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At least 415 records · Page 23Linked to original sources
PubMed1986

[Histamine liberation from rat mast cells by culture supernatants of human lymphocytes and rat spleen lymphocytes].

The supernatant of mitogen- or antigen-stimulated mononuclear cell cultures is known to contain a large number of biologically active molecules. In the present study, we have stimulated human mononuclear cells and rat spleen cells with Con A or antigen (PPD) respectively to produce lymphokines, such as histamine releasing factor (HRF), which is capable of causing histamine release from rat mast cells and human basophils. Histamine was measured fluorimetrically by Shore et al. This assay is sensitive and reproducible: replicates varied by less than 15% in triplicate samples.

Adult↗
PubMed1988

[Intragastric provocation and antigen-induced in vitro histamine liberation by the food additive E 102].

Adverse reactions to tartrazine have been known since 1958. The mechanism of this reaction, a not IgE-mediated, anaphylactoid reaction, is not fully understood. The demonstration of this adverse reaction by provocative challenge feeding may be problematic by a score of subjective symptoms because of the placebo effect. This report deals with the intragastral provocation under endoscopic control with tartrazine and tartrazine-induced histamine release in vitro from gastric mucosa and from blood. Two patients with anamnestically suspected adverse reactions to tartrazine were studied. Correspondence of in vivo and in vitro testing with tartrazine could be demonstrated.

Azo Compounds↗
PubMedDate not supplied

[Effect of pyridoxine on histamine liberation and degranulation of rat mast cells].

Pyridoxine, one of the B vitamins, has been shown to be useful in the treatment of childhood bronchial asthma by Collip et al. (1975). A double-blind study with 76 asthmatic children followed for five months indicated significant improvement in asthma following pyridoxine therapy (200 mg daily) and a reduction in dosage of bronchodilators and cortisone. Other reports have shown that nicotinamide, another B vitamin shows inhibitory activity in rat mast cell degranulation and histamine release (Bekier et al. 1974, Wiczolkowska and Maslinski, 1975, 1976). These results induced us to investigate if pyridoxine, like nicotinamide or disodium cromoglycate, exhibits pharmacological inhibitory activity in rat mast cell degranulation and histamine release induced by antigen or other non-immunological stimulants. We found that pyridoxine at concentrations of 10 (-3) M, or greater significantly inhibited rat mast cell degranulation and histamine release induced by phospholipase A, compound 48/80, antigen (egg albumin) or a mixture of dextran and phosphatidyl serine, respectively. In these experimental models, pyridoxine shows a pharmacological profile similar to nicotinamide and disodium cromoglycate, although weaker than the latter. In spite of this, the lack of toxicity of this vitamin at relatively high doses (1 or 1.5 g), the possibility that other mechanisms of action may be involved, such as the improvement in tryptophan metabolism reported by Collip following pyridoxine therapy, suggest that this vitamine merits additional research.

Animals↗
PubMed1995

[Inhibition of histamine liberation in allergic rhinoconjunctivitis in relation to the season].

An increased activity of the cAMP-degrading enzyme phosphodiesterase (PDE) has been observed in peripheral leukocytes from atopic patients. We studied 9 patients with seasonal allergic rhinoconjunctivitis and 9 controls during (summer) and out of symptomatic season (following winter). Dextran sedimented peripheral mixed leucocytes (pML) were preincubated with the nonspecific PDE inhibitor isobutyl-methylxanthine (IBMX), with the PDE III selective inhibitor motapizone and with the PDE IV selective inhibitor rolipram and subsequently histamine release was induced by anti-IgE antibodies. The anti-IgE induced histamine release (anti-IgE HR) showed no significant seasonal differences in atopic patients and in controls. All PDE inhibitors reduced anti-IgE HR over the whole investigated concentration range (from 10(-8) mol/l to 10(-4) mol/l) in a dose dependent manner. Comparing the PDE inhibitors rolipram was the most potent inhibitor on anti-IgE HR from pML of acute and symptomless patients, while there were no significant differences on anti-IgE HR from pML of controls. During symptomatic season rolipram inhibited anti-IgE HR from pML of patients significantly more efficient than out of season. This could be the result of a seasonal increased PDE IV activity in the pMI of patients with allergic rhinoconjunctivitis.

Adult↗
PubMed1985

[Hemodynamic changes following heparin injection in aortocoronary bypass operations. Sequela of histamine liberation].

Prior to cannulation for extracorporeal circulation, 375 Units of Heparin/kg body weight were applied to 22 patients (group 1) into the right atrium. A few minutes later, characteristic changes in haemodynamics were observed. In a second group of 10 patients, the same amount of heparin was injected directly into the ascending aorta to avoid the passage of an undiluted bolus of heparin through the pulmonary vessels. In this group, the haemodynamic effects of heparin seemed to be slightly weakened. Immediately after administration of heparin, a significant increase of plasma histamine was measured (in 12 patients of group 1). This might be the main reason for the heparin-dependent haemodynamic effects.

