Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HISTAMINE LIBERATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed1989

Pathogenesis of naturally acquired bovine respiratory syncytial virus infection in calves: evidence for the involvement of complement and mast cell mediators.

Indicators of immune-mediated disease were studied in calves with severe natural bovine respiratory syncytial virus infection. Although antigen and antibody were detected concurrently in most calves, immune complexes were not detected by use of immunofluorescence, ELISA, and binding of the 1q component of complement. Complement component C3, however, was observed by immunofluorescence in the cranioventral, virus-infected portion of the lungs of 19 of 25 calves. Reductions in the amount of histamine and in the numbers of mast cells and mast cell granules in the virus-positive cranioventral and virus-negative caudodorsal portions of the lungs, indicated activation of mast cells and liberation of their granule contents. On the basis of these and previous findings, a model for the pathogenesis of bovine respiratory syncytial virus-induced disease was proposed.

Animals↗
PubMed1980

Platelet-activating factor in anaphylaxis and phagocytosis. I. Release from human peripheral polymorphonuclears and monocytes during the stimulation by ionophore A23187 and phagocytosis but not from degranulating basophils.

Platelet-activating factor (PAF) is a mediator of a anaphylaxis found initially in basophils and later in mouse and rat macrophages. The purpose of this paper was to determine the cellular origin of PAF released from human leucocytes and to establish if phagocytosis is a more important stimulus for PAF release than anaphylactic reactions. Phagocytic leucocytes (monocytes and PMNs) released PAF, physicochemically analogous to the PAF obtained by anaphylactic reactions in rabbits when challenged with zymosan, zymosan coated with complement, immune complexes, immunoglobulin aggregates or calcium ionophore A23187. Basophils failed to release PAF by anti-human IgE antibody, although positive degranulation and histamine liberaton were found. Pre-incubation of phagocytosing leucocytes with cytochalasin B or colchicine produced a diminution of PAF release, whereas beta-glucuronidase liberation was increased. The addition of carboxypeptidase B did not significantly modify PAF or beta-glucuronidase release. These data indicate that PAF obtained from preparations of human leucocytes comes from monocytes and polymorphonuclears; human basophils do not liberate measurable quantities of PAF, either by anaphylactic stimulus or by neutrophil cationic proteins; liberation of PAF and lysosomal content follow different mechanisms as they have different kinetics and are modified in an opposite way by drugs acting on the cytoskeleton.

Anaphylaxis↗
PubMed1987

Structure of a biologically active neurotensin-related peptide obtained from pepsin-treated albumin(s).

Using a radioimmunoassay toward the COOH-terminal region of neurotensin, an immunoreactive and biologically active neurotensin-related peptide (NRP) has been isolated from pepsin-treated fractions of bovine, canine, human, and rat plasma. Bovine NRP was identified as H-Ile-Ala-Arg-Arg-His-Pro-Tyr-Phe-Leu-OH, which is similar in structure to both neurotensin and angiotensin I. Canine and human NRP also had the above amino acid composition, whereas that obtained from rat plasma had valine substituted for isoleucine. At their concentrations in pepsin-treated plasmas (2-6 microM) rat, human and canine NRP were shown to increase vascular permeability when injected intradermally into rats and to release histamine from rat mast cells in vitro. The pure peptides also cross-reacted very effectively at nanomolar concentrations in a radioreceptor assay for neurotensin. The protein(s) which liberated NRP upon pepsin treatment were purified about 7-fold and shown to behave like albumin during sodium dodecyl sulfate-polyacrylamide gel electrophoresis, isoelectric focusing, and high pressure liquid chromatography on muBondapak C4. In addition, the purified preparations were found to react with anti-albumin antisera during immunodiffusion. Although the amino acid sequence of NRP was not found in albumin, a partial sequence homology was noted for NRP and various segments of bovine albumin. Using V8 protease, glutamyl residues were shown to lie within 3-4 amino acids of each end of NRP, as also occurs for the related segments in albumin. These results suggest that a subset of albumin-related protein(s) could serve as precursor(s) to biologically active neurotensin-related peptide(s).

Amino Acid Sequence↗
PubMed1976

Release of creatine kinase by antigen, histamine, and catecholamines.

