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[Participation of the lungs in the absorption and liberation of biogenic amines in the postresuscitation period].

After revival from a 10-minute clinical death caused by acute blood loss the transport of biogenic amines to the lungs in dogs did not increase for 3 hours. Their absorption by the lungs was replaced periodically by their liberation; both processes were intensified for serotonin but weakened for histamine. In 6-9 hours during the period of hypoperfusion and reduction of the transport of amines to the lungs the intensity of absorption and liberation of serotonin by the lungs were normalized, while these processes for histamine remained diminished. The content of biogenic amines in arterial blood reduced. Twenty-four hours later, under conditions of normalization of hemodynamics, the transport of histamine to the lungs and its concentration in blood were still reduced, while the transport and absorption of serotonin by the lungs, as well as its content in arterial blood, increased; this was attended by an increase in total pulmonary resistance and the development of moderate hypoxemia. Animals who died subsequently had a higher level of serotonin in arterial blood but a lower level of histamine. The role of the lungs in homeostasis of blood biogenic amines in the postresuscitation period is discussed.

Animals↗

PubMed1980

Mast cells and eosinophils as regulators of functional homeostasis in the gastric mucosa.

The numerous mast cells of the interstitial tissue of the gastric mucosa are the sites of histamine synthesis and storage. If this biogenic amine is liberated from these cells it transmits simulation of gastric acid secretion to the epithelial cells. However, the effect of this released histamine is limited by the eosinophilic leukocytes, which find their way to the origin of histamine and decompose it. The functional level of these two kinds of cells is controlled by the neuroendocrine system.

Animals↗

PubMed1984

Thromboxane formation in human polymorphonuclear leukocytes is inhibited by prednisolone and stimulated by leukotrienes B4, C4, D4 and histamine.

Human polymorphonuclear leukocytes (PMNL) were incubated for 60 min at 37 degrees C with 20 microM or 100 microM prednisolone, and stimulated thereafter for 1 min with 10 nM LTB4, 10 nM LTC4, 10 nM LTD4 or 10 microM histamine. The amount of thromboxane B2 (TXB2) formed by PMNLs was measured by radioimmunoassay. PMNLs spontaneously released TXB2 during 60 min incubation, and the rate of formation was significantly reduced in the presence of 20 microM or 100 microM prednisolone. LTB4, LTC4, LTD4, and histamine stimulated the rate of TXB2 production during 1 min incubation to 93-, 49-, 60-, and 55-fold, respectively. Preincubation with prednisolone for 60 min had a slight inhibitory effect on the stimulated TXB2 formation but TXB2 production still remained many fold as compared to its spontaneous rate of formation. The present study indicates that human PMNLs are capable of synthetizing TXB2, and its spontaneous rate of formation is inhibited by a synthetic glucocorticoid, prednisolone. The great stimulatory effect of LTB4, LTC4, LTD4, and histamine suggests that these agents may activate phospholipases or other acylhydrolases which liberate arachidonate for eicosanoid biosynthesis.

Histamine↗

PubMed2004

Histamine-cytokine connection in immunity and hematopoiesis.

A number of recent studies have led to a reappraisal of the functional capacities of histamine in immunity and hematopoiesis. This change of perspective was provided by the following findings: (1) the evidence for multiple cellular sources of histamine, differing from mature basophils and mast cells by their ability to newly synthesize and liberate the mediator without prior storage, (2) the discovery of a novel histamine receptor (H4R), preferentially expressed on hematopoietic and immunocompetent cells, (3) the potential intracellular activity of histamine through cytochrome P450 and (4) the demonstration of a histamine-cytokine cross-talk. Indeed, cytokines not only modulate the degranulation process of histamine but also control its neosynthesis by the histamine-forming enzyme, histidine decarboxylase (HDC), at transcriptional and post-transcriptional levels. In turn, histamine intervenes in the intricate cytokine network, regulating cytokine production by immune cells through distinct receptors signaling distinct biological effects. This type of regulation is particularly relevant in the context of TH1/TH2 differentiation, autoimmunity and tumor immunotherapy.

Animals↗

PubMed1984

Inhibitory effect of cloxacepride on compound 48/80-induced histamine and serotonin release from rat mast cells.