Blood Pressure↗
PubMed1989

Stimulation by McN-A-343 and blockade by telenzepine of acid secretion in the mouse isolated stomach at histamine-liberating cells.

(1) In the lumen-perfused mouse stomach in vitro, potential sites of gastric antisecretory action of the muscarine M1-receptor antagonist telenzepine were investigated. Acid secretion was stimulated by the muscarinic agonist McN-A-343 (1-1000 mumol/l). Neither basal nor McN-A-343-stimulated acid secretion was affected by 1 mumol/l TTX indicating that neuronal structures were probably not involved. (2) Acid secretion stimulated by 10 mumol/l McN-A-343 was inhibited by telenzepine (0.1-1.4 mumol/l) and cimetidine (10-140 mumol/l). Neither of the antagonists affected basal acid secretion. TTX had no inhibitory influence on the antagonist effect of telenzepine and cimetidine. (3) Compound 48/80 (100 mumol/l), which depletes histamine stores, initially mimicked but subsequently prevented the effect of McN-A-343. Prenylamine (50 mumol/l), which prevents histamine release, also abolished the secretagogue effect of subsequently administered McN-A-343. (4) Up to concentrations greater than 100 mumol/l, McN-A-343 did not stimulate acid production in rabbit isolated fundic glands and guinea-pig isolated parietal cells. Thus, parietal cells are not directly stimulated by McN-A-343. (5) Based on the site of action of the agonist McN-A-343 in the mouse isolated stomach and its failure to stimulate parietal cells from different species directly, it is concluded that telenzepine blocks, in the mouse isolated stomach, muscarine receptors located on paracrine cells to reduce endogenous histamine release.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1989

Ultrastructural study of the response of eosinophil granule cells to Aeromonas salmonicida extracellular products and histamine liberators in rainbow trout Salmo gairdneri Richardson.

Intraperitoneal injections of Aeromonas salmonicida extracellular products (ECP), Compound 48/80 and Concanavalin A were found to degranulate the eosinophil granule cells (EGC) in the lower intestine and rectum of the rainbow trout Salmo gairdneri Richardson. Ultrastructurally, the EGC response resembled the anaphylactic granule extrusion of mammalian mast cells. Varying degrees of granule vacuolation and loss of electron density occurred. Labyrinthine channels were observed at the peak of degranulation. EGC response however, differed from mammalian mast cells in two respects. Firstly, degranulation involved the release of intact electron lucent granules and the subsequent disintegration of the granule matrix extracellularly. Mammalian mast cells on the other hand, release their granules by direct exocytosis. Secondly, the 48/80 and Con A-stimulated EGC degranulation was inhibited by antihistamines, promethazine and cimetidine. In mast cells, antihistamines do not prevent granule release but block histamine receptors in target cells. The degranulation of the ECGs was a non-cytotoxic event and the cells were capable of regeneration. As soon as the cells lost most of their granules, increased cytoplasmic activity was observed. This involved the expansion of the Golgi-endoplasmic reticulum complex.

Aeromonas↗
PubMed1975

The mast cells of the newborn rat diaphragm and their response to histamine liberators.

The mast cell population of rat diaphragm was estimated between birth and adulthood and found to rise with an increase in the age of rat studied. Degranulation of these cells was observed in rats from all age groups, following treatment with compound 48/80 and dextran. The association of mast cells with the blood vessel wall in adult rat diaphragm was not observed in the comparable tissues of newborn rats. These findings are discussed in relationship to the poor vascular permeability reactions exhibited by newborn and young rats.

Aging↗
PubMed1985

[Reassessment of the respective risks of anaphylaxis and histamine liberation with anesthetic substances].

A search of the French and English language literature of the last 20 years (1964-1984) yielded 975 cases of immediate anaphylactoid reactions due to anaesthetic drugs given parenterally. The accident mechanism was confirmed in only half the patients, and nearly always at a later date. The immunoallergological tests most often used in the diagnostic process were skin tests and Prausnitz-Küstner tests. Although all drugs could be responsible for an anaphylactic reaction, the greatest number of cases was due to muscle relaxants (51%) and hypnotic drugs (42.3%). The signs most often described were cutaneous, cardiovascular, respiratory and occasionally gastro-intestinal. Whilst hypnotic drugs were responsible for cutaneous signs, muscle relaxants gave cardiovascular signs. A past history of drug allergy was found in 37% of cases, and atopy in 38%; virtually all patients had already had one or more anaesthetics.

Anaphylaxis↗