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At least 1,225 records · Page 68Linked to original sources
PubMed1980

Release of mediators from free bronchoalveolar cells: effect of ionophore A23187 and antigen challenge.

The ionophore A23187 stimulated the release of prostaglandins and SRS-A (now identified as leukotriene D4) from guinea-pig bronchoalveolar macrophages. Upon specific antigen challenge of the cells obtained from ovalbumin-sensitized animals or of normal cells preincubated with the serum of sensitized animals, prostaglandins, SRS-A or histamine were undetectable. Furthermore, treatment of "sensitized" cells with the ionophore resulted in a reduced liberation of prostaglandins in comparison to control cells. It is suggested that sensitization produce in bronchoalveolar macrophages some functional alterations of arachidonic acid oxygenation products.

Animals↗
PubMed1990

[Plasma histamine and exercise-induced bronchospasm].

The pathogenesis of bronchospasm of effort is not yet elucidated and it is probable that is determined by multiple factors. In this study we have tested the role of mastocytes in taking as an index of their activation the fluctuation of plasma histamine levels during repeated exercise tests. We will show that asthmatic subjects who develop bronchospasm on effort have a significant rise (times 3) in their level of serum histamine whilst normal subjects don't show much change. Furthermore in a repeated effort test we have observed a strict parallelism between the occurrence of bronchospasm of effort and a rise in plasma histamine levels. These different observations enable us to consider that the activation of mastocytes and the liberation of mediators which follow play an important role in the pathogenesis of bronchospasm of effort.

Adolescent↗
PubMedDate not supplied

The metabolism of roxatidine acetate hydrochloride. Liberation of deuterium from the piperidine ring during hydroxylation.

The metabolism of roxatidine acetate hydrochloride (RA), a new histamine-2 receptor antagonist, was studied by GC/MS in rats and dogs in vivo. The co-administration of 14C-RA and RA-d10 labeled with deuterium in the piperidine ring expedited the isolation and identification of 15 urinary metabolites. The major metabolites in both animals were M-1, M-8, M-10, and M-11; M-4 could be found only in the rat. The aromatic and piperidine ring-hydroxylated metabolites were found in small amounts in both species. Following the administration of RA-d10 to rats and dogs, oxygenated metabolites on the piperidine ring, such as M-3 and M-4, were isolated and their analysis indicated the unexpected loss of three or four deuterium atoms from the ring. Also, first and second isotope effects were observed on the conversion rate in vivo and retention time in HPLC, respectively.

Administration, Oral↗
PubMed1968

Isolated 5-hydroxytryptamine organelles of rabbit blood platelets: physiological properties and drug-induced changes.

1. In isolated 5-hydroxytryptamine (5-HT) organelles of rabbit platelets, the concentrations of 5-HT, histamine and adenosine-triphosphate (ATP) respectively are about 200 times higher than in intact platelets. Organelles incubated in plasma at 37 degrees C gradually lose endogenous 5-HT, histamine and ATP and take up (14)C-5-HT against a considerable concentration gradient. Liberation and uptake of 5-HT markedly decrease with dimishing incubation temperature.2. Exposure to reserpine in vitro strongly counteracts the uptake of (14)C-5-HT by isolated organelles, whereas the (14)C-5-HT uptake of intact isolated platelets is less affected by the drug. 5-HT organelles of platelets from reserpinized rabbits also take up very little (14)C-5-HT.3. Imipramine inhibits the uptake of (14)C-5-HT in isolated organelles less markedly than in isolated platelets.4. It is concluded that in the organelles 5-HT and possibly histamine may be associated with ATP. Reserpine probably impairs the uptake of 5-HT at the level of the organelles (possibly by interfering with the association 5-HT/ATP), whereas imipramine seems to act preferentially on the cell membrane.

Adenosine Triphosphate↗
PubMed2003

Therapeutic immunoglobulin reduces Ca2+ mobilization and von Willebrand factor secretion, and increases nitric oxide release in human endothelial cells.