Cloxacepride, a potent inhibitor of passive cutaneous anaphylaxis (PCA) in the rat, was evaluated for in vitro inhibitory effect on 48/80-induced histamine and serotonin release from rat mesenterial mast cells. Significant inhibition and linearity of concentration and effect was found in the concentration range of 10 to 50 microM. The IC50 was determined to 21 microM (histamine) and 19 microM (serotonin). A simultaneous liberation of both mediators from mast cells is indicated from nearly identical IC50. LDH increase in the supernatant of the incubation mixture by cell damage resulted from higher concentrations of cloxacepride (greater than 50 microM). The high concentration of 10 micrograms/ml releaser 48/80 did not affect or diminish the effect of cloxacepride, while the reference compounds cromolyn sodium (DSCG) and theophylline were inactive under these conditions. The substantial inhibition of the PCA reaction and of the mediator release from mast cells provides cloxacepride a promising potential antiallergic drug.

Animals↗

PubMed1995

Influence of alpha-helicity, amphipathicity and D-amino acid incorporation on the peptide-induced mast cell activation.

Mast cell activation by polycationic substances is believed to result from a direct activation of G protein alpha subunits and it was suggested that the adaption of amphipathic, alpha-helical conformations would allow the peptide to reach the cytosolic compartment to interact with G proteins (Mousli et al., 194, Immunopharmacology 27, 1, for review). We investigated the histamine-releasing activity of model peptides as well as analogues of magainin 2 amide and neuropeptide Y with different amphipathicities and alpha-helix content on rat peritoneal mast cells. Amphipathic helicity is not a prerequisite for mast cell activation. Moreover, non-helical magainin peptides with high histamine-releasing activity were less active in the liberation of carboxyfluoresceine from negatively charged liposomes, indicating that peptide-induced mast cell activation and peptide-induced membrane perturbation do not correlate. In contrast to the negligible influence of the secondary structure, amino acid configuration may exert a striking influence on peptide-induced mast cell activation. Thus histamine-release by substance P was markedly impaired when the L-amino acids in the positively charged N-terminal region were replaced by D-amino acids, with [D-Arg1)substance P being the most inactive substance P diastreoisomer.

Amino Acid Sequence↗

PubMed2004

The role of human mast cell-derived cytokines in eosinophil biology.

Eosinophil-mediated diseases, such as allergic asthma, eosinophilic fasciitis, and certain hypersensitivity pulmonary disorders, are characterized by eosinophil infiltration and tissue injury. Mast cells and T cells often colocalize to these areas. Recent data suggest that mast cells can contribute to eosinophil-mediated inflammatory responses. Activation of mast cells can occur by antigen and immunoglobulin E (IgE) via the high-affinity receptor (FcepsilonRI) for IgE. The liberation of proteases, leukotrienes, lipid mediators, and histamine can contribute to tissue inflammation and allow recruitment of eosinophils to tissue. In addition, the synthesis and expression of a plethora of cytokines and chemokines (such as granulocyte-macrophage colony-stimulating factor [GM-CSF], interleukin-1 [IL-1], IL-3, IL-5, tumor necrosis factor-alpha [TNF-alpha], and the chemokines IL-8, regulated upon activation normal T cell expressed and secreted [RANTES], monocyte chemotactic protein-1 [MCP-1], and eotaxin) by mast cells can influence eosinophil biology. Stem cell factor (SCF)-c-kit, cytokine-cytokine receptor, and chemokine-chemokine receptor (CCR3) interactions leading to nuclear factor kappaB (NF-kappaB), mitogen-activated protein kinase (MAPK) expression, and other signaling pathways can modulate eosinophil function. Eosinophil hematopoiesis, activation, survival, and elaboration of mediators can all be regulated thus by mast cells in tissue. Moreover, because eosinophils can secrete SCF, eosinophils can regulate mast cell function in a paracrine manner. This two-way interaction between eosinophils and mast cells can pave the way for chronic inflammatory responses in a variety of human diseases. This review summarizes this pivotal interaction between human mast cells and eosinophils.

Cell Adhesion Molecules↗

PubMed1975

[Effects of colchicine and of emetine on capillary permeability].

