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At least 685 records · Page 38Linked to original sources
PubMed1975

Effects of intensive application of retinoic acid on human skin.

The daily application of 0-3% retinoic acid to the back produced an acute irritant dermatitis which resolved to a near-normal clinical appearance within 40 days despite continued daily exposure. Hardened skin was markedly altered physiologically. The responses to DMSO, histamine and the histamine liberator, compound 48/80, were sharply enhanced. This reflected enhanced permeability resulting from reduction of the horny layer to less than one-half its normal thickness. Phototoxic and irritant substances produced exaggerated reactions owing to greater penetration. A paradoxical decrease in delayed sinsitivity to streptodornase-streptokinase was attributed to enhanced clearance of the antigen.

Adult↗
PubMed2000

Compound 48/80, a histamine-depleting agent, blocks the protective effect of morphine against electroconvulsive shock in mice.

We have shown that morphine has an anticonvulsive effect against maximal electroconvulsive shock (MES) in mice, and this effect is antagonized by histamine H1-receptor antagonists. Brain histamine is localized both in neurons and in mast cells, and morphine is known to enhance the turnover of neuronal histamine and to release histamine from mast cells. In the present experiments, compound 48/80 was injected chronically (0.5 mg/kg on day 1, 1 mg/kg on day 2, 2 mg/kg on day 3, 3 mg/kg on day 4, and 4 mg/kg on day 5, twice daily, ip) to deplete mast cell contents. Morphine (0.001-10 mg/kg, ip; N = 20) produced a dose-dependent anticonvulsive effect against MES seizure in mice with non-depleted mast cells, whereas it did not exert any anticonvulsive effect in mice with depleted mast cells. These results indicate that morphine produces its anticonvulsive effect against maximal electroconvulsive shock in mice by liberating histamine from mast cells.

Animals↗
PubMed1989

Total and specific IgE in sera from patients with invasive amoebiasis.

Total and specific IgE antibodies were determined in 20 patients with invasive amoebiasis. Using a histamine release assay by passive sensitized human leukocytes, a significant increase of Entamoeba histolytica induced IgE-mediated histamine liberation was found in basophils sensitized with sera from patients with amoebiasis as compared to those of control groups. Concerning the total serum IgE, no statistically significant changes were found in different serum groups. Our results suggest that E. histolytica can induce a detectable level of circulating specific IgE without change in total serum IgE.

Amebiasis↗
PubMed1976

Cryptogenic pulmonary eosinophilia.

The clinical and immunological features of fifteen cases of cryptogenic pulmonary eosinophilia are reported. There were ten women (mean age 35.4 years) and five men (mean age 42 years). Eight gave a previous history of asthma and seven had none. Thirteen of the fifteen patients had negative skin test to common allergens. Many features of a systemic illness were present in the asthmatic and non-asthmatic groups including anaemia, weight loss, fever and a grossly raised ESR. An absolute polymorphonuclear leucocytosis was frequent as well as the obligatory increase in blood eosinophils used as one of our criteria for inclusion. Hepatomegaly (three cases), splenomegaly (four cases) and hilar node enlargement (one case) were seen in the group without asthma. Evidence of renal involvement or necrotizing vasculitis was notably absent and the response to small doses of corticosteroids was dramatic. Immunologically the striking feature was a disproportionate increase in blood eosinophils compared with only minor elevations in the total serum IgE levels. This stands in contrast to patients with bronchopulmonary aspergillosis and helminth infestation. Studies of cytophilic antibodies using histamine liberation after challenge with antibodies to immunoglobulin sub-classes in six patients showed a marked increase in IgG2 and lesser increases of IgE and IgG3. No evidence of antibodies specific to A. fumigatus was found. The amount of cytophilic antibody was also in contrast to that found in bronchopulmonary aspergillosis.

Adolescent↗
PubMed1961

Some effects of corticosteroids on the metabolism of histamine and 5-hydroxytryptamine in the rat.

Daily intramuscular injections of cortisone, prednisolone, triamcinolone, fludrocortisone and 2-methylfludrocortisone reduced the histidine decarboxylase activity of the rat liver, but increased the enzyme activity of the pyloric stomach. Injections of histamine liberators or exposure to cold produced similar changes. After adrenalectomy, the histidine decarboxylase activities of the liver and pyloric stomach were unaltered, but the histaminase activity of the ileum was reduced. The 5-hydroxytryptophan decarboxylase activities of rat liver and kidney were not altered by treatment with corticosteroids.

Adrenal Cortex Hormones↗
PubMed1975

[Allergic reactions following dextrane infusions (author's transl)].

