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[Effect of biologically active splenic factors on the functional state of mast cells in rats].

The effects of "splenic protein-free extract" and its fractions as well as splenin on the functional activity of the rat mast cells have been studied. It is established that this extract unlike splenin has no histamine-releasing activity, however it is able to inhibit histamine release from mast cels under the influence of specific liberator--substance 48/80. The found effect is associated with biologically active substances contained in fraction III of splenic protein-free extract.

Animals↗

PubMed1984

Synthesis of prostaglandin F by cultured human endometrial cells.

Human endometrial cells were dispersed with collagenase and maintained in culture overnight. The synthesis of PGF by the dispersed cells incubated at 37 degrees C in serum-free medium was stimulated by estradiol (10(-7)M - 10(-5)M), histamine (5X10(-7)M - 5X10(-5)M), bradykinin (10(-6)M), phorbol myristate (PMA, 3X10(-8)M) and arachidonate (5X10(-6)M). Preincubation of the cells for 3 h with cortisol (5X10(-7)M - 5X10(-5)M), progesterone (10(-6)M) or mepacrine (10(-6)M - 2X10(-4)M) inhibited the response to histamine, bradykinin and PMA but not to arachidonate. Perfusion of the cultured cells in filtration chambers yielded similar results to those obtained in the incubation system but differences in the onset and duration of the responses to stimuli were found. In the perifusion system the responses to histamine and bradykinin were rapid and of short duration (peak response in less than 60 min) while the responses to PMA and arachidonate were of longer duration with a slower onset. We conclude that these observations using dispersed endometrial cells are consistent with previous work showing that histamine, bradykinin and PMA act by stimulating acylhydrolase activity, thereby liberating precursors such as arachidonic acid which are converted to prostaglandins by the cyclo-oxygenase complex.

Arachidonic Acid↗

PubMed1980

The role of prostaglandin F2 alpha in byssinosis.

Female guinea pigs were perfused via the pulmonary artery with Tyrode's solution containing 0, 10(-6), 10(-5), or 10(-4) g/mL of lyophilized aqueous extracts of cotton dust. The perfusate was collected via the pulmonary vein and analyzed for prostaglandin F2 alpha, its metabolite 15-keto-13, 14-dihydro-prostaglandin F2 alpha and histamine. The histamine content of the pulmonary parenchyma was also analyzed. Prostaglandin F2 alpha, its metabolite, and the percentage of total histamine released increased in a dose related fashion and were significantly higher in the perfusate of the animals which had received the two highest doses than that of the controls. Since prostaglandin F2 alpha can increase airway resistance and bronchial smooth muscle contraction and decrease pulmonary tidal volume, its liberation into the respiratory system could play a role, along with histamine, in the acute bronchial constriction that follows the inhalation of cotton, flax, or hemp dust.

Animals↗

PubMed1988

Ovulation.

Three events lead to the ovulation of a normal oocyte: cytological and biochemical changes in the follicle wall, disintegration of the follicle apex and oocyte maturation. The remodelling of the follicle wall results from plasmin and collagenase activities. The thinning of the follicular apex, in addition to these enzymes, involves hydrolases liberated by dying ovarian epithelial cells. PGF2 alpha and histamine are also involved but it is not known precisely how they contribute to the apical dissociation. The nuclear and cytoplasmic maturation of the oocyte is highly dependent on the synthetic activities of granulosa cells which are regulated by LH and FSH. The pulsatile secretion of these gonadotrophins is not necessary for the final phase of Graafian follicle growth and rupture. Why high levels of gonadotrophins, normally reached during the preovulatory surge, completely change the structure and the biochemical activities of all follicular compartments remains unknown and in fact has never been studied. Moreover, there is very little information concerning the mechanisms involved both in the increase of blood flow during the LH surge and later in the blood stasis at the follicular apex. Steroids, whatever their levels and ratio, are of little if any concern in follicle rupture and nuclear maturation. However, their importance has been clearly demonstrated in the cytoplasmic maturation of the oocyte of some species.

Animals↗

PubMed1984

Mechanisms of control of intestinal transport: a review.