Colchicine and emetine administered locally in the hind paw of the rats increased markedly the capillar permeability. The action may be strongly inhibited by methysergide (0.2 mug). Mepyramine (0.5 mug) is not so active and indomethacine (1 mg/kg per os), even less. As some prostaglandines release serotonine and histamine (8) it is possible that some liberation of these mediators may be attribuable to a previous release of prostaglandines, but the experiments suggest also the possibility of a direct and concomitant release of those two mediators by the alkaloids assayed.

Animals↗

PubMed1977

Isolation of the cytoplasmic granules of guinea pig basophilic leukocytes: identification of esterase and protease activities.

Procedures were developed for isolating highly purified cytoplasmic granules of basophilic leukocytes from guinea pig peripheral blood. The methods involved disruption of cells in 0.34 M sucrose followed by a series of membrane filtrations and fractionation on sucrose density gradients. These preparations, up to 95% pure basophil granules by electron microscopy, contained a mixture of neutral esterases-proteases including caseinolytic activity; both trypsin- and chymotrypsin-like serine hydrolases were identified by means of appropriate inhibitors. Localization of at least one such activity to the basophil granule was confirmed by a cytochemical method; this activity was absent in contaminating lymphocytes and eosinophils. By contrast, several lysosomal enzymes, lactic dehydrogenase, and plasminogen activator activity, present in cell homogenates, were absent from purified granules. The granule matrix of guinea pig basophils, unlike the cytoplasmic granules of other granulocytes or mast cells, was little altered by high or low salt concentration but was disrupted into insoluble fragments by 0.01 N HCl and by Triton X-100. Granules were solubilized by papain and by urea-SDS but enzyme activity was destroyed. Triton X-100 incubation with freeze-thawing proved to be the optimal method for extracting esterase activities. Esterase activities were not released from basophils under conditions of anaphylactic degranulation that liberated the great majority of basophil granule histamine.

Animals↗

PubMed1998

[Allergic immunobiology and anesthesiology].

A protocol has been produced for the study of anaphylactic accidents that occur post-operatively that allows definition of the anaphylactic origin, and so reactions that are mediated by IgE in post-operative accidents. This protocol occurs in two stages, the first is done in the minutes and hours that follow the anaphylactic accident, and the second a month or 6 weeks afterwards. At first, we evaluate the sequential study of the liberation of the mediators of anaphylaxis, plasma histamine, serum tryptase, urinary methylhistamine and, more recently, leucotriene E4. The second study is devoted to reactions that are mediated by IgE, essentially, specific serum IgE, tests of activation of basophils by flow cytometry, measurement of leucotriene C4 and skin tests. A study on 16 subjects has evaluated and validated the protocol and shown a significant level of correspondence of results between the sequential measurement of mediators on one hand and on the other the search for IgE-mediated reactions every time that there was an anaphylactic reaction.

Adolescent↗

PubMed1982

Hypoxic pulmonary vasoconstriction in conscious sheep: role of mast cell degranulation.

We used pharmacologic and histologic techniques to investigate the role of mast cells in the mediation of hypoxic pulmonary vasoconstriction in conscious sheep. Breathing a hypoxic gas mixture (13%, 02, 87% nitrogen) caused hypoxic pulmonary vasoconstriction (HPV) with increases in mean pulmonary artery pressure and pulmonary vascular resistance by 97 and 90%, respectively. Intravenous pretreatment with the mast cell membrane stabilizing agent cromolyn sodium (3 mg/kg/min) completely blocked HPV, whereas the H1-histamine receptor antagonist chlorpheniramine, alone or in combination with the H2-receptor antagonist metiamide and the prostaglandin synthetase inhibitor indomethacin, failed to prevent HPV. Cromolyn sodium failed to modify the pulmonary pressor response to infusions of norepinephrine (alpha-agonist), tyramine (catecholamine-releasing agent), and histamine, indicating the specificity of cromolyn sodium action on the mast cells. Electromicroscopic studies of pulmonary perivascular mast cells showed that a 90-min exposure to the hypoxic gas mixture reduced the total number of granules per mast cell to 75% of control. This was blocked by cromolyn sodium pretreatment. We conclude that in conscious sheep], HP[V is initiated by the liberation of a mast cell product (other than histamine) that either directly or indirectly causes pulmonary vasoconstriction.