Intravenous gamma-immunoglobulin (i.v.Ig) is commonly used in the treatment of autoimmune and inflammatory vascular disorders to prevent thrombotic complications. The mechanism of action of i.v.Ig is, however, not yet elucidated. In view of this, we investigated the ability of i.v.Ig to modulate i) Ca(2+) signals of fura-2 loaded endothelial cells, and ii) the associated release of nitric oxide (NO) and von Willebrand factor (vWf). NO was measured either indirectly by radioimmunoassay of cGMP in unstimulated cells or directly by electrochemistry at the surface of stimulated endothelial cells from human umbilical cord veins (HUVEC). Short-term treatment of unstimulated HUVEC with intact i.v.Ig decreased the basal cytosolic Ca(2+) concentration by 20% while it activated the NO/cGMP synthesis. Following i.v.Ig treatment of HUVEC, the Ca(2+) liberation from internal stores and the vWf secretion induced by ATP, thrombin or histamine were significantly reduced by 38 and 60%, respectively. The effects on Ca(2+) signals were observed with intact i.v.Ig as well as with the F(ab')2 or the Fc fragments indicating that both portions are involved in the mechanism of action. The i.v.Ig treatment of HUVECs had no effect on the NO release induced by thrombin or histamine. By contrast, the i.v.Ig treatment increased the ATP-activated NO release by amplifying the Ser1177-eNOS phosphorylation. The i.v.Ig also activated the NO-dependent cGMP release in resting and collagen-stimulated platelets. Since NO is a potent inhibitor of platelet activation and vWF is a platelet adhesion cofactor, the beneficial effects of therapeutic i.v.Ig may lie in the inhibition of platelet adhesion to damaged endothelium.

Blood Platelets↗
PubMed1983

Postprandial exercise-induced anaphylaxis.

A variety of systemic reactions associated with exercise are increasingly being recognized. We studied an atopic individual whose job-related activities involved strenuous running that often terminated in an episode of syncope and hypotension preceded by cutaneous pruritus, warmth, urticaria, and angioedema. These attacks occurred only after meals, but no foods appeared to elicit symptoms without subsequent exercise. The subject underwent three exercise challenges in the laboratory under the following conditions: (1) fasting state, with heat-dissipating clothing. (2) fasting, with heat-retention clothes, and (3) after a meal. Blood pressure decreases and minimum skin reactivity were observed for (1) and (2), and reproduction of syncope, hypotension, and further cutaneous manifestation were observed only after (3). Venous and arterial plasma determinations for complement activation (C4, C4d, and CH50) and histamine before, during, and after exercise were not abnormal. Although other vasodepressor mediators may have been liberated, at least part of the mechanism for postprandial exercise-related syncope may be attributed to a shift of blood flow to the splanchnic as well as skeletal muscle vasculature.

Adult↗
PubMed1998

[Mechanism of severe, immediate reactions to iodinated contrast material].

Immediate reactions to iodinated contrast material are usually supposed to be due to complement activation. Histamine has not been proved responsible for signs. However the results described in the literature are controversial: they have been obtained from non-reacting patients or during minor or moderate reactions. We suggest to study mediator release during unexpected severe reactions and to perform skin tests and IgE measurements in patients with proved liberation of mediators.

Anaphylaxis↗
PubMedDate not supplied

[Histamine and serotonin contents in human tissues].

Fluorometry of histamine and serotonin in cadaveric blood revealed a threefold increase of their concentrations in comparison with those in whole blood of live subjects. This indicates liberation of amines in the course of death and after it when factors inactivating them cease to function. However, the authors consider it possible to validate their conclusions about changes in the content of histamine and serotonin in cadaveric tissues in different diseases, provided certain conditions of selecting the material are adhered to. The distribution of amines in the viscera is not sex-dependent, little depends on the blood content of tissues, and is determined by the organ-specific features of metabolism of these bioactive substances. To illustrate this, the authors consider the content of histamine and serotonin in the organs of patients dead from hemorrhagic fever with the renal syndrome.

Adult↗
PubMed1990

Endothelium and mechanical responses of isolated monkey pulmonary veins to histamine.