Of the long list of substances which are capable of influencing intestinal transport, corticosteroids and aldosterone probably exert a prolonged, modest, controlling influence on salt and water absorption. They are likely to be important in situations where variation in colonic absorption occurs, such as in the rabbit, or in circumstances where salt depletion or salt overload are likely. There is modest evidence in favour of the possibility that the gastrointestinal hormones liberated locally after a meal limit the rate of absorption of salt and water at that time, perhaps to maintain the fluidity of luminal contents for digestion to occur. More rapid short-term regulation of salt and water absorption in localized areas of the intestine may be exerted by peptide secretions from the enteric nervous system and paracrine cells. Cholinergic and adrenergic effects on secretion and absorption respectively may be responsible for maintaining an overall balance, and there is reasonable evidence in favour of this view. There is also strong circumstantial evidence to support a role for VIP in intestinal secretion. VIP may also play a part in mediating secretory diarrhoea. A role for the large number of other neurotransmitters remains uncertain but it is likely that overall control is maintained by a combination of counter-balancing factors. Finally, under pathological circumstances, where damage to the intestine liberates such mediators of the inflammatory response as prostaglandins, histamine and bradykinin, intestinal secretion may occur and be responsible for the diarrhoea associated with these diseases.

Animals↗

PubMed1989

Anaphylactic death: the effect of aminoguanidine and heparin on histamine and stress hormones in guinea pigs.

The modifying effect of aminoguanidine (a histaminase inhibitor) and heparin (a histaminase liberator) on anaphylactic shock in guinea pigs was studied using ovalbumin as an antigen and trigger. The animals died of the shock, the time to death remaining unaltered by the drugs. Serum histamine and cortisol values were high after shock, but were reduced by heparin. Both noradrenaline and adrenaline in plasma were also elevated after shock, the final concentration of the latter being lowered by heparin. The lungs were dilated, indicating bronchoconstriction. The results confirm the role of histamine in anaphylactic shock and its potential value for the diagnosis in this kind of rapid death, in which morphological signs are scarce or lacking. Its diagnostic value still requires confirmation, however, which only autopsy studies can supply. It also appears that pretreatment of the animals with heparin affected the blood cortisol and catecholamines, which are involved in the shock mechanism as countermeasures, although aminoguanidine did not have any effect.

Anaphylaxis↗

PubMed1973

The release of spasmogenic substances from human chopped lung tissue and its inhibition.

1. Human lung tissue, passively sensitized with reaginic antibodies, released prostaglandins E(1), E(2) and F(2alpha) in addition to histamine and slow reacting substance (SRS-A), when exposed to the appropriate antigen. No rabbit aorta contracting substance (RCS) was detected.2. Experiments with rats and guinea-pigs showed that the release of RCS is not confined to anaphylactic reactions mediated by non-reaginic antibodies but may be a feature of anaphylaxis in guinea-pigs alone.3. Human lung tissue gently agitated with a blunt nylon rod liberated an E-type prostaglandin and RCS in addition to histamine and SRS-A.4. Human isolated bronchial muscle was contracted by RCS.5. Disodium cromoglycate antagonized the release of prostaglandins during anaphylaxis but not during agitation of human lung tissue, whereas indomethacin blocked the release of prostaglandins during agitation and anaphylaxis.6. The release of an E-type prostaglandin during anaphylaxis in human lung tissue, which inhibits the further release of histamine could be another example of the regulatory role of prostaglandins in body functions.

Anaphylaxis↗

PubMed1991

Hydrogen peroxide alters signal transduction in human endothelial cells.

Lytic H2O2-induced injury to human umbilical vein endothelial cells provides a model for endothelial cell damage in diverse states including acute respiratory distress and septic shock. Endothelial cell lysis is an extreme result of inflammatory cell activation. Functional alterations such as responsiveness to endothelial cell agonists and eicosanoid production might be impaired by exposure to inflammatory cell products including H2O2. Soluble mediators such as thrombin or histamine cause endothelial cell activation via a signal transduction mechanism that hydrolyzes phosphatidylinositol 4,5-bisphosphate (IP), liberating inositol trisphosphate (IP3). Accordingly, pretreatment of endothelial cells with H2O2 blocked the subsequent production of IP3 in response to thrombin and histamine. H2O2 inhibition of IP3 was time- and concentration-dependent. The endothelial cells were viable by trypan blue dye exclusion and chromium release. H2O2 inhibition of signaling was completely prevented by catalase. Iron-dependent oxidant radical formation appears critical because deferoxamine (10(-4) mol/L) pretreatment of endothelial cells prevented H2O2 inhibition of IP hydrolysis. Prostacyclin and platelet activating factor production in response to thrombin have been linked to IP hydrolysis. Pretreatment of endothelial cells with H2O2 reduced prostacyclin and platelet-activating factor production by thrombin by at least 50%. It appears H2O2 can induce defects in signaling pathways with sequelae (decreased prostacyclin and platelet-activating factor) short of endothelial cell death. The possible consequences of H2O2 interaction with endothelial cells is reviewed with the aim of presenting a hypothesis to integrate these various observations.