Animals↗

PubMed1976

Anaphylactic hypersensitivity in sheep lung in vitro: (vascular Schultz-Dale response and bioamine liberation).

Two aspects of anaphylactic hypersensitivity in sheep lung were studied. Isolated pulmonary vein constricted in response to histamine, acetylcholine, dopamine and bradykinin, whereas serotonin or specific antigen in sensitized tissue caused relaxation of the vessel. Tryptaminergic antagonists did not inhibit vessel relaxation caused by either serotonin or antigen. Antigenic challenge of chopped sheep lung caused significant liberation of serotonin and dopamine but not of histamine. It is suggested that anaphylactic release of serotonin may counteract the inflammatory response in sheep lung; which may explain the relative resistance of sheep to pulmonary hypersensitivity and tryptamine toxicity compared with other species.

Anaphylaxis↗

PubMed1993

Endogenous histamine in cultured bovine adrenal chromaffin cells.

Histamine releases catecholamines and opioids in primary cultured bovine adrenal medullary (BAM) chromaffin cells. We have studied whether histamine is synthesized and localized in BAM cells, and whether it can be released upon activation with secretagogues. In BAM cells histamine is immunohistochemically co-localized with tyrosine hydroxylase in 45 +/- 8% of all cells. Only histamine immunoreactivity was observed in 8 +/- 2% of all BAM cells. No mast-cell-like cells were observed in our system. Histamine can be released from BAM cells by high potassium (56 mM K+) in a calcium-dependent manner. Compound 48/80 did not release histamine from BAM cells but nicotine caused a dose-dependent liberation of the amine. Cultured BAM cells have histidine decarboxylase activity which is inhibited by alpha-fluoromethylhistidine. These results indicate that endogenous histamine is synthesized, stored and released in BAM chromaffin cells in vitro.

Adrenal Medulla↗

PubMed2003

Cytokine profiles after nonionic dimeric contrast medium injection.

RATIONALE AND OBJECTIVES: Mediators of contrast media (CM)-induced allergic/pseudoallergic side effects are largely unknown. We evaluated the possibility of cytokines released as surrogate markers for allergic/pseudoallergic responses in patients who tolerated CM injection well. MATERIALS AND METHODS: Interleukin-1beta (IL-1beta), -2, -4, -5, -6; tumor necrosis factor-alpha; plasma histamine level; and the anaphylatoxin C5a were measured by enzyme-linked immunosorbent assay technique in 9 patients who received the nonionic dimeric iodinated CM iotrolan under routine computed tomography examination conditions. Serum samples were collected before, 1 hour, 6 hours, and 24 hours after contrast medium injection. RESULTS: The cytokine values did not correlate with the hematocrit. Kinetic studies revealed a trend, although not statistically significant (P>0.05), for an early increase of IL-2 (1 hour after CM), followed by delayed increase of IL-4 and IL-6. Histamine significantly decreased after iotrolan injection and C5a increased 6 hours (P>0.05) after CM administration in parallel to IL-6. IL-1beta decreased (with the lowest value measured 6 hours after CM injection; P>0.05), and tumor necrosis factor-alpha did not show any tendency. Patients with late adverse reactions had a T helper 1 to T helper 2 shift and 24 hours after CM injection had the highest histamine values. CONCLUSION: The results suggest CM-related liberation of cytokines with a sequential T helper type 1 (IL-2 after 1 hour), and T helper type 2-like pattern (IL-4, -5, and -6).

Adult↗

PubMed1986

Age-related decrease in endothelium-dependent dilator response to histamine in rat mesenteric artery.

The effect of aging on the vasodilator responses to histamine, 2-pyridylethylamine and 4-methylhistamine of ring segments of rat mesenteric arteries were investigated. The maximal extent of histamine-induced dilatation of the arteries previously contracted with norepinephrine was greatest for arteries from rats aged 2 and 8 weeks. The maximal response decreased progressively with an increase in age to 13 and 56 weeks. Arteries from 99 week old rats scarcely responded to histamine. Under these conditions, the dilatation induced by papaverine showed no change with age. The vasodilatation caused by 2-pyridylethylamine and 4-methylhistamine also decreased age dependently. The dilatation of the arteries induced by these agents was inhibited by the H1-antagonist chlorpheniramine, but not by the H2-antagonist cimetidine. Removal of the endothelium completely abolished the vasodilator effect of histamine, leaving the effect of papaverine unaffected. Hydroquinone and methylene blue reversed the dilatation induced by histamine, without affecting that caused by papaverine. These results suggest that the age-related decrease in dilatation of rat mesenteric artery in response to histamine is mainly due to a decrease in the ability of the endothelium to liberate a mediator(s).

