Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dose of 0.5 mg/kg i.v. of compound 48/80 was lethal in 97.2% of the injected rats. Observations before death and at autopsy were in accordance with the basic effect of compound 48/80 in rats i.e. the sustained release of mast cell mediators, whose action on the cardiovascular system leads to circulatory collapse. The administration of drugs with various pharmacological effects before the intravenous challenge with compound 48/80 allowed us to conclude that the following effects are not sufficient to prevent the lethal shock: inhibition of prostaglandin biosynthesis; H2-histamine antagonism; cholinergic, alpha- or beta-adrenergic blockade; beta-adrenergic stimulation; CNS-effects of antidepressants, hypnotics, sedatives, neuroleptics or narcotic analgesics; ganglion blockade; glucocorticoid or cromoglycate-like activity. Dose-dependent protection from the lethal reaction was obtained with compounds known to exert a single or several actions of the following types: oxatomide-like inhibition of mast cell mediator release; h1-histamine antagonism; serotonin antagonism. Quantitatively, however, when measured in in vitro systems these effects are poorly related to the protection from lethal compound 48/80 challenge. The new test offers the advantage of a simple, comprehensive measure of the potency of a compound to prevent mast cell-mediated shock.
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PMID:Protection of rats from compound 48/80-induced lethality. A simple test for inhibitors of mast cell-mediated shock. 3 Apr 20

Exercise is a physical cause of allergic reactions, including exercise-induced anaphylaxis (EIAna), exercise-induced urticaria (EIU), exercise-induced asthma (EIA), and exercise-induced rhinitis (EIR). Since its first description in 1979, EIAna has been reported with variable clinical manifestations, with exercise alone, and in combination with food ingestion. Elevated serum histamine levels and cutaneous mast cell degranulation have been noted. Exercise-induced urticaria appears as small, punctate lesions that differ from the classic coalescent type seen with EIAna. Variant forms of EIAna with cholinergic urticarial lesions manifesting systemic collapse and/or respiratory distress have been studied. Exercise-induced urticaria and cold-induced urticaria may cause elevated plasma histamine levels coincident with the onset of pruritus and hives. Theories accounting for EIA include respiratory heat loss, water loss, and mast cell activation. Although some studies have shown increased plasma histamine with EIA, others have not. Recently, bronchoalveolar lavage in atopic subjects with EIA has been evaluated preexercise and postexercise, with no significant differences in histamine or tryptase, suggesting a pathogenesis of EIA independent of the mast cell. Exercise-induced rhinitis, with varying degrees of rhinorrhea, congestion, and sneezing, has been increasingly recognized in athletes who run, cycle, and ski. Cold-air-induced rhinorrhea in laboratory challenges displays a mediator release pattern similar to that produced by allergen-induced nasal challenges. Therapeutically, H1 antihistamines are recommended for EIAna both as pretreatment and acute therapy. H1 antihistamines may be helpful in EIU, but are recommended for EIAna both as pretreatment and acute therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise-induced allergies: the role of histamine release. 137 Oct 41

T-2 toxin-induced alterations in rat mesenteric mast cell granulation were measured by cytophotometric analyses of the metachromatic reaction of mast cell granules with azure B. Hypogranulation (diminution of metachromatic material) was observed 8 h following injections of T-2 toxin (0.5-1.5 LD50, i.p.). These data suggest that mast cell activation occurs during acute T-2 intoxication and raise the possibility that mast cell mediators may contribute to toxin-induced cardiovascular collapse.
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PMID:Mesenteric mast cell degranulation in acute T-2 toxin poisoning. 150 4

