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PubMed1977

[Factors favoring anaphylactic reactions to general anesthetics].

The prevention of anaphylactic reactions to general anesthetics depends on the definition of a high risk group owing to special risk factors in these subjects. This study based on a study of the world literature over 20 years and on the cases of anaphylactic reaction observed in Nancy (more than 30) led the authors to carry out a special study of 7 with an atopic background, a history of drug allergy of immediate type, the repetition of general anesthetics at short intervals, latent spasmophilia, aptitude to histamine liberation, and/or hyper-reactivity to histamine, type of anesthesia and association of various factors. This method of approach permits in turn a prevention of complications by appropriate premedication.

Anaphylaxis↗
PubMed1958

The pressor effect of peptone in the rat.

Peptone normally causes a rise of blood pressure in rats. Since the pressor response was not abolished or even diminished by adrenalectomy, it could not have been caused by a release of pressor substances from the adrenal glands. The group of drugs (dibenamine, dihydroergotamine, ergotamine, tolazoline, nicotine and hexamethonium) which antagonize or block the peptone-induced pressor action suggests that the pressor effect may be secondary to a release of sympathin by the stimulation of sympathetic ganglia. Since it was not possible to duplicate the pressor response to peptone by either 48/80 or histamine, the hypothesis that peptone acts by liberating histamine can be ruled out.

Adrenal Glands↗
PubMed1982

Regulation of allergic reaction by aerobic Corynebacterium equi extract, CEF. III. Inhibition of histamine release from rat peritoneal mast cells.

Effects of a water soluble fraction of Corynebacterium equi (CEF) on the histamine release from rat peritoneal mast cells (RPMC) were investigated. The treatment of RPMC with CEF resulted in a significant inhibition of the histamine release from RPMC which was induced by IgE antibody-antigen interaction as well as nonimmunological histamine liberators. CEF was much more effective in inhibition of IgE-mediated histamine release and compound 48/80 or polymyxin B-induced histamine release when the mast cells were treated with CEF prior to the incubation with the antigen or the liberators. In contrast, CEF was equally effective in inhibition of the histamine release by concanavalin A with phosphatidyl serine when the mast cells were treated with CEF prior to or simultaneously with the liberator. Evidence was also presented that CEF inhibits degranulation of mesenteric mast cells induced by immunological as well as nonimmunological mechanisms.

Animals↗
PubMed1991

The intracerebroventricularly administered mast cells degranulator compound 48/80 increases the pituitary-adrenocortical activity in rats.

The effect of brain mast cells degranulation by compound 48/80 on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, and the involvement of a histaminergic mechanism in that stimulation was investigated in conscious rats. All the drugs were given intracerebroventricularly (icv), histamine antagonists 15 min prior to compound 48/80. Compound 48/80 induced a significant dose- and time-related increase in the serum corticosterone levels. That increase, measured 1 h after administration of compound 48/80, was moderately diminished by icv pretreatment of rats with mepyramine and cimetidine, histamine H1- and H2-receptor antagonists. Three hours after administration of compound 48/80 mast cells of the thalamus and the hypothalamus were completely degranulated. At the same time the thalamus and the whole brain histamine levels were substantially higher than in the saline-treated control rats. The above results suggest that histamine liberated from the brain mast cells and central histamine receptors play a moderate role in increasing the pituitary-adrenocortical activity by compound 48/80.

Adrenal Cortex↗
PubMed1991

The cardiovascular effects of thyrotropin-releasing hormone (TRH) are attenuated by cimetidine in rats.