Aging↗

PubMed1989

Metabolism of picumast after administration of picumast dihydrochloride and antiallergic activity of the main metabolites.

The present experiments were carried out to elucidate the chemical structure and the pharmacological activity of the main metabolites of picumast (3,4-dimethyl-7-[4-(4-chlorobenzyl)piperazine-1-yl]propoxycoumarin ). The metabolic pathways were identical in animals and man, but there were major quantitative differences. The fraction of the radioactivity in the plasma attributable to the parent compound 0.5 to 3 h after oral administration of picumast dihydrochloride was less than 15% in animals but 95% to 57% in man. Inhibition of the C3-zymosan-induced chemilumiescence of human leucocytes was taken as an indicator of the diminished liberation of mediators and inhibition of the histamine-induced contraction of isolated guinea-pig lung strips as an example for the antagonism of picumast dihydrochloride to mediators of allergic reactions. Stepwise oxidation of the 3-methyl substituent of the coumarin ring to the alcohol and the carbonic acid increased the histaminolytic potency, but decreased the inhibition of chemiluminescence. Another metabolite formed by cleavage of the piperazine-containing side chain was inactive in both tests.

Animals↗

PubMed1978

[Non-enzymatic fibrinolytic agents].

Non-enzyme fibrinolytic agents include pharmacological agents which are active in vivo but inactive in vitro and synthetic chemical compounds which when added to blood or plasma in vitro directly induce fibrinolysis. There are a number of drugs with a short duration of action such as adrenalin, nicotinic acid, vasopressin and histamine. Vasoactive drugs probably act by stimulating the liberation of vascular activator. The effect of nicotinic acid is rapidly exhausted when injections are repeated. By contrast, the biguanides and certain anabolic steroids are capable of exerting a long term stimulation of endogenous fibrinolysis. Amongst these substances, phenformin, metformin, ethyloestrenol, stanozolol and a new substance, moroxydine chloride, have been studied. The biguanides appear to be capable of exerting an effect upon the synthesis and liberation of plasminogen vascular activator. The combination of an anabolic steroid and a biguanide would appear to be the most powerful. These various drugs have been used with success in cases of recurrent venous thrombosis in patients with an abnormally low level of plasminogen activator in the venous walls and/or low fibrinolytic activity after venous stasis. Chemical fibrinolytic agents were studied only in vitro, since the use of these substances in human therapeutics would seem to be still difficult in view of the fact that they are active only in a narrow range of concentrations.

Anabolic Agents↗

PubMed1988

Detection of histamine in human placental perfusate and the effect of histamine releasers.

Studies on full-term human placentas were conducted to determine whether the vasogenic actions of certain agents on perfused placental vasculature are due to histamine release. Compound 48/80 and morphine were selected because they liberate the autacoid via different mechanisms. Initially, a control effluent was collected prior to each drug challenge and again collected throughout the rise and fall in perfusion pressure. The drugs were given alone and in the presence of a 50 mcg dose of histamine free base (HFB) to assess the release of stored histamine and also to serve as a control. Following extraction in n-butanol and recovery in 0.1 N HCl, all effluents were fluoresced with o-phthalaldehyde and assayed for histamine content via spectrophotofluorometry. A baseline histamine level was discovered in the majority of placental effluents collected prior to the administration of any agent. No significant increases above this initial level occurred following treatment with compound 48/80 alone. However, small but significantly elevated amounts of histamine appeared in the placental effluent when compound 48/80 was given 10 minutes after the initial 50 mcg dose of HFB. This agent also caused a slight increase in placental perfusion pressure after each administration. Results obtained with morphine do not appear to support the hypothesis that significant amounts of histamine are released by this agent in the perfused human placenta.

Female↗