Ring strips of monkey pulmonary veins precontracted with a high concentration of prostaglandin F2 alpha (PGF2 alpha) relaxed in a concentration-dependent manner in response to histamine. Treatment with mepyramine and/or famotidine attenuated the relaxation. 2-Pyridylethylamine (2PEA) and dimaprit caused relaxations in the precontracted preparations, which were inhibited by pretreatment with mepyramine and famotidine, respectively. Removal of endothelium reversed the histamine- and 2PEA-induced relaxations to dose-related contractions. On the other hand, the removal had no effect on the dimaprit-induced relaxations, which were significantly reduced by pretreatment with famotidine. Histamine-induced relaxations in the precontracted strips with endothelium in the presence and absence of famotidine were suppressed or abolished by treatment with methylene blue or hemoglobin but were unaffected by aspirin. It may be concluded that histamine-induced relaxation in monkey pulmonary veins precontracted with PGF2 alpha is mediated by H2-receptors in smooth muscle and H1-receptors in endothelium. Also, stimulation of the endothelial H1-receptors liberates an endothelium-derived relaxing factor.

Animals↗
PubMed1987

The role of intracellular Ca2+ in the degranulation of skinned mast cells.

The intracellular pH of rat peritoneal mast cells was slightly acidic and compound 48/80 induced a decrease in the cytoplasmic pH of these cells. By means of chemical skinning, it was revealed that perfusion with Ca2+ or inositol 1,4,5-trisphosphate (IP3) induced degranulation dose-dependently in mast cells at concentrations higher than 10 microM and 0.1 microM, respectively. Na+ was essential for the release of histamine from mast cells. An assay based on the binding of 45Ca to mast cell fragments revealed that the intracellular Ca store of the mast cell is located in the endoplasmic reticulum. IP3 liberated Ca from the endoplasmic reticulum.

Animals↗
PubMed1986

Adrenergic and cholinergic stimulation of arachidonate and phosphatidate metabolism in cultured astroglial cells.

Primary cultures of neonatal rat brain polygonal astroglia, or cells of the C62B glioma line, were incubated with [1-14C]arachidonic acid (AA) in culture for 18 hr. In both culture systems, more than 80% of the added [1-14C]AA was taken up into cellular glycerolipids; less than 1% of the radioactivity in the cells was present in an unesterified form. When prelabeled C62B cells were stimulated with acetylcholine (ACh), there was a rapid accumulation of arachidonyl-phosphatidic acid (PA) accompanied by a liberation of [1-14C]AA. A variety of other neurotransmitters failed to activate this response in C62B glioma cells. In contrast to the agonist specificity of the response in C62B glioma cells, primary astroglia generated PA and liberated [1-14C]AA in response to several neurotransmitters (i.e., ACh, norepinephrine, glutamate, and histamine) Treatment of astroglia with a combination of norepinephrine, ACh, and histamine resulted in a greater production of PA and free [1-14C]AA than did treatment with any one of these neurotransmitters alone. The results suggest that cultures of astroglia can respond to several different neurotransmitters with specific changes in AA and PA metabolism. Thus, a variety of neurotransmitters initiate cascades of lipid metabolism which may be of physiological significance in glial function.

Animals↗
PubMed1980

Identification of sulfated mucopolysaccharides including heparin in the lesional skin of a patient with mastocytosis.

Comparison of the [35S]mucopolysaccharides extracted after in vitro incubation of skin biopsy specimens from nonlesional and lesional sites of a patient with mastocytosis showed that lesional sites incorporated sulfate into heparin. After in vitro incorporation of the [35S]sulfate, the tissues were extracted sequentially by a 3-step procedure which utilized high salt concentrations, enzymatic digestion and base hydrolysis to liberate essentially all the counts. The extracted [35S]mucopolysaccharides were separated from free [35S]sulfate, histamine, protein, and hyaluronic acid by ion-exchange chromatography utilizing Dowex 1. The [35S]mucopolysaccharide extracts of the nonlesional skin were completely degraded by treatment with chondroitinase ABC, as they age predominantly dermatan sulfate with small amounts of chondroitin sulfates. The absolute quantity of sulfated mucopolysaccharides after Dowex 1 chromatography in micrograms of uronic acid per mg wet weight of starting tissue was higher in the lesional than the nonlesional specimen, while the specific incorporation of [35S]sulfate per microgram of uronic acid was the same. Approximately one-half of the [35S]mucopolysaccharides obtained in the 3 sequential extracts of lesional tissue was resistant to degradation by chondroitinase ABC as determined by gel filtration before and after enzyme treatment, indicating the presence of sulfated mucopolysaccharides in addition to chondroitin and dermatan sulfates. Heparinase treatment of the chondroitinase ABC-resistant [35S]mucopolysaccharides followed by gel filtration revealed an equal distribution of label between heparin and heparinase-resistant material presumed to be heparan sulfate. Heparin was also directly demonstrated in extracts of lesional mastocytosis skin by chemical and functional criteria.