In mepyramine treated, ovalbumin sensitized anaesthetized guinea pigs protracted anaphylactic shock was produced by i.p. injection of antigen, and serum creatine kinase (CK) activities were determined 4, 6, or 17 hrs thereafter. Significant increases above nonsensitized controls were obtained. In nonanaesthetized guinea pigs shock course and serum CK increase were considerably accelerated. Histamine increased the serum CK only when given in high amounts (10 mg/kg) s.c., in the presence or absence of mepyramine. I.p. injection of histamine in mepyramine treated animals had no effect. Adrenaline (1 or 10 mg/kg) given as a s.c. depot in oil produced a significant increase of serum CK, as well as noradrenaline (0.1, 1, or 10 mg/kg). Dibenamine reduced the effect of adrenaline. In isolated perfused guinea pig hearts a significant CK liberation occurred already within the first hour after eliciting anaphylaxis. Nonanaphylactic hearts released CK too, but significant amounts were obtained only in the total 4 hrs after ovalbumin administration. Isolated anaphylactic hearts incubated in Tyrode solution liberated significantly more CK than did nonsensitized control hearts. The findings are discussed in view of a possible myocardial damage in anaphylaxis.

Anaphylaxis↗
PubMed1985

The effect of 8-methoxypsoralen plus long-wave ultraviolet (PUVA) radiation on mast cells: PUVA suppresses degranulation of mouse skin mast cells induced by compound 48/80 or concanavalin A.

In order to see whether 8-methoxypsoralen (8-MOP) plus long-wave ultraviolet (UVA) radiation (PUVA) has an influence on immediate-type skin reactions, we have undertaken an animal study. Ears of mice were treated with a 0.5% 8-MOP solution topically plus UVA radiation (1.5-2.5 J/cm2). After PUVA radiation, skin responses to intradermal injection with mast cell liberators, including compound 48/80 (2.5 mg/ml, 10 microliter) and concanavalin A (Con-A) (2.0 mg/ml), or with a mixture of 5-hydroxytryptamine (5-HT) and histamine as vasodilator (1.0 mg/ml and 50 mM, respectively) were examined with time (2 h-14 days). At each time point, an ear swelling response (ESR) was measured with a dial thickness gauge. The rate of mast cell degranulation and mast cell numbers were assessed by light microscopy using toluidine blue-stained semithin (1 micron) sections. ESR induced by compound 48/80 or Con-A was significantly suppressed dose-dependently (greater than 42% inhibition) by PUVA between 2 h-3 days postirradiation as compared with that in nonirradiated control mice, and the value returned to normal levels by 7-14 days. Compound 48/80- or Con-A-induced mast cell degranulation (%) was remarkably decreased between 2 h-3 days (greater than 48% inhibition) in accordance with the suppression in ESR and it was restored to the rates in nonirradiated controls by 7-14 days. Neither ESR nor percent degranulation was affected by UVA radiation only (less than 3.5 J/cm2) or application of 8-MOP only. 5-HT plus histamine-mediated ESR was not altered at all by PUVA throughout the experimental period. Since PUVA radiation itself at given doses did not produce measurable ESR, mast cell degranulation, or a reduction in mast cell numbers, and since PUVA did not affect a normal vascular response to vasodilator, it seemed that decreased skin reactivity to mast cell degranulators by PUVA might be due to a PUVA-induced noncytolytic alteration in mast cell release mechanisms.

5-Hydroxytryptophan↗
PubMed2004

Expression of L-histidine decarboxylase in granules of elicited mouse polymorphonuclear leukocytes.

Infiltrating polymorphonuclear leukocytes (PMN) in the peritoneal cavity were found to express L-histidine decarboxylase (HDC), the rate-limiting enzyme of histamine synthesis, in a csein-induced peritonitis model. Expression of HDC was detected in the elicited PMN, but not in the peripheral blood leukocytes. The peritoneal lavage fluids in this model were found to augment histamine synthesis in PMN isolated from the bone marrow. Rapid post-translational processing of HDC was observed in PMN, and the dominant form of HDC was the mature 53-kDa form, which was found to co-localize with a granule enzyme, matrix metalloproteinase-9 (MMP-9). Treatment of PMN with the phorbol ester PMA, which stimulates the release of MMP-9, did not liberate the granular HDC. Immunofluorescence studies using an anti-HDC antibody strongly suggested that HDC is bound to the cytosolic side of the granule membranes. These observations suggest that HDC is induced upon infiltration of PMN into the mouse peritoneal cavity and that histamine is synthesized by HDC attached to the granule membranes of PMN.

