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At least 775 records · Page 43Linked to original sources
PubMed1954

Cytological and pharmacological observations on the release of histamine by mast cells.

Experimental solutions known to affect mast cells or to cause liberation of histamine from the tissue were introduced into the peritoneal cavity of rats. Samples of the peritoneal fluid were withdrawn at intervals afterward and assayed for histamine and the condition of the mast cells was subsequently ascertained by microscopic examination of stained spreads of the mesenteries. Intraperitoneal injection of distilled water caused osmotic disruption of the mast cells and the appearance of an appreciable amount of histamine in the peritoneal fluid. Injection of Tyrode solution alone was not particularly damaging to the mast cells and little or no histamine was released. Injection of Tyrode solution containing compound 48/80 resulted in extensive release of granules from mast cells and the appearance of large amounts of histamine in the fluid. Solution of 48/80 failed however to cause histamine release when injected into rats whose subserosal mast cells had previously been destroyed. A series of increasing doses of compound 48/80 had a graded morphological effect upon mast cells and resulted in a graded increase in the amount of histamine that appeared in the peritoneal fluid. It is unlikely therefore that this compound acts by simply lysing the plasma membrane. It is concluded that mast cells in the rat are extraordinarily rich in histamine which is liberated under conditions which cause mast cells to release their granules. The histamine set free by the potent histamine liberator, compound 48/80, appears to come principally from the tissue mast cells.

Animals↗
PubMed1975

[Characteristics of the phlogistic action of melittin, its C-terminal fragment and some basic peptides in the rat paw (author's transl)].

Injection into the rat paw of either melittin, its C-terminal dekapeptide, tetralysine or triarginine causes an inflammatory response with melittin having the highest and the last mentioned peptides the lowest activity. The inflammatory action of melittin and the dekapeptide has the following characteristics: 1. it is mainly due to the liberation of histamine, since on both compounds the anti-histaminic diphenhydramine has a pronounced inhibitory effect; 2. di-sodium-cromoglycate inhibits only the inflammatory action of the dekapeptide but has no effect on the activity of melittin. Melittin and its fragment thus liberate histamine via different routes.

Animals↗
PubMed1986

The effect of compound 48/80, substance P and pentagastrin on the isolated guinea pig atrium.

It has been shown that histamine is present in guinea pig hearts. In the present work, the effect of some substances, known to liberate mast cell histamine, on the isolated guinea pig atria was studied. Compound 48/80 (100 micrograms/ml), pentagastrin (10(-6) M) and substance P (10(-5) M) were added 2-3 times to the isolated organs and the frequency of contractions was measured. At the end of experiments, the atria were examined histologically for mast cell degranulation. Compound 48/80 and pentagastrin increased the frequency of contractions of isolated atria. Substance P provoked a dose-dependent decrease of contraction frequency; this effect was diminished by atropine (10(-5) M). All three substances provoked pronounced degranulation of mast cells present in the atrium, the effect of substance P being significantly greater than the effects of the other two substances. It can be concluded that mast cells, present in guinea pig atrium, are sensitive to the histamine liberators used; histamine is released in quantities high enough to produce an effect.

Animals↗
PubMed1977

[Endogenous histamine. Principles of prevention].

After recalling the machanisms of liberation of endogenous histamine and its fate; the author discusses the pharmacological methods of protection of the organism against histamine liberation.

Animals↗
PubMed1992

Isolated bronchi from asthmatics are hyperresponsive to adenosine, which apparently acts indirectly by liberation of leukotrienes and histamine.

Bronchial hyperresponsiveness can be demonstrated in asthmatic subjects by inhalation of adenosine, but the action of adenosine at the level of the human airway smooth muscle has received comparatively little attention. We have previously observed that bronchi isolated from one asthmatic patient contracted in response to adenosine. We have therefore, during the course of a 3-yr study, further characterized the effects of adenosine in bronchi prepared from surgical specimens of lung tissue of asthmatics and of nonasthmatics. Contraction responses were always studied in vitro the same day the tissues were obtained. Bronchi from asthmatics (19 strips from six patients) were more sensitive to adenosine than were bronchi from nonasthmatics (21 strips, seven patients). In contrast, there was no difference in sensitivity to histamine or leukotriene C4 between the two groups, nor was the maximal tissue contractility different. The contractile effect of adenosine was inhibited by the adenosine A1-antagonist 2-thio-[(1,3-dipropyl)-8-cyclopentyl]-xanthine as well as by the dual A1 and A2 antagonists 8-(p-sulfo)-phenyltheophylline and theophylline. The combination of leukotriene antagonism (receptor-antagonist ICI 198,615 or biosynthesis inhibitor MK-886) and histamine antagonism (antihistamines mepyramine and metiamide) blocked the contractile effects of adenosine, suggesting that adenosine acts indirectly by liberation of leukotrienes and histamine, possibly from mast cells. The findings of increased sensitivity to adenosine in bronchi from asthmatics to our knowledge represents the first evidence of increased bronchial reactivity in vitro in asthmatics.