Glycosaminoglycans↗
PubMed1980

Differential inhibitory effects of the ionophore RO2-2985 (X537A) on contractile responses to potassium and histamine in coronary artery smooth muscle.

The effects of the ionophore RO2-2985 (X537A) on KCl- and histamine-induced contractions in porcine coronary vascular smooth muscle were studied in vitro. Cumulative dose-response curves were constructed for KCl and histamine in the presence and absence of RO2-2985. The dose-response curve to KCl in the presence of RO2-2985 was shifted to the right with no change in the maximal response attained. Lineweaver-Burk and Hill plots indicated that responses to KCl involved a positive cooperative interaction between excitation and some step or steps in the contractile event and that RO2-2985 increased this cooperativity. The dose-response curve to histamine in the presence of the ionophore was significantly shifted to the right with a 40 to 50% depression in the maximal response. Propranolol inhibited norepinephrine-induced relaxation of KCl-contracted coronary strips but did not affect RO2-2985-induced relaxation. These results suggest that RO2-2985 competitively inhibits KCl-induced contractions but inhibition of histamine-induced contractions are of a mixed mechanism. Also, RO2-2985 does not appear to induce relaxation of coronary artery smooth muscle by liberating enodgenous catecholamines. Preliminary evidence supports involvement of prostaglandins in the mechanism of ionophore-induced coronary relaxation.

Animals↗
PubMed1994

Responses to histamine and acetylcholine in isolated monkey mesenteric veins versus arteries.

OBJECTIVE: The aim was to analyse and compare mechanisms of histamine or acetylcholine action in mesenteric venous and arterial strips obtained from Japanese monkeys. METHODS: Monkey mesenteric arterial and venous strips were suspended for isometric tension recording in modified Ringer-Locke solutions, and responses of the strips precontracted with prostaglandin F2 alpha to histamine or acetylcholine were compared. RESULTS: Histamine (2 x 10(-8) M-10(-5) M) produced a concentration related relaxation in the arteries and veins. The arterial relaxation was slightly but significantly attenuated by endothelial denudation [57.1(SEM 11.2)% inhibition at 10(-7) M, n = 14, p < 0.05] and treatment with 10(-6) M chlorpheniramine [26.7(6.7)% inhibition at 10(-7) M, n = 10, p < 0.05] or 10(-5) M methylene blue [31.5(11.2)% inhibition at 10(-7) M, n = 9, p < 0.05], and markedly suppressed by 10(-5) M cimetidine [96.8(1.2)% inhibition at 10(-7) M, n = 13, p < 0.001]. Indomethacin (10(-6) M) was without effect. On the other hand, relaxant responses to histamine of the venous strips were not influenced by endothelial denudation and treatment with chlorpheniramine or indomethacin but were abolished by treatment with cimetidine. Removal of the endothelium did not alter the venous relaxation caused by acetylcholine (10(-8) M-10(-4) M) but almost abolished the response to Ca2+ ionophore A23187 (10(-7) M) and substance P (10(-7) M). The acetylcholine induced relaxation was reversed to a contraction by indomethacin. CONCLUSIONS: Histamine-induced relaxations of monkey mesenteric arteries seem to be associated mainly with activation of the H2 receptor subtype in smooth muscle and partially mediated by relaxing factor liberated by stimulation of the H1 subtype in the endothelium, whereas the mesenteric venous relaxation seems to be due exclusively to a mediation of H2 receptors. Acetylcholine-induced relaxations of venous strips appear to be caused by vasodilator prostanoids, possibly prostaglandin I2, liberated from subendocardial tissues.

Acetylcholine↗