Catalase↗

PubMed1994

Reliability of skin prick tests during terfenadine treatment in adults with pollen rhinitis. A clinical study.

The variation in skin prick test (SPT) results was evaluated clinically during terfenadine treatment in 39 adult patients with pollen rhinitis. A change in the perceived state of the patient as regards sensitization to a specific pollen allergen or atopic constitution was judged to be clinically important. A randomized, double-blind, crossover design was used, comprising 2 weeks on terfenadine 120 mg once a day and 2 weeks on placebo. SPT for two pollen allergens and histamine (10 mg/ml) were evaluated at the start of the study and at the end of each period. When SPT was used as a discovery test and liberal definitions were applied, predictive values for a positive test were 100%. 1-Sensitivity ranged between 10 and 54% with substantially lower values when a histamine wheal reaction was noted. The inhibitory effect of terfenadine was detectable 2 weeks after withdrawal as a reduction in the median of the mean diameter for the histamine-induced wheal response of 1 mm (0-1.5). The data implied that a positive SPT is reliable when liberal definitions are adopted for sensitization and atopy; a negative SPT is presumably reliable when the measurement artifact is considered and the wheal reaction to histamine is detectable.

Adolescent↗

PubMed2003

[H1 histamine antagonists].

Histamine is an important mediator for early phase allergic reactions that are involved in atopic diseases, mediated by specific IgE antibodies. After allergenic contact, its liberation induces unpleasant symptoms like itching, several manifestations as local vasodilatation, bronchoconstriction, mucus hypersecretion. Antagonists of H1 histamine receptors are the most prescribed drugs, due to their symptomatic effects at the levels of nasal or conjunctival mucosa, and the skin. Their major indications cover allergic rhinitis, either seasonal or perennial, and idiopathic chronic urticaria, as a first line medication. The pharmacological evolution allows to distinguish three generations of products differing at the levels of specificity, long acting period, and toxicity. The authors are discussing the respective benefits of two recent molecules presented as 3rd generation molecules: fexofenadine and levocetirizine, while repositioning their use among available treatment strategy.

Acetates↗

PubMed1994

Contribution of phospholipases A2 and D to arachidonic acid liberation and prostaglandin D2 formation with increase in intracellular Ca2+ concentration in rat peritoneal mast cells.

The contribution of phospholipases A2 (PLA2) and D (PLD) activation to arachidonic acid liberation and prostaglandin D2 (PGD2) formation was studied in stimulated rat peritoneal mast cells. Stimulation of the cells with ionomycin induced time-dependent and Ca(2+)-concentration-dependent increase in arachidonic acid liberation and PGD2 formation, and the Ca(2+)-dependent increase was especially remarkable at extracellular Ca2+ concentration higher than 200 microM. Staurosporine did not induce any effect on the arachidonic acid liberation, indicating that protein kinase C is not involved in the liberation. Addition of ethanol to the cells decreased the ionomycin-stimulated arachidonic acid liberation to 40% of the control, while it decreased the PGD2 formation almost completely, with the increase in phosphatidylethanol formation. Propranolol, a phosphatidate phosphohydrolase inhibitor, caused similar effects. p-Bromophenacyl bromide, a PLA2 inhibitor, inhibited partially the arachidonic acid liberation. The inhibition of the liberation by combination of p-bromophenacyl bromide and ethanol was additive and reached approximately 90%. Under the conditions used p-bromophenacyl bromide did not influence significantly the PLD activity assessed by the phosphatidylethanol formation. Histamine release was decreased by ethanol treatment to 35% of the control. These results suggest that more than half of the total arachidonic acid liberation is mediated by the sequential pathway of PLD/phosphatidate phosphohydrolase/diacylglycerol lipase and more than half of histamine release is also dependent on PLD activation, while the PGD2 formation is fully mediated by the pathway. PLA2 also contributes to arachidonic acid liberation but to a lower extent.

Acetophenones↗

PubMed1984

Anaphylactic- and calcium-dependent generation of prostaglandin D2 (PGD2), thromboxane B2, and other cyclooxygenase products of arachidonic acid by dispersed human lung cells and relationship to histamine release.