SK&F 101926 is a synthetic octapeptide which was designed to promote free water excretion by antagonizing the action of antidiuretic hormone. The clinical and pathologic changes in rats resulting from lethal doses of SK&F 101926 have suggested that death is associated with respiratory failure and/or cardiovascular collapse. To define the relationships between respiratory failure, cardiovascular collapse, and death, respiratory and cardiovascular parameters were monitored in anesthetized rats following the intravenous administration of SK&F 101926 at a dosage (3 mg/kg) which resulted in 70% mortality. Within 5 min after receiving this dosage, mean arterial blood pressure was reduced to values between 30 and 40 mm Hg in all rats. This degree of hypotension was well tolerated by some rats and, consequently, was not considered to be the cause of death. Deaths occurred between 9 and 58 min after dosing and were preceded by respiratory depression involving marked reductions in respiratory rate and the lack of compensatory increases in tidal volume. At the time of respiratory arrest, heart rates remained above 200 beats/min, mean arterial blood pressure remained between 30 and 40 mm Hg, and there were no consistent changes in dynamic lung compliance or total pulmonary resistance. Pretreatment of rats with a mast cell stabilizing agent (disodium cromoglycate), a mast cell degranulating agent (compound 48/80), or a histamine/5-hydroxytryptamine blocking agent (cyproheptadine) prevented the reductions in respiratory rate and death caused by SK&F 101926. These pretreatments also reduced the effect of SK&F 101926 on blood pressure, but were not able to completely prevent the hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory and cardiovascular changes associated with toxic doses of a peptide antagonist of vasopressin in the rat. 160 Dec 32

The intragranular pH of isolated mast cell granules was measured. Because of the minute amounts of isolated granules available, two techniques were developed by modifying aminoacridine fluorescence and [14C]methylamine accumulation techniques to permit measurements with microliter sample volumes. Granule purity was demonstrated by electron microscopy, ruthenium red exclusion, and biochemical (histamine, mast cell granule protease) analysis. The internal pH was determined to be 5.55 +/- 0.06, indicating that the pH environment within mast cell granules is not significantly different from that of previously studied granule types (i.e., chromaffin, platelet, pancreatic islet, and pituitary granules). Collapse of the pH gradient by NH+4 was demonstrated with both techniques. No evidence of Cl-/OH- or specific cation/H+ transport was found, and major chloride permeability could not be unequivocably demonstrated. Ca2+ and Cl- at concentrations normally present extracellularly destabilized granules in the presence of NH+4, but this phenomenon does not necessarily indicate a role for these ions in the exocytotic release of granule contents from intact cells. The pH measurement techniques developed for investigating the properties of granules in mast cells may be useful for studying other granules that can be obtained only in limited quantities.
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PMID:Measurement of the internal pH of mast cell granules using microvolumetric fluorescence and isotopic techniques. 357 99

Exercise-induced anaphylaxis (EIA) is a unique and an increasingly recognized syndrome consisting of premonitory symptoms and signs of generalized body warmth, pruritus, and erythema, which progresses on continued exertion to confluent urticaria, laryngeal edema with stridor or hoarseness, and gastrointestinal colic and frequently culminates in vascular collapse. Previous studies of five individuals with this condition have demonstrated significant elevations of serum histamine concurrent with the early clinical manifestations after experimental exercise. To assess relevant morphologic alterations in the skin of these patients, cutaneous mast cells were examined by light and transmission electron microscopy before and during the initial erythema elicited by exertion. The marked alterations observed in mast cells immediately after exercise consisted of (1) loss of electron density and internal substructure of granules, (2) fusion of granule membranes with those of adjacent granules and with mast cell membranes creating conduits to the extracellular space, and (3) an apparent decrease in the number of intact granules per cell. Biopsy specimens obtained before exercise from patients with EIA and from two normal individuals who served as control subjects were identical, and the control subjects had normal mast cell morphology after exercise. Serum histamine levels were significantly elevated in patients with EIA after exercise at the time of biopsy, whereas control subjects had normal levels. These observations provide evidence that EIA is a distinct form of physical allergy associated with mast cell degranulation similar in morphology to that of human pulmonary mast cell IgE-Fc-dependent activation secretion. Characterization of this disorder is important because its prevalence may be underestimated, and its clinical consequences, which may include some morbidity, are not fully known.
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PMID:Exercise-induced anaphylaxis: a serious form of physical allergy associated with mast cell degranulation. 398 Aug 83