The modulation of cardioventilator effects of thyrotropin-releasing hormone (TRH) by histaminergic mechanisms was studied in anaesthetized rats pretreated with histamine receptor antagonists. TRH (1-100 nmol/kg) into the lateral cerebral ventricle dose-dependently elevated mean arterial pressure, heart rate and stimulated respiration. The respiratory stimulating effect of TRH remained unchanged after pretreatments with histamine H1-receptor antagonist diphenhydramine or H2-receptor antagonists cimetidine and ranitidine, while the TRH-induced hypertension and tachycardia were attenuated by cimetidine. This antagonism was not due to an interaction between TRH and cimetidine at their central binding sites, since there was no displacement of [3H]MeTRH binding in the presence of cimetidine nor did TRH displace [3H]cimetidine in rat brain homogenates. Inability of diphenhydramine to modify the cardiovascular effects of TRH indicates that these effects are not due to histamine liberation, as cardiovascular stimulation after central administration of histamine is mainly mediated via H1-receptors. The antagonism of the cardiovascular responses to TRH by cimetidine was not due to blockade of H2-receptors, since another potent H2-receptor antagonist ranitidine was unable to affect the cardiovascular effects of TRH. Therefore, we suggest that cimetidine exerted antagonism of TRH by some non-specific action.

Animals↗
PubMed1984

[Characteristics of the effect of ketotifen on the selective and non-selective histamine release from human basophils].

Administration of ketotifen at concentrations from 0.125 to 1.0 mM did not lead to the release of histamine from basophils of normal persons but induced a dose-dependent inhibition of histamine release provoked by IgE antibodies or Con A. The inhibitory action of ketotifen developed shortly after addition to the cells, being retained in the presence of the drug throughout the whole time of experiment (up to 40 min). Washing of the cells from ketotifen was followed by rapid recovery (at any rate within the first 5 min) of cell sensitivity to the histamine liberator. Ketotifen did not produce any influence on histamine release provoked by the cytotoxic secretion activators, chlorpromazine and mellitin.

Adult↗
PubMed1986

Lack of effect of compound 48/80 on human umbilical vein endothelium.

Human umbilical veins have been treated with compound 48/80, a histamine liberator factor, in order to obtain information about the histamine content in the Weibel-Palade bodies. Ultrastructural observations show a lack of effect in the morphology of this organelle. Our findings suggest that the Weibel-Palade bodies are not histamine storage organelles in human umbilical vein.

Endothelium↗
PubMed1982

Intrinsic asthma and bacterial histamine release.

In this study of intrinsic asthma (IA) in children the pathogenic role of bacteria in respiratory disease was elucidated by a basophil histamine liberation technique. Several strains of bacteria caused release of histamine from peripheral leukocytes in vitro. Normal, non-infectious and non-atopic children frequently responded in a similar fashion, although positive responses were less frequent. It seems that two different mechanisms of bacterial histamine release exist: interaction with the basophil-bound IgE and a direct interaction with the cell surface. It is suggested that the histamine release takes place only in the lung of IA patients, where a defective pulmonary barrier could permit the bacteria to enter, but not in healthy individuals.

Adolescent↗
PubMed1990

Effect of inhibitors on histamine release from mast cells recovered by bronchoalveolar lavage in basenji-greyhound and mongrel dogs.

Studies of rodent mast cells have demonstrated that subpopulations differ in regard to their response to inhibitors of histamine release. To determine whether such compounds have different effects on mast cells from Basenji-Greyhound (BG) dogs with airway hyperreactivity and from mongrel dogs, we investigated the effect of cromolyn sodium, nedocromil sodium, theophylline, and quercetin on calcium ionophore A23187-induced histamine release from mast cells recovered by bronchoalveolar lavage. Mast cells recovered from BG and mongrel dogs were similar in respect to morphology and spontaneous and calcium ionophore-induce histamine release. Histamine release from mast cells from both BG and mongrel dogs was inhibited by quercetin (10(-4) M) and nedocromil sodium (5 x 10(-5) M). In contrast, only the histamine release from mast cells recovered from mongrel dogs was inhibited by cromolyn sodium (10(-4) M) and theophylline (5 x 10(-3) M). Thus, mast cells that are similar in regard to morphology and response to histamine liberators may differ in their response to inhibitors of histamine release.

Animals↗
PubMed1989

[Alpha-thrombin stimulation of heparin secretion by the peritoneal mast cells in rats].