14 allergic reactions to dextran 60 and dextran 75 are reported. In 8 patients the peripheral pulse became impalpable; Medical history and clinical examination did not reveal any predisposition. Histamine liberation is to be discussed. Antihistamines did not protect against allergic reactions of colloid plasma expanders. All the patients were treated with prednisolone and fluids. After rapid infusion of Ringer-lactate and plasma protein solution to an amount of 2000-2775 ml adequate circulation was restored.

Adult↗
PubMed1982

Studies on the inhibition of rapid expulsion of Trichinella spiralis in rats.

A variety of inhibitors was examined for their ability to interfere with the expression of rapid expulsion (RE) of challenge Trichinella spiralis infections in rats. Inhibitors of immediate hypersensitivity, prostaglandin release, peristalsis, or complement function, did not impair RE when administered to immune rats. Induction of intestinal anaphylaxis against T. spiralis or ovalbumin by passive serum transfer to intestinally primed rats (prior infection with Heligmosomoides polygyrus) or administration of the histamine liberator 48/80 also failed to stimulate RE. In contrast, irradiation or cortisone treatment 1, 3 or 5 days before challenge inhibited RE. We conclude that immediate hypersensitivity is not the terminal mediator of RE and plays a minor role or none at all. The effects of cortisone and irradiation suggest a major involvement by lymphoid cells in the RE reaction.

Anaphylaxis↗
PubMed1979

The effects of compound 48/80 on the fibrinolytic activity of dogs.

It has been demonstrated that histamine by itself, did play some role in the activation mechanism of fibrinolysis. In this particular work, it was demonstrated that histamine at doses not affecting blood pressure levels, did not exert any direct immediate effect on fibrinolytic activity. Compount 48/80, a powerful mast cell depleter and histamine liberator, by itself, has no direct molecular effect on fibrinolytic activity, but rather, through the release of activators and/or inhibitors form mast cells, will exert either an activating or inhibiting action, according to the dose used. Low doses, such as 0.2 mg/kg i.v. will achieve a higher degree of activator release, while doses of 1.0 mg/kg will result in higher inhibitors release from mast cells.

Animals↗
PubMed1976

Stimulation and suppression of rat mast cell functions by alloantibodies.

The stimulatory as well as the inhibitory capacity of alloantisera has been investigated with respect to rat mast cell functions. Alloantibody against alloantigens coded for by the major histocompatibility (H-1) gene region promoted histamine release from purified LEW mast cells. This process was found to be complement-independent but demonstrated an absolute requirement for calcium. Pretreatment of mast cells with anti-H-1 antisera in the absence of calcium markedly suppressed the IgE-dependent histamine release challenged either by antigen or by anti-IgE antibody. The alloantisera, however, did not interfere with the ability of compound 48/80-associated histamine liberation. Additionally, antibodies specific for H-1 antigens were highly effective in inhibiting the binding of IgE to the mast cell surface. Alloantisera absorbed with erythrocytes lost their capacity to block mast cell functions. Based on these data the possible ralationship between H-1 alloantigens and the IgE receptor on the mast cell surface is discussed.

Animals↗
PubMed1979

Effects of 16, 16-dimethyl prostaglandin E2 on bile-induced histamine release and permeability alterations in canine oxyntic mucosa.

Damage to the stomach results in excessive movement of hydrogen ion (H+) out of the lumen, and increased movement of sodium (Na+) and potassium (K+) into the lumen. Histamine liberation during damage probably adds to the destruction by increased capillary permeability and formation of edema. Previous reports have shown that the synthetic prostaglandin analogue 16,16-dimethyl prostaglandin E2 (Dm PGE2) protects dog gastric mucosa from aspirin- and ethanol-induced gastric mucosa damage. The effects of dm PGE2 on bile salt (sodium taurocholate) induced injury has not been investigated. Using the canine Heidenhain pouch, the present study examined the action of dm PGE2 on gastric mucosal damage induced by 5 mM sodium taurocholate in 100 mM HCl. Bile salt damaged the pouch mucosa as evidenced by an increased loss of H+, and increased net fluxes of both Na+ and K+. There was also an increase in the histamine content of the fluid irrigating the Heidenhain pouch. Intravenous injection of dm PGE2 in the doses 0.1 and 1.0 microgram/kg 1/2 h before administration of the sodium taurocholate in HCl significantly reduced the net loss of H+ and the gain of Na+, K+, and histamine. It is concluded the dm PGE2 effectively protects the canine gastric mucosa from the damaging effects of bile salt and that the mechanism of dm PGE2 protection of canine oxyntic mucosa may be mediated in part via inhibition of the gastric mucosal release of histamine.

Animals↗
PubMed1988

[Acute use of adrenergic drugs in asthma and anaphylactic shock in clinical practice].