Proteolytic digestion of human lung tissue dispersed a population of cells (HDLC) containing 1 to 8% mast cells but which were free from bronchial and vascular smooth muscle. Incubation of HDLC with anti-human IgE, which released a net 24.8 + 4.3% of mast cell-derived histamine, stimulated a 14-fold increase in the generation of PGD2, a seven-fold increase in TXB2, and less than a twofold increase in PGF2 alpha, immunoreactive PGE, (i-PGE) and 6-keto-PGF1 alpha. A similar profile of prostanoid release was observed when cells were challenged with epsilon-specific anti-IgE, indicating that the response was specific to the coupling of IgE Fc receptors. The calcium ionophore A23187 also released prostanoids from HDLC in approximately the same proportions as anti-IgE. This stimulus, however, released only 50% as much PGD2 per nanogram histamine than did IgE-dependent activation, thereby showing a fundamental difference in the mechanisms by which the two agents activate mast cells and liberate arachidonic acid for oxidative metabolism. In concentration-response and time course experiments, both secretory stimuli released prostanoids and histamine in parallel. After separation of lung cells by isopyknic centrifugation, challenge with anti-IgE or A23187 released PGD2 only from those fractions containing mast cells, the amount released corresponding closely to both the mast cell concentration and net histamine release. On pooling data from all experiments, the closest correlation was found between release of PGD2 and histamine when cells were stimulated with either anti-IgE (r = 0.813, p less than 0.001) or A23187 (r = 0.763, p less than 0.001), supporting a mast cell origin for PGD2. The release of other prostanoids in fractions not containing mast cells demonstrates that macrophages, monocytes, and lymphocytes have the capacity to generate TXB2, PGF2 alpha, and i-PGE both in the absence and presence of mast cells. Thus, although mast cells are likely to be the major source of PGD2 generated upon IgE-dependent stimulation of HDLC, other cells dispersed from lung tissue have the capacity to generate prostanoids directly after activation of their IgE-Fc receptors and, indirectly after the secretion of mast cell mediators.

Anaphylaxis↗

PubMed2002

Cationic amphiphilic drugs and platelet phospholipase A(2) (cPLA(2)).

The aim of the study was to verify and compare the effect of cationic amphiphilic drugs (CAD) from different pharmacological groups on activation of platelet phospholipase A2 (PLA2)--the essential enzyme of arachidonic pathway in blood platelets. Beta-adrenoceptor-blocking (BAB) drugs inhibited platelet aggregation in the rank order of potency: propranolol>alprenolol>metipranolol>atenolol. The higher the inhibition of arachidonic acid (AA) liberation by BAB drugs, the higher the inhibition of aggregation. Similarly did the H1-histamine antagonists bromadryl (BRO) and dithiaden (DIT) as well as the antimalarial chloroquine (CQ) show antiplatelet effect in vitro in the rank order of potency: DIT>BRO>CQ. Dose-dependent inhibition of aggregation was followed by the inhibition of AA liberation from membrane phospholipids of platelets stimulated either at the receptor site (thrombin) or by a stimulus bypassing membrane receptors (Ca2+ ionophore A23187). The rank order potency for inhibition of stimulated 3H-AA liberation from membrane phospholipids was: (a) for BAB drugs: propranolol>alprenolol>metipranolol, (b) for other drugs: DIT>BRO>CQ. The investigated drugs' interference with stimulated liberation of AA showed nonspecific inhibition of platelet cytosolic PLA2 (cPLA2) by these drugs at intracellular level. The results revealed that besides the inhibition of cyclooxygenase pathway and receptors for adenosine diphosphate (ADP) and glycoproteins Gp IIbIIIa, the interaction of drugs with cPLA2 may represent a further site for antiplatelet action.

Alprenolol↗

PubMed1986

Leukocyte diapedesis and plasma extravasation after leukotriene B4: lack of structural injury to the endothelium.

Leukotriene B4 (LTB4) is a derivative of arachidonic acid which causes neutrophil diapedesis, endothelial swelling and increased permeability of post-capillary venules. To detect whether these effects are accompanied by degranulation of leukocytes and visible injury to the microvessels, the vasculature of rabbit skeletal muscle (tenuissimus) was exposed to LTB4 (10-20 nM). Some preparations were pre-treated with prostaglandin E1, (PGE1). When leukocytes started to adhere markers of plasma leakage were infused. Ultrastructural examination of leakage areas revealed that neutrophils and eosinophils appeared structurally intact, but many basophils and mast cells had been partially degranulated which indicated that vasoactive substances may have been liberated. However, endothelial gaps, such as may form in response to histamine released during degranulation, were not observed and there was no obvious injury to the endothelial cells. The apparent swelling observed by light microscopy was due to pseudopods of migrating leukocytes. Electron dense markers occurred in some endothelial vesicles and in the vicinity of neutrophils which had reached the abluminal side. These particles are interpreted to have escaped concurrent with leukocyte migration. After treatment with both PGE1 and LTB4 a few post-capillary venules showed endothelial gaps. However, leakage of markers was insignificant where the basement membrane persisted. It is concluded that exposure to LTB4 per se and the resulting leukocyte diapedesis are not structurally damaging to the vasculature.