The interaction of alpha-thrombin with connective tissue-type mast cells (CTMC) purified by Ficoll density gradient centrifugation has been examined. It was demonstrated that exposure of CTMC to polymixin (widely used histamine liberator) (3 mg/ml) induced the release of heparin and histamine. Exposure of CTMC to 10(-11) M alpha-thrombin resulted in increase of heparin secretion by 75.5% in relation to basal level. CTMC which were stimulated by very low concentrations of alpha-thrombin (10(-11)-10(-8) M) can release high level of heparin, but not histamine. We have a suggestion that the thrombin specificity is connected with the additional recognition binding site for high molecular substrates (HMS) distinct from the active centre. Unlike alpha-thrombin which has both the active centre and the recognition site for HMS, beta/gamma-thrombin with catalytic activity but with disrupted recognition site induced the heparin release from mast cells only at higher concentrations than alpha-thrombin. It was revealed that DIP-alpha-thrombin without proteolytic activity was unable to activate mast cells in contrast to alpha-thrombin. We consider that alpha-thrombin induced release of heparin by CTMC account for proteolytic and hormone-like activity enzyme by means of both the active centre and the additional recognition site for HMS.

Animals↗
PubMed1976

[The effect of mepyramine and 48/80 on the histamine content of pleural exudates in the rat].

The influence of pretreatment with the antihistaminic, mepyramine, or with the histamine liberator 48/80 was studied on the volume and the histamine content of pleural exudates induced in rats by intrapleural injection of turpentine, silver nitrate or carrageenan. The fluorometric determination of histamine was performed in the exudates collected at different times after injection of the irritant. In control animals the histamine levels were different from those previously found by the authors using biological assays. In rats pretreated with mepyramine or compound 48/80, the effects observed varied according to the nature of the irritant used to induce pleurisy.

Animals↗
PubMed1986

Effect of 8-methoxypsoralen plus long-wave ultraviolet (PUVA) radiation on mast cells. II. In vitro PUVA inhibits degranulation of rat peritoneal mast cells induced by compound 48/80.

Rat peritoneal mast cells incubated with a histamine liberator, compound 48/80, showed a significantly reduced capacity for releasing histamine following in vitro treatment with 0.1 micrograms/ml of 8-methoxypsoralen (8-MOP) plus 1-5 J/cm2 of long-wave ultraviolet (UVA) irradiation (PUVA). No remarkable inhibition in histamine release was observed in the cells treated with 8-MOP only. Irradiation with 5 J/cm2 of UVA alone exerted an inhibitory effect on histamine release, to a lesser extent than PUVA. PUVA irradiation did not bring any decrease in cell viability or any spontaneous release of histamine from irradiated cells as shown by phase-contrast microscopy and by histamine assay, respectively. These results suggest that PUVA treatment may cause a noncytotoxic disturbance at mast cell membranes or on surface receptors, leading to a decreased capacity for secreting chemical mediators.

Animals↗
PubMed1982

[Histamine content of the sputa of patients with chronic obstructive bronchitis].

The sputa of patients with chronic obstructive lung disease show high histamine concentrations with large individual variations. The fluorometric and the biologic method correlate statistically significantly. Histamine concentrations decrease significantly, during 60 min at 37 degrees C, by different amounts in different patients. The measured histamine concentration can cause bronchoconstriction. The histamine and the NaCl control solutions have been found to liberate histamine into the blood, measured as free plasma histamine. There are still many questions open which should be solved because the histamine concentration in the sputum could play an important role in chronic obstructive lung disease.

Adult↗
PubMed1977

Protein concentration in immunological preparations and pyrogenic reaction of rabbits.

The drop of arterial pressure was found to be caused by proteins injected intravenously into test animals. The drop was related to the protein concentration and the volume of the dose. Low pressure was caused neither by the histamine nor by the protein characterized by its property of liberating histamine. Antihistamines had no influence on quantitative or qualitative depressory reaction, caused by the presence of dissolved proteins. Concentrated protein solutions, when applied intravenously, did not contribute to identifying the pyrogenic reaction, but had a damaging effect on the organism and homeostasis of animals used in the experiments.

Animals↗
PubMedDate not supplied

Alcohol-histamine interactions.