Adenosine↗
PubMed1987

Mast cell histamine release induced by intermediate products of arachidonic acid metabolism.

This study was performed to evaluate the role of intermediate products of arachidonic acid metabolism on histamine release from rat serosal mast cells. Arachidonic acid in concentrations ranging from 10(-9) to 10(-4) M caused no histamine release from purified rat peritoneal mast cells. High concentrations (10(-6)-10(-6) M) of the terminal products of the arachidonic acid metabolism were also devoid of any significant histamine-releasing properties. The metabolic activation of arachidonic acid with prostaglandin-H-(PGH)-synthase isolated from calf seminal vesicles, evoked a significant release of histamine from rat serosal mast cells. The liberation of histamine was not accompanied by a significant leakage of lactic dehydrogenase (LDH) and the electron microscopical features were consistent with an exocytotic release. The phenomenon was blocked by reduced glutathione (GSSH) and by D-mannitol, a hydroxyl free-radical scavenger. These results suggest that free radical derivatives of arachidonic acid are generated during the catalysis which triggers mast cell histamine release.

Animals↗
PubMed1989

Comparison of histamine and 5-hydroxytryptamine content and secretion in rat mast cells isolated from different anatomical locations.

Rat mast cells, isolated from different anatomical locations, were found to exhibit heterogeneity with respect to histamine and 5-hydroxytryptamine (5-HT) content. Unlike peritoneal mast cells, those derived by enzymatic digestion of rat lung and mesentery tissues contained amounts of 5-HT in excess of histamine. Both compound 48/80 and A23187 were more effective liberators of histamine than 5-HT in each cell type, despite their differences in relative amine content. However, in response to a mixture of specific antigen and phosphatidylserine, the pattern of secretion of both amines from each mast cell type was observed to be essentially colinear. These results are discussed in terms of amine release mechanisms and post-secretory events.

Animals↗
PubMed1982

Significance of sustained gastric hypersecretion by the emulsified histamine solution.

Experimental production of gastric and duodenal ulcers was investigated in dogs by administration of histamine emulsified in Freund's incomplete adjuvant. Acid secretory responses were also checked. The results are as follows: Intramuscular administration of 10 mg/day of the emulsified histamine solution caused sustained gastric hypersecretion due to gradual liberation of histamine but produced no apparent side effects. However, neither gastric nor duodenal ulcer was observed within 2 months with the dosage of 10 mg/day. These results suggest that intramuscular administration of the dosage of 10 mg/day within 2 months would be a valuable means to elucidate the pathogenesis of ulcer under the sustained gastric hypersecretion.

Animals↗
PubMed1979

[Histamine levels in blood of patients with allergic bronchial asthma (author's transl)].

The investigation of 10 patients with allergic asthma showed histamine levels of 79.8 +/- 50.0 ng/ml in blood during symptom-free intervals. They were not significantly different from those in 12 patients with chronic obstructive bronchitis (54.0 +/- 25.9 ng/ml) and in 13 healthy probands (56.9 +/- 21.5 ng/ml). It could be shown that allergen-induced bronchial obstruction in patients with allergic asthma had no demonstrable influence on blood histamine levels. The absence of increased blood histamine levels in allergic bronchial obstruction supports the assumption that allergen-induced liberation of histamine and its biological effects are mainly limited to the bronchial system. Local metabolisation of the liberated mediator can be supposed to a large extent.

Adult↗
PubMed1989

Ischemia-reperfusion injury and histamine release in isolated guinea-pig heart: the role of free radicals.

Free radicals produced by the occlusion and opening of the left anterior descending coronary artery and/or by perfusion of isolated guinea-pig heart with FeCl3/ADP (10 microM/100 microM) induce a differential release of histamine and lactate dehydrogenase (LDH) in the perfusates with a preferential liberation of histamine in the reperfusion phase, associated with an increase of ventricular arrhythmias. The release of histamine has been correlated with malonyldialdehyde (MDA) production and tissue calcium content in left ventricular tissue. MDA increased during ischemia, while the calcium content increased when the tissue was reperfused. Under these conditions, N-t-butyl-alpha-phenylnitrone (BPN), a molecule capable of forming spin adducts with free radicals, and D-mannitol are active in preventing reperfusion-induced arrhythmias.

Animals↗