Effects of the organophosphate neurotoxin soman on rat mesenteric mast cell granule content were determined using scanning-integrating microdensitometric analysis of individual cell metachromasia. Mast cell degranulation was evidenced both with sublethal (0.5 LD50) and lethal (1.5 LD50) dosages and as early as 3-10 min post-injection. These data indicate a possible contribution of mast cell autacoids in the genesis of organophosphate-induced respiratory and circulatory collapse.
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PMID:Quantitative cytophotometric analyses of mesenteric mast cell granulation in acute soman intoxicated rats. 406 5

REV 3164 has been evaluated in a variety of intact rodent models to reveal potential utility in the prophylactic treatment of asthma. REV 3164 was found a potent, orally active inhibitor of rat (IgE) passive cutaneous anaphylaxis (PCA, ED50 = 0.9 mg/kg). By contrast, at 50-200 mg/kg p.o., it did not affect guinea-pig (IgG1) PCA. In PCA rats, both REV 3164, 1-36 mg/kg i.p., and the known inhibitor of mast cell mediator release, disodium cromoglycate (DSCG), 2-54 mg/kg i.p., blocked cutaneous wheals caused by i.v. antigen challenge but not by intradermal serotonin or histamine. Neither REV 3164 (0.1-10 mg/kg i.p.) nor DSCG (2-54 mg/kg i.p.) affected Compound 48/80-induced wheals. REV 3164 (0.01-1 mg/kg i.v. or 10 mg/kg i.p.) abolished rat (IgE) passive lung anaphylaxis (PLA, ED50 = 0.05 mg/kg i.v. for inhibition of elevated airway resistance). At 10 mg/kg i.p., REV 3164 did not affect active lung anaphylaxis in guinea-pigs pharmacologically manipulated to enhance the production and action of slow reacting substance of anaphylaxis (SRS-A), nor did it exhibit anticholinergic activity in the rat. REV 3164 (100 mg/kg i.p.) did not protect conscious guinea-pigs from histamine aerosol-induced collapse. It is concluded that REV 3164 is an oral inhibitor of IgE-dependent immediate hypersensitivity in the rat with biological activities in rats and guinea-pigs similar to DSCG.
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PMID:In vivo anti-allergic and bronchopulmonary pharmacology of REV 3164 in rats and guinea-pigs. 649 6

Exercise-related anaphylaxis is a novel form of physical allergy that is being recognized with increasing frequency in a society with a growing commitment to health through planned exercise. The clinical manifestations progress from pruritus, erythema, and urticaria to some combination of cutaneous angioedema, gastrointestinal and laryngeal symptoms and signs of angioedema, and vascular collapse. The finding of an elevated serum histamine level during experimentally-induced attenuated attacks indicates mast cell participation, as in a physical allergy, and the signs and symptoms are characteristic of a classic anaphylactic reaction to a foreign substance in an allergic human.
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PMID:Exercise-induced anaphylaxis. 671 33

Exercise induced anaphylaxis (EIA) is a relatively new syndrome described in 1980. It is associated with different kinds of exercise, although jogging is the most frequently reported. The clinical manifestations progress from pruritus, erythema and urticaria to some combination of cutaneous angioedema, gastrointestinal and laryngeal symptoms and signs of angioedema and vascular collapse. In the full-blown phase a differential diagnosis must be done with the following syndromes: exercise-induced asthma, idiopathic anaphylaxis, cardiac arrhythmias, carcinoid syndrome. An elevated serum histamine level during experimentally-induced attacks and cutaneous degranulation of mast cells after attacks proved a mast cell participation in the pathogenesis of the syndrome. As predisposing factors, a specific or even aspecific sensitivity to food has been reported and such cases are called "food-dependent EIA". Another precipitating factor includes drug intake; moreover a familial tendency has been reported in some studies. Although the prognosis of this syndrome is not well defined, a reduction of attacks occurs in 45% of patients by means of elimination diets and behavioural changes. Treatment of attacks should include all the manoeuvres efficacious in the management of conventional anaphylactic syndrome, including the epinephrine administration. Prevention of attacks may be achieved by limitation of the exercise program or interruption of the program at the appearance of the first premonitory symptoms. The use of H1 antihistamine-receptor antagonists in maintenance therapy seems to be useful, although no controlled data are available.
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PMID:[Anaphylaxis induced by exertion]. 809 51


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