Animals↗
PubMed1982

Effect of vagotomy on gastric acid secretion in the rat.

The effects of pentagastrin, histamine or feeding on gastric acid secretion were studied in conscious rats with total gastric by-pass, achieved by transection of the cardia and pylorus, followed by an oesophago-duodenostomy. After closure of the cardia, the by-passed stomach was connected to the small intestine through a Roux-en-Y loop. A chronic gastric fistula was fitted into the rumen. Basal acid output was low in chronically vagotomized rats, being 6% of that in the innervated animals. A clear-cut stimulation was observed after both pentagastrin and histamine in innervated as well as denervated rats, although the maximal acid output in the denervated group was less than 10% of that in the innervated group. In previous studies on acid secretion in vagotomized rats with chronic gastric fistulas, neither basal nor stimulated acid secretion could be detected. Apparently, by-passing the stomach eliminates sources of error associated with the conventional gastric fistula technique (for instance, neutralization of acid gastric juice by swallowed saliva or regurgitated duodenal juice). Nonetheless, the greatly reduced acid output following vagotomy indicates that normal basal as well as normal stimulated acid secretion is dependent upon an intact vagus. Pentagastrin- and histamine-stimulated acid secretion was blocked by atropine and cimetidine in both the innervated and denervated rats. Feeding caused a significant inhibition of acid secretion in the by-passed, innervated stomach. In the denervated stomach feeding was without effect. The mechanism behind the postprandial inhibition of acid secretion in the innervated stomach is obscure. Direct vagal inhibition as well as humoral substances, liberated by vagal stimulation or by the presence of food in the intestine, may be responsible.

Animals↗
PubMed1997

Medical therapy of gastroesophageal reflux and management of esophageal strictures.

The goals of modern medical therapy for gastroesophageal reflux disease are threefold: first, eliminate symptoms; second, heal injured esophageal mucosa; third, manage and/or prevent complications. Selection of a particular medical regimen depends on the severity of the disease, effectiveness of the therapy, cost, and convenience of the medical regimen. An accurate diagnosis needs to be made in patients suspected with esophageal strictures. If there is a treatable underlying disease, specific therapy is essential. The goal of dilation therapy should be established and set about to accomplish in a timely, but unhurried fashion. Fluoroscopy and wire-guided dilators should be used liberally, especially for difficult strictures.

Diagnosis, Differential↗
PubMed1975

Action of morphine sulfphate on stimulated gastric secretion in dogs.

In dogs morphine sulphate suppresses both 2-deoxy-D-glucose and pentagastrin-stimulated acid and pepsin secretion, but not histimaine- and pilocarpine-stimulated acid. This is consistent with the view that morphine both depresses acetylcholine release from cholinergic endings in the stomach and that pentagastrin acts by liberation of acetylcholine from these endings.

Acetylcholine↗
PubMed1988

Biochemical and cellular basis for circadian rhythms in obstructive lung disease and implications for theophylline therapy.

In the majority of patients one of the primary features of bronchial asthma is the occurrence of nocturnal symptoms. There are significant bioperiodicities for hormonal, neural, cellular and humoral factors and for mediators, which are all in favour of reducing bronchial patency during the night. In the morning hours between 2 and 6 a.m. the histamine concentration shows a peak, the adrenaline and cyclic AMP have their minimum, while the cortisol secretion with its delayed onset of action is already ascending. The kallikrein kinin system is activated by histamine. Circadian variations have also been found for the receptor density of beta-receptors, cAMP, adenylcyclase and phosphodiesterase. While circadian rhythms are not known for the platelet activating factor (PAF) at the present time, the known nocturnal peak of thromboxane A2 may influence PAF-liberation as well. The bronchodilating metabolite of the cyclooxygenase pathway, PGE2, was found to have depressed levels during the night. Total plasma, total protein as well as IgA, IgM, IgG and IgE have a minimum during the night, cellular elements like T11-, T4-, B-lymphocytes and Leu8 have a maximum. Slow release theophylline is today the most important drug for nocturnal asthma. Theophylline is known to interfere with histamine release from mast cells, mediator release of arachidonic acid metabolites, the cyclic AMP concentration and suppressor cell activity. Important work remains to be done to clarify the therapeutic and immunological role of theophylline in nocturnal asthma and to identify the subgroups of patients having the greatest benefit of theophylline treatment.

