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[Standardization of the histamine liberation test].

The application of the histamine liberation test to the diagnosis and follow-up of allergic processes has been pursued by many authors. Since Shore first described a manual fluorimetric technique, efforts have been directed at automating the system and reducing the sample volume. According to the latest contributions by Moneo et al., from 300 to 400 determinations can be carried out in a single work day, and from 40 to 50 determinations with 10 ml of blood. In the present work we present our experienced in updating the technique and the system of preparation of a histamine standard, which we consider of great practical use in the application of this technique routine. Using the standard solution as reference, we calculated total and basal histamine levels in 342 presumed healthy individuals; the mean values were 69.5 ng/ml for total histamine and 8% for basal histamine in males, and 71 ng/ml for total histamine and 6% for basal histamine in females. Age range was from 17 to 57 years, and there were no differences between sexes. The maximum value was 176 ng/ml and the minimum 32 ng/ml. The reaction of O-phthaldialdehyde with histamine is not chemically specific. In the presence of light, aldehydes self-polymerize; moreover, O-phthaldialdehyde can react with other products in addition to histamine. The first problem is avoided by protecting the reagents from light, and the second by using specific absorption and emission filters which do not pick up signals from reaction side products. Nevertheless, at the quantitative level these effects are negligible when compared to other causes which, although not part of the chemical reaction, are also involved in the process (antigen standardization, etc). By means of this technique, from 300 to 400 determinations can be carried out in a single work day, making it possible to use this technique in the daily work routine.

Adolescent↗
PubMed1977

[Prevention of complications of histamine liberation occurring after administration of anesthetic agents and adjuvants].

To protect the organism against histamine liberated during anesthesia specific premedication is used including:--hydroxyzine (Atarax) which blocks the H1 histamine receptors, and is an anxiolytic,--tritoqualine (Hypostamine) which inhibits histamine synthesis,--epsilon aminocaproic acid (Hemocaprol) which prevents the antigen-antibody reaction and blocks the alternate route of complement. Twenty five patients were thus premedicated, 25 others received no premedication. All were put to sleep with Alfatesine. The results were judged on the clinical symptoms and the variations of histamine in whole blood. This premedication seems very efficacious, in particular in subjects with a high risk of histamine liberation.

Adjuvants, Anesthesia↗
PubMed1985

Potency of various peptides as histamine liberators in the rat hind limb.

The potency of several peptides and drugs as histamine liberators was assessed using the rat isolated hind limb preparation. Neurotensin (NT) and compound 48/80 (C48/80) were effective in concentrations as low as 10(-9) M and 10(-8) M, respectively. Threshold concentrations of vasoactive intestinal peptide (VIP) and substance P (SP) varied between 5 X 10(-7) to 5 X 10(-6) M while somatostatin (SS) was barely active at 6 X 10(-6) M. No histamine release could be detected following the use of high concentrations of thyrotropin releasing hormone (TRH) (6 X 10(-6) M), dynorphin (DYN) (6 X 10(-6) M) bradykinin (BK), des-Arg9-BK or bombesin (BB) (at 10(-5) M). Poly-L-Lysine and the calcium ionophore A23187 were about 100 times less active than NT. Concanavalin A (Con A) was inactive at 10(-6) M. These results indicate that NT is more potent (on a molar basis) as histamine liberator in the rat hind limb preparation (which contains a large population of cutaneous and subcutaneous mast cells) than any of the other compounds tested. Histamine release by NT was inhibited by preexposure of the rat hind limb mast cells to a high concentration of SP (1.5 X 10(-6) M). This result adds further support to the hypothesis suggesting that NT and SP might share a common mechanism of action and/or act through common receptors at least in rat mast cells.

Animals↗
PubMed1996

Histamine liberation related to cardiopulmonary bypass in children: possible relation to transient postoperative arrhythmias.

Tumor necrosis factor-alpha production and products of mast cell, basophil, and eosinophil degranulation (prostaglandin D2, histamine, and eosinophil cationic protein) were prospectively studied in 26 children undergoing cardiac operations. The relationship between inflammatory response to cardiopulmonary bypass and transient postoperative arrhythmias was analyzed. Cardiopulmonary bypass was conducted with circulatory arrest and deep hypothermia in 10 patients and with continuous low-flow and moderate hypothermia in 16 patients. Transient postoperative arrhythmias diagnosed on standard or atrial electrocardiograms (or both) were seen in eight of the 26 examined children: accelerated junctional rhythm (n = 3), junctional ectopic tachycardia (n = 3), second-degree atrioventricular block (n = 1), and third-degree atrioventricular block (n = 1). Children with transient postoperative arrhythmias were younger than those without (p < 0.05). Compared with baseline values, there was in all patients a significant release of histamine and eosinophil cationic protein (p < 0.05) related to cardiopulmonary bypass, reaching peak values 4 hours after the operation. In contrast, tumor necrosis factor-alpha production and prostaglandin D2 release were not significant. This suggests that activated basophils but not mast cells are the major sources of histamine liberated during and after cardiopulmonary bypass. Histamine release but not eosinophil cationic protein release correlated with circulatory arrest and deep hypothermia (p < 0.05), suggesting the participation of physicochemical alterations of circulating basophils leading to histamine liberation. Four hours after the operation, patients with transient postoperative arrhythmias had significantly higher blood concentrations of histamine (p < 0.02) and eosinophil cationic protein (p < 0.05) than did those without transient postoperative arrhythmias. On the first postoperative day, four of the eight patients with transient postoperative arrhythmias had persisting elevated histamine levels, whereas in patients without transient postoperative arrhythmias histamine reached baseline values. The multivariate analysis retained histamine release and eosinophil cationic protein variations related to cardiopulmonary bypass for the emerging model to predict transient postoperative arrhythmias. The results of this study show significant histamine release related to cardiopulmonary bypass. Furthermore, they document a possible relationship between circulating histamine and transient postoperative arrhythmias. The latter may therefore be suspected among the consequences of the inflammatory response to cardiopulmonary bypass.