Animals↗

PubMed1986

Histamine stimulates prostaglandin E production by rheumatoid synovial cells and human articular chondrocytes in culture.

Histamine stimulates prostaglandin E (PGE) production by cultures of adherent rheumatoid synovial cells and human articular chondrocytes. When subcultured synovial fibroblasts or human articular chondrocytes were "primed" by preincubation with conditioned media from primary adherent rheumatoid synovial cell cultures (synovial factor), each produced even higher PGE levels upon histamine exposure. This histamine stimulation was prevented by histamine H1, but not H2, antagonists and was more marked if serum was absent from the culture media. Thus, histamine-induced PGE production by these cells is mediated via H1 receptor activation and subsequent arachidonic acid liberation.

Arthritis, Rheumatoid↗

PubMed1976

The histamine release process and concomitant structural changes in rat peritoneal mast cells. In vitro study on effects of compound 48/80 and the dependence of the process on cell preparation, temperature and calcium.

Two morphologically different populations of rat peritoneal mast cells were observed in response to incubation with compound 48/80. Type 2 mast cells: cells with distinct contours exhibiting intracellular vacuoles containing altered granules and without signs of granule liberation; Type 3 mast cells: cells with indistinct countours and with varying number of granules liberated. The absence of calcium in the medium, high temperature (37 degrees C) in the presence as well as in the absence of calcium favoured type 2 versus the type 3 cells. The isolated mast cell population was less morphologically heterogeneous than the mixed cell population in response to the addition of compound 48/80. It is concluded that mast cells might release a great part of their histamine content without a concomitant liberation of the granule matrixes. The varying morphological pictures observed after incubating of mast cells with compound 48/80 is due to variable factors inherent to the experimental procedures.

Analysis of Variance↗

PubMed1984

Enhanced carnosine (beta-alanyl-L-histidine) breakdown and histamine metabolism following treatment with compound 48/80.

We have previously suggested that carnosine may serve as a reservoir for histidine to be used as a source of histamine in the trauma response of rats. In this study we report the effect of stimulation of histamine-forming capacity by compound 48/80 on muscle carnosinase (C'ASE) and histidine decarboxylase (HDC) activities as well as on muscle carnosine and histamine concentrations. Male rats (180 g) were injected i.p. with 5 mg/kg bw of compound 48/80 and C'ASE and HDC activities as well as carnosine, histidine and histamine concentrations were monitored over a 72 h period post-injection. This treatment resulted in an 120% increase in muscle HDC activity and an 110% increase in muscle histamine concentration at 15 min post-injection, followed by an 80% increase in muscle C'ASE activity at 1 h and a 100% reduction in muscle carnosine concentration at 24 h post-injection when compared to control animals injected with 0.9% saline. Histidine concentration was not affected by treatment. The time frame of response, a rapid increase in muscle HDC activity and in muscle histamine concentration followed by an increase in muscle C'ASE activity and a later decrease in muscle carnosine concentration, suggests that carnosine is hydrolysed to liberate histidine and that carnosine, as a reservoir for histidine, is mobilized to maintain a constant muscle concentration of histidine for histamine synthesis.

Animals↗

PubMed1990

Magainin-2 releases histamine from rat mast cells.

The magainins are basic 23 amino acid peptides with a broad spectrum of antimicrobial activity. Their bactericidal effect has been attributed to their capacity to interact with lipid bilayer membranes. We observed histamine release by magainin-2 amide from rat peritoneal mast cells (ED50 = 13 micrograms/ml) but not from human basophils. This histamine-releasing reaction from peritoneal mast cells was due to a secretory rather than cytolytic effect, i.e., release occurred without concomitant liberation of lactic dehydrogenase. Furthermore, the pretreatment of mast cells with magainin-2 amide did not desensitize cells against subsequent challenge with other secretagogues. Maximum histamine release occurred in less than a minute at 25 and 37 degrees C. The addition of Ca2+ was not required for histamine release, although release was enhanced by the addition of 0.3-1 mM Ca2+. The addition of 3 mM Ca2+ or Mg2+ was markedly inhibitory. The presence of Na+ or Cl- ions in the medium was not required for release. Therefore, histamine release is not due to the formation of anion-selective channels in the membrane of mast cells. The results indicated that the characteristics of histamine secretion induced by magainin-2 amide were unlike IgE-mediated release but were similar to the mechanism of release attributed to some other basic peptides and to compound 48/80.

Amino Acid Sequence↗