Asthma↗
PubMed1996

Inhibition of ultraviolet-induced formation of reactive oxygen species, lipid peroxidation, erythema and skin photosensitization by polypodium leucotomos.

The acute reactions of human skin to solar ultraviolet radiation (290-400 nm) are recognized as a form of inflammation reactions that are mediated by several possible mechanisms including (a) direct action of photons on DNA, (b) generation of reactive free radicals and reactive oxygen species involving the formation of O2.-, 1O2, H2O2, OH, etc., (c) generation of prostaglandins (PGD2, PGE2, etc.), histamine, leucotrienes, and other inflammatory mediators. It is conceivable that UV-induced reactions represent oxidative stress mediated by the formation of free radicals, reactive oxygen, lipid peroxidation, liberation of membrane phospholipids, and subsequent formation of prostaglandins by cyclo-oxygenase pathway. In this study, we examined the role of reactive oxygen species and lipid peroxidation in in vitro reactions as well as in vivo skin inflammation reactions induced by (a) UVB radiation (290-320 nm), and (b) skin photosensitization reaction by PUVA treatment involving 8-methoxypsoralen and UVA (320-400 nm) radiation and presented data for the generation of superoxide anion O2.-) and lipid peroxides. We have also evaluated, both in vitro as well as in vivo systems, the quenching or the inhibition of O2.- by a plant extract known as Polypodium leucotomos. The P. leucotomos extract was found to exhibit interesting antioxidant and anti-inflammatory as well as photoprotective properties against photo-oxidative stress involving the generation of reactive oxygen, lipid peroxidation under in vitro reactions as well as in vivo experimental conditions. Significant inhibition of UVB-induced erythemal response, and 8-methoxypsoralen plus UVA-induced phototoxic reaction after topical application or oral administration of the photosensitizer could be demonstrated in guinea pig skin and human skin following the topical application of P. leucotomos extract. The photoprotective mechanism of P.leucotomos involving interaction with reactive oxygen species or free radicals appears to have potential clinical usefulness in preventing sunburn and inhibiting phototoxic reaction.

Animals↗
PubMed1983

The significance of liberated cyclooxygenase products for the pulmonary and cardiovascular actions of leukotriene C4 in the guinea pig depends upon the route of administration.

Leukotriene C4 (LTC4), given as an aerosol or by the intravenous route, was at least 100 times more potent than histamine in causing an increase of the tracheal insufflation pressure in pentobarbital anaesthetized artificially ventilated guinea pigs. Indomethacin or meclofenamate enhanced the longlasting bronchoconstriction elicited with aerosols of LTC4, but antagonized the relatively short lived airway response to intravenously injected LTC4. However, by increasing the injected dose of LTC4, a slowly developing but maximal bronchoconstriction could be obtained in the presence of indomethacin. Indomethacin did not affect the airway response to histamine, administered by either route. Intravenous injection of LTC4 had little effect on the heart rate, but evoked a biphasic change of the systemic arterial blood pressure. An initial pressor response, which was attenuated but not abolished by indomethacin, was followed by a longlasting reduction of blood pressure. The hypotensive period evoked with higher doses of LTC4 occurred earlier and was of greater magnitude in indomethacin treated animals. Thus, LTC4 has a potent cyclooxygenase-independent bronchoconstrictor action in the intact guinea pig, which supports the possibility that LTC4 and its metabolites are important mediators of airway anaphylaxis in this animal. Depending upon the route of administration, secondarily released prostaglandins and/or thromboxanes may amplify or reduce the direct pulmonary effects of LTC4.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