Alcohol and histamine metabolic pathways in the body have the common enzymes aldehyde dehydrogenase and aldehyde oxidase. The metabolite of ethanol, acetaldehyde, can effectively compete with the metabolites of histamine, methylimidazole acetaldehyde, and imidazole acetaldehyde. At the periphery, alcohol and acetaldehyde liberate histamine from its store in mast cells and depress histamine elimination by inhibiting diamine oxidase, resulting in elevated histamine levels in tissues. Histamine mediates alcohol-induced gastric and intestinal damage and bronchial asthma as well as flushing in Orientals. On the other hand, alcohol provokes food-induced histaminosis and histamine intolerance, which is an epidemiological problem. There are many controversial reports concerning the effect of H2 receptor antagonists on ethanol metabolism and the activity of alcohol dehydrogenase in the stomach. In addition, alcohol affects histamine levels in the brain by modulating histamine synthesis, release, and turnover. Histamine receptor antagonists can affect ethanol metabolism and change the sensitivity of animals to the hypnotic effects of alcohol. In contrast to other neurotransmitters, the involvement of the brain histamine system in the mechanisms of the central actions of alcohol and in the pathogenesis of alcoholism is poorly studied and understood.

Alcohol Deterrents↗
PubMed1966

Skin histamine in cats: Its depletion and subsequent recovery after injection of compound 48-80.

1. The histamine content of the skin has been determined in untreated cats, in cats injected with the histamine liberator, compound 48/80, and in cats injected subcutaneously with an oily suspension of histamine or histidine after treatment with compound 48/80.2. Skin histamine in cats varied from 2.2 to 37.5 mug/g. Apart from regional variations in the histamine content of the abdominal skin, lower values were obtained from cats kept on a laboratory diet which included aureomycin (mean 8.5 mug/g, range 2.2-13.1) than from cats on a high protein diet without aureomycin (mean 17.5 mug/g, range 5.2-37.5).3. Compound 48/80 caused a depletion of skin histamine which was never complete, and a residue of 3-7% remained; in cats which originally had a low histamine content of skin, depletion was even less and up to 20% of the original histamine remained.4. Recovery of skin histamine in cats after injections of compound 48/80 was slow, at least 110 days being required for full restoration. The rate of recovery was not altered by daily subcutaneous injections of histidine, but an effect was found with daily subcutaneous injections of histamine. Histamine had no effect for the first 33 days, but at 55 days the percentage histamine content of the skin was greater than in the cats treated with histidine or the oily suspending vehicle, and at 110 days the histamine content was not only much greater than the other two groups but was greater than that before injection of compound 48/80.5. No in vitro histamine formation was detected in the skin samples either before compound 48/80 treatment or at any time during the subsequent recovery of the histamine to control levels.6. The results support the theory that the histamine found in skin tissues of the cat is not formed there but is taken up from the blood stream.

Animals↗
PubMed1976

[Skin tests for 48/80 and histamine].

The variability in time of the cutaneous response, resulting from morbid and specially from therapeutic physiological interferences, restrains the credibility of cutaneous allergological investigations. The authors present the first results, established on control population considered as normal, of an approach to cutaneous reactivity by means of a non-specific histamine liberation, induced by a tween: 48/80 coupled with appreciation of the reactivity to histamine injected by the intra-dermal route. The study objectively demonstrates the variability in the response in terms of the doses injected, age, and especially in terms of drug interferences which usually, go in the direction of a hyporeactivity. On the contrary, hyper-reactivity is frequently observed in certain morbid conditions, in particular in spasmophilia. In conclusion, before including the 48/80 and histamine tests in the battery of allergological investigations, it seems indispensable to specify the limits in normal subjects and to better aprehend interferences which modify its expression.

Anaphylaxis↗
PubMed1991

[Role of pain component in the organization of chemosensory taste reaction].

The investigation of algoinductor (histaminergic) and peptidergic relations in peripheral pain reaction of taste was performed by using of different histamine liberators (applied on tongue). By fluorescence-histochemical methods it was shown that histamine in the apical portion of papilla is derived from cells of taste buds and in the basal zone--from connective tissue cells (including mast cells). It was established in behavior trials on peptidergic system that consumption of taste solutions became changed. It was suggested that histaminergic structures together with SP-containing fibers ensure food controlling in oral cavity.

Animals↗