There are two situations where these products may be used and their justifications are quite different. For anaphylactic shock, the treatment should be aimed at limiting the effects of the acute reduction of volume due to vasoplegia and peripheral diapesis provoked by the liberated histamine. The medullary-suprarenal hormones are the first recourse, efficacious on the alpha and beta receptors. The alpha action is of the excitative type and provokes peripheral vasoconstriction. The beta-action suppresses the contraction of the smooth muscle, but in isolation can facilitate vasodilation. This is why adrenalin is suitable for strict control of arterial pressure: Immediate administration in IM (0.25 to 1 mg), by slow I.V. (dilution 1/10) It is appropriate, where possible to restore the blood volume with a volume expander. Cortico-therapy, both general and by aerosol is used in relays. For asthma: The question is, whether to use beta-2-agonists that have an action on muscle relaxation, on mucosal oedema, also on the secretion of mucus and indirectly on liberation of intermediate substances. Acute use of beta-2-agonists is: Perhaps for a specific purpose, for example to prevent effort-induced asthma: use of a spray is simple and efficacious. Perhaps for a greater and more prolonged use to treat an attack of asthma or a bad state of asthma before hospitalisation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗
PubMed1998

In vitro effects of the pyrethroid S-bioallethrin on lymphocytes and basophils from atopic and nonatopic subjects.

Synthetic pyrethroids are increasingly used as insecticides and marketed as having relatively low human toxicity. The aim of this study was to examine the in vitro effects of the synthetic pyrethroid S-bioallethrin on human blood lymphocytes and basophils in atopic individuals and nonatopic control subjects. S-bioallethrin caused inhibition of lymphocyte proliferation after a 72-h culture period in a concentration-dependent manner. The inhibition of the lymphocyte proliferation by S-bioallethrin at the concentration 6.5 microM correlated well with the total serum IgE values (r = -0.89, P < 0.001). Samples from atopic subjects were more sensitive to this inhibition than those from nonatopic volunteers. The regulatory interleukin-4/interferon-gamma (JL-4/IFN-gamma) balance showed a significant difference between atopic and nonatopic subjects after a short-term culture period (24 h) in the presence of the same concentration range of S-bioallethrin (P < 0.001). Additionally, IFN-gamma secretion was consistently lower in cells from the atopic donors. Furthermore, S-bioallethrin induced histamine release from human basophils in a concentration-dependent manner. Although the effect was small compared to histamine liberators such as N-formyl-Met-Leu-Phe and anti-IgE, the response to S-bioallethrin was significantly different in atopic donors from nonatopic (P = 0.0431). These findings are the first demonstration of the immunotoxicologic properties of the synthetic pyrethroid S-bioallethrin by this combined in vitro approach with human lymphocytes and basophils. Further studies will investigate the responses of lymphocytes from patients who are sensitive to these agents.

Adolescent↗
PubMed1993

[Anaphylactic shock during the use of high doses of aprotinin in cardiac surgery].

A 77-year-old man was admitted for mitral valve replacement, 46 days after a failed conservative mitral surgery where he received high-dose aprotinin. Twenty minutes after induction of anaesthesia, 250 UPh E of aprotinin were infused intravenously; before the end of this infusion, bronchospasm, systemic hypotension and generalized rash were noted. Immediate treatment included intravenous adrenaline and methylprednisolone; cardiovascular stability was restored after 10 minutes. Immediate histamine liberation was confirmed by the analysis of the time course of the clinical events, a previous contact and positive skin tests. Aprotinin has the antigenic molecular structure of natural proteins. Since 1987, it is used in cardiac surgery to reduce postoperative blood loss: to prevent serious allergic reactions to aprotinin, it is necessary, in patients known to have had previous aprotinin therapy, to perform skin testing with diluted aprotinin before infusion.

Aged↗
PubMedDate not supplied

Reliability of the prick-test in comparison to other techniques.

This paper aims to establish the diagnostic reliability of the Prick test and its correlation to other techniques used in allergologic diagnosis: intracutaneous testing, RAST, hemagglutination, histamine liberation test. All of these tests were realized in 55 patients with bronchial asthma and with marked sensitization to diverse inhaled allergens and in a control group of 20 healthy subjects. A low correlation is observed between the Prick test and a positive intracutaneous test for house dust, somewhat higher correlation is seen for dermatophagoides and even higher for pollen. Greater reliability is demonstrated for the intracutaneous test as compared to the other in vitro techniques.

Adolescent↗
PubMed1985

Peptides and histamine release from rat peritoneal mast cells.