Adolescent↗
PubMed1980

Relationship of hydrogen ion back-diffusion to histamine liberation from canine oxyntic mucosa.

Pharmacological damage to gastric mucosa results in excessive movement of hydrogen out of the lumen and increased movement of sodium and potassium into the lumen. It has been previously reported that one consequence of H+ back-diffusion is the release of intramucosal histamine which probably adds to the damage by increasing capillary permeability and edema formation. In the present study histamine concentration in the solution irrigating an isolated pouch of the gastric fundus was measured following 15% (w/v) ethanol (EtOH) in either 100 mM HCl, 10 mM HCl, or 0.03 M phosphate buffer. All three solutions effectively broke the mucosal barrier as evidenced by increased net fluxes of sodium and potassium. Significant (P less than 0.05) increases in the histamine content of the fluid irrigating the pouch were observed after all treatments. The histamine output in response to EtOH in acidic solution was significantly greater than the response to EtOH at neutral pH. Instillation of 150, 200, 225, or 250 mM HCl alone into the pouch resulted in progressive increases in H+ back-diffusion. Application of 250 mM HCl alone resulted in a proportionally greater back-diffusion of H+, increases in Na+ and K+ fluxes indicating barrier damage, and the appearance of histamine. These results indicate that the damaging agent ethanol probably acts at two points: (1) it breaks the mucosal barrier, and (2) it liberates histamine. These results suggest that an increase in H+ back-diffusion per se is not solely responsible for gastric mucosal histamine liberation but that histamine is released as a general consequence of breaking the gastric mucosal barrier.

Animals↗
PubMed1989

[Experimental study of histamine-liberating properties of eremomycin].

Eremomycin, a new glycopeptide antibiotic showed the same as ristomycin, polymyxins B and M and kanamycin histamine liberating properties. Liberation of endogenic histamine induced destructive lesions on the mucosa of the gastrointestinal tract. The most pronounced lesions were observed after intraperitoneal administration of the antibiotic. When eremomycin was administered intravenously or subcutaneously the affection of the gastrointestinal tract epithelium was less pronounced. After subplantar administration of the antibiotics pad edema in albino rats was observed. The most pronounced edema was after the use of ristomycin and the polymyxins. After the use of eremomycin and kanamycin it was at the average 2 times less pronounced. Preliminary administration of dimedrol decreased intensity of the pad edema induced by the antibiotics.

Animals↗
PubMed1975

[Disodiumcromoglycate and histamine liberation by cotton dust extract in the rat (author's transl)].

1. Disodiumcromoglycate (DSCG) had no influence on the microscopical appearance of rat peritoneal mast cells either by i.p. injection (2 times 10(-5) g/ml) or by i.v. infection (10 mg/kg) nor by local application (2 times 10(-5)/1 times 10(-4) g/ml). 2. A particular effect of DSCG (2 times 10(-6)/2 times 10(-5) on the tonus of guinea pig ileum or an interaction with contractor activity due to histamine (3 times 10(-8)/1 times 10(-7) g/ml) has not been established. 3. Histamine liberation from rat peritoneal mast cells by i.p. injection of aqueous cotton dust extract was not inhibited by DSCG (2 times 10(-8)/2 times 10(-7) g/ml), histamine liberation was rather increased.

Administration, Topical↗
PubMed1982

Influence of ultraviolet light on itch and flare reactions in human skin induced by histamine and the histamine liberator compound 48/80.

The itch and flare responses induced by intradermal injection of histamine and the histamine liberator compound 48/80 were studied in healthy volunteers before and after exposure to UVB, UVA or PUVA administered 2-3 times weekly for 4 weeks. All three modalities were found to inhibit the responses induced by compound 48/80. The degree of tanning was most pronounced after PUVA and weakest after UVB, without any correlation between tanning and inhibition of itch. In contrast, when induced by histamine, the responses were not inhibited to the same extent, pronounced and significant inhibition being observed only for itching in subjects exposed to UVB. It is concluded that UVB, UVA and PUVA all might be of benefit in treating pruritic states if histamine release is involved and that UVB might have an additional effect by inducing hyposensitivity to itching stimuli.

