement) histamine liberators. 3 Nonidet P40 (0.005%) was found to reduce the activity of a mast cell membrane 'ecto-enzyme', calcium-activated ATPase, by about 45% when presented at the time of its assay.

Animals↗
PubMed1984

The effect of H1 and H2 receptor blockers on immunological and nonspecific histamine release from isolated target cells.

The investigations were carried out on isolated peritoneal rat mast cells and human basophils. Cell histamine release was induced by a specific antigen, anti-IgE and by compound 48/80. Mepyramine and Diphenhydramine were used as H1 receptor blockers and Cimetidine as H2 receptor blocker. It was shown that effect of H1 and H2 receptor blockers on histamine release depends on concentration of drugs used in experiments, on the presence of exogenous histamine in the medium, on the kind of histamine liberators and also on the type of investigated target cells. The results obtained seem to indicate the presence of H2 receptors not only on basophils but also on mast cells.

Animals↗
PubMed1991

Characteristics of histamine secretion from mast cells stimulated with sodium orthovanadate and other vanadium compounds.

Sodium orthovanadate was found to be an effective histamine liberator from serosal mast cells of the rat and mouse. The release process was slow, non-cytotoxic and strongly dependent on pH and extracellular calcium. The effect was highly tissue and species specific and human basophil leucocytes, human lung mast cells and tissue mast cells of the rat and guinea pig were only weakly responsive or essentially unreactive. Other oxyanions of vanadium with the metal in the (+V) oxidation state also evoked histamine release from rat peritoneal mast cells but neither vanadyl sulphate (+IV oxidation state) nor the analogous orthophosphate anion were effective secretagogues. On the basis of these results, the possible mechanism of action of vanadate is discussed.

Animals↗