Various vasoactive peptides were compared for their histamine releasing effects on rat mast cells. Neurotensin, substance P (SP), and kallidin were the most active natural peptides, followed by bradykinin; neurokinin A and B, bombesin, angiotensin and tuftsin were practically inactive. Several kinins and tachykinin-related peptides were tested in an attempt to characterize the receptors mediating histamine liberation. The order of potency of the kinins was the following: kallidin greater than [Tyr(Me)8]bradykinin = bradykinin greater than [desArg10]kallidin greater than desArg9-bradykinin, the same as that found in smooth muscle possessing receptors of the B2 type. Tachykinin-related peptides were potent stimulants and followed the order: [D-Tryp7,9,10]SP-(1-11) greater than [D-Pro2,D-Tryp7,9,10]SP-(1-11) greater than SP-(1-11) greater than SP-(1-9) greater than [D-Pro4,D-Tryp7,9,Leu11]SP-(4-11) greater than SP-(1-7) greater than SP-(4-11) greater than neurokinin A = neurokinin B, indicating that: (a) undecapeptide antagonists of SP behave as superagonists; (b) both N- and C-terminal portions of SP-(1-11) are essential for activity; and (c) receptors for the tachykinins mediating histamine release appear to be of the SP-P type.

Animals↗
PubMed2002

Effects of beta-endorphin on nasal allergic inflammation.

BACKGROUND: Beta-endorphin is a derivative of pro-opiomelanocortin. Cells of the immune system can also synthesize and secrete beta-endorphin. Its concentration is increased during the allergic reaction and during stress. Increased reactivity during psychological stress of allergic subjects is also well known. OBJECTIVE: Is beta-endorphin one physiological link between stress and an exacerbation of the allergic reaction? METHODS: First, intranasal beta-endorphin challenges with subsequent lavages to determine histamine and albumin levels and measurements of nasal flow and resistance in dose-response and time course experiments were performed. Secondly, we examined whether beta-endorphin pre-treatment increased the antigen-induced release of histamine and albumin in nasal lavages and the clinical symptoms. RESULTS: Exogenous beta-endorphin (100 pM-10 microM/mL) induced a dose-dependent increase in nasal symptoms in asymptomatic allergic subjects with rhinitis (n = 14) as well as in non-allergic controls (n = 10), but did not release any mediators into nasal secretion. However, comparing the antigen-evoked release of mediators into nasal secretions with that of a beta-endorphin pre-treated antigen challenge we could note a significant enhancement of human serum albumin influx (P < 0.05) and histamine liberation (P < 0.05) 10 min after antigen challenge compared with the allergen challenge alone, with also a correlation with the more pronounced decrease in nasal flow (P < 0.05). CONCLUSION: These results suggest that beta-endorphin-induced increase in nasal congestion is mediated through direct neuroendocrine receptor activation independent of mast cell activation and that during the allergic reaction there is a beta-endorphin/mast cell interaction that enhances the mediator response to nasal allergen challenge.

Administration, Inhalation↗
PubMed1979

[The antiexudative and anti-edematous action of sympathomimetics].

The anti-exudative and anti-edematous effects and the dose-effect relationship of a-sympathomimetics, especially of l-phenylephrine-HCl (PE), have been demonstrated using as model the rat pad-carrageenan edema and the histamine liberator test, the dosage being administered cutaneously, orally, and intraperitoneally. The beta-receptor activating compound bamethane sulfate was not effective when used on the same models. Evidence of percutaneous penetration of PE was provided both on isolated skin and in viro. PE, when injected intravenously or subcutaneously, produced a rise of blood pressure in experimental animals. When PE was administered orally and cutaneously, it did not, however, alter the blood pressure. The anti-inflammatory and anti-exudative effects remianed unchanged.

Animals↗
PubMed1977

[Diagnostic, etiologic and therapeutic problems confronting the anesthesiologist in cases of bronchial spasm. Apropos of 4 cases].

The authors recall the symptoms of peroperative and early postoperative bronchospasm. They emphasise the etiology and the treatment. In fact, bronchospasm may be induced by several causes:--mechanical or chemical vagal stimulation;--direct or allergic-induced histamine liberation, induced by certain drugs (mainly curare);--taking beta-blockaders before operation, favoured by the use of morphine during operation;--finally, any irritation of the bronchi (inhalation of gastric juice, pulmonary embolism, pulmonary oedemal). The treatment is etiological but also symptomatic:--enrich the inspired air with oxygen;--inject I.V. 1/2 to 1mg of atropine;--in case of failure, one should use Salbutamol I.V. which is very effective during contraction of the bronchial muscles;--massive corticosteroid therapy will be effective in mucosal oedema.

Adrenal Cortex Hormones↗