Adult↗
PubMed1985

[Evolution of plasma histamine after midazolam in patients at risk of histamine liberation].

Changes in plasma histamine levels 2 min (t1) and 10 min (t2) after the intravenous injection of 0.2 mg X kg-1 midazolam were measured in 10 subjects at risk of releasing histamine (group I) and compared with those of 15 other subjects free from any risk of releasing histamine (group II). There was mean increases in plasma histamine levels of 0.78 ng X ml-1 between t0 and t1 (p less than 0.01), and of 0.41 ng X ml-1 between t0 and t2 (p less than 0.01) in group I; they only rose by 0.18 ng X ml-1 between t0 and t2 (p less than 0.01) in group II. The only statistically significant variation between the two groups was that at t1 (p less than 0.03): plasma histamine levels rose higher at the second minute in those cases at risk. This was a rather small increase, within physiological limits, and without any clinical or haemodynamic manifestation.

Adult↗
PubMed1976

[Histamine liberation in extracorporeal circulation].

Extra-corporeal circulation (E.C.C.) has been held responsible for histamine liberation incidents, essentially by a mechanical cause. In order to prove this, the authors assayed the overall histaminaemia at different times during E.C.C. in 11 patients. The results are discussed in terms of the patients' backgrounds, temperature, hematocrit, blood gases and the acid-base balance, and electrolyte balance. Histaminaemia, corrected depending on the dilution, did not show any significant variation, even in two patients who clinically had anaphylactic manifestations.

Acid-Base Equilibrium↗
PubMed1989

[Plasma histamine liberation after the application of nonionic contrast media].

In 94 patients the levels of plasma histamine have been measured after application of three nonionic contrast media (iopromide, iopamidol, iohexol) and after application of blood-isotonic saline solution. A significant liberation of histamine could be observed after administration of contrast media and also after administration of saline solution. Neither between the three nonionic contrast media nor between the contrast media and the saline solution significant differences could be measured. Administering contrast media after subsequently saline solution the levels of histamine were lower than in case of pure contrast media application. Psychogenically induced histamine liberation is discussed.

Contrast Media↗
PubMed1976

[Histamine liberation and its mechanism].

The author, on the basis of his personal work, proposes a classification of the mechanisms of histamine liberation: a metabolic mechanism (acting like anaphylaxis) and a mechanism by amine displacement. Subsequently, the action on histamine of two hydrosoluble vitamins: ascorbic acid and nicotinamide is considered, in the animal as a whole and on the mastocytes of rat peritoneum.

Anaphylaxis↗
PubMed1990

The effect of beta-adrenoceptor blocking drugs on histamine liberation, prostaglandin synthesis and phospholipid turnover in isolated mast cells stimulated with concanavalin A.

Exaprolol, metipranolol and propranolol decreased significantly histamine liberation, degranulation, 45Ca uptake and thromboxane B2 formation in isolated rat mast cells stimulated with concanavalin A and phosphatidylserine. Moreover, exaprolol and metipranolol decreased 32P incorporation into membrane phospholipids and metipranolol and propranolol reduced the liberation of arachidonic acid from membrane phospholipids of stimulated mast cells. Exaprolol significantly increased the arachidonic acid liberation from these cells. Possible mechanisms of interaction of beta-adrenoceptor blocking drugs with isolated mast cells are discussed.

Adrenergic beta-Antagonists↗
PubMed1983

[Effect of ketotifen and oxatomide on histamine liberation due to exposure in cold urticaria].

Four patients suffering from cold urticaria were treated with ketotifen and oxatomide for one week each. Histamine liberation was measured after the exposure to cold before and after the treatment. A significant inhibition was demonstrated for either product, much more so, however, for oxatomide. This inhibition was associated with a pronounced improvement of complaints.

Adult↗
PubMed1976

In vitro effects of histamine liberator compound 48/80 on rat superior cervical ganglia with special regard to the small granule-containing cells.

The effect of the histamine liberator compound 48/80 on the rat superior cervical ganglia in vitro has been investigated. After incubation of the ganglia with compound 48/80: (1) ganglionic mast cells degranulate in the same manner as in other tissues; (2) cell bodies of the postganglionic neurons are not affected by compound 48/80; (3) there is evidence that ganglionic interneurons, the monoamine-containing cells are activated. The ultrastructural aspects of this process are characterized by degranulation of perikarya and accumulation of dense core vesicles in cell processes and in terminals adjacent to presynaptic membranes. These vesicles vary in size between 200-800 A in diameter. They may represent storage sites of the neuro-transmitter complexes that have undergone exocytosis. The results are discussed with special reference to models of exocytotic processes involving the adrenergic transmitter. It is concluded that monoamine-containing cells represent interneurons in sympathetic ganglia which inhibit ganglionic transmission and which are stimulated by low concentrations of compound 48/80 in vitro.

Animals↗