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A patient suffering from an eczema of the right hand showed after routine patch testing an immediate urticarial reaction to cinnamaldehyde. The same reaction could be noted in three out of eight control persons. Laboratory investigations revealed cinnamaldehyde to have a histamine liberating effect, a fact not previously mentioned in reports on untoward reactions to this compound.
The effect of platelet-activating factor (PAF) on histamine release from peritoneal mast cells of adult and young male rats was investigated. PAF alone tended to release histamine from the mast cells of adult and young rats, although very slightly. On the other hand, PAF significantly inhibited the histamine release induced by the Ca2+ ionophore A23187 in mast cells obtained from rats of either age group, but not that by compound 48/80. Such inhibition was not seen with lyso-PAF. CV-3988, a PAF antagonist, antagonized the inhibitory effect of PAF on the A23187-induced histamine release in mast cells from adult and young rats. These results suggest that PAF does not have a strong histamine-liberating action on mast cells, and that PAF inhibits the calcium influx into mast cells through the activation of PAF receptors.
1 A newly synthesized substance P (SP) analogue, (D-Pro2, D-Trp7,9)-SP, specifically antagonizes the contractile effects of SP on the guinea-pig isolated taenia coli. In addition, previous studies had indicated that the SP analogue per se is capable of contracting this preparation. The results of the present study on the guinea-pig taenia suggest that the smooth muscle contractions produced by the SP analogue are due to histamine release. No contractions were observed following blockade of histamine H1-receptors by mepyramine or following pretreatment with the histamine liberating agent, compound 48/80. 2 Analysis of the inhibition of SP-induced contraction by the analogue suggests that the inhibition is of the competitive type; pA2 was calculated to be 6.1. 3 We conclude that (D-Pro2, D-Trp7,9)-SP is a competitive SP antagonist with histamine-releasing properties.
In addition to the classical microtubule inhibitors (antimitotic agents), transganglionic degenerative atrophy of central terminals of primary sensory neurons can be induced also by means of applying to a peripheral nerve basic polypeptides (Polymyxin B and Colimycin) and two basic derivatives of glutamic acid that do not exert any microtubule inhibition. This effect is independent of other pharmacological effects (histamine liberation, Ca2+ -binding, etc.) of the applied compounds, and probably it is based on a competitive reaction with nerve growth factor.
The recent discovery of the protective action of xanthic bases towards histamine-release consecutive to the antigen-antibody reaction led the authors to study the importance of this protection induced by various theophylline derivatives. The technique used was that described by LICHTENSTEIN and OSLER: isolation of leucocytes, measurement of histamine liberated in the presence of antigen, same measurement done in the presence of antigen and theophylline. The antigens used were: house dust, Dermatophagoides pteronyssimus (DP), graminaceae pollens. The tested theophyllines were: the theophylline base, aminophylline, bamiphylline, diprophylline, thio theo, piperazine acefilinate. All these substances studied brought a reduction of the histamine-release but according to a variable frequency and intensity: the thio theo, the diprophylline and the piperazine acefilinate gave the best results. Besides the latters are clearer when the antigen was dust or DP. This study enables the confirmation of the inhibiting action of theophyllines on histamine-release induced by antigen, but complementary studies on a larger number of cases seem necessary in order to determine precisely the most efficient derivatives.
The histamine release from basophils induced by hypo-osmolarity was investigated in 75 healthy persons and in 43 patients with chronic obstructive airway disease. Leukocyte suspensions were diluted with destilled water in cell/water ratio volumen of 1:1, 1:3, and 1:7. Basophils, sequentially treated with increasing amounts of water, show an activation of the release process. A statistically significant age-dependent hypo-osmolar histamine liberation could be demonstrated. Furthermore, a significant higher cell stability was found for the group of patients.
The histamine concentration was determined by enzymatic isotopic method in biopsy specimens of oxyntic mucosa from 37 children. Nineteen of the 37 had Helicobacter pylori associated gastritis (9 with duodenal ulcer). The histamine concentration in the H pylori negative group was mean (SD) 54.1 (23.1) micrograms/g fresh weight, and that in the H pylori positive group was 26.3 (14.2) micrograms/g (p less than 0.01). There was also a significant difference between H pylori positive patients with duodenal ulcer (19.8 (6.3) micrograms/g) and those without ulcer (31.4 (17.9) micrograms/g) (p less than 0.05). These results suggest that H pylori positive patients, especially those with duodenal ulcer, have reduced 'stored' histamine, perhaps because of increased histamine liberation.
1. The predominant effect of morphine, diamorphine, pethidine or nalorphine on the blood pressure of the anaesthetized cat or rabbit is hypotension although, occasionally, a pressor action may predominate or intervene.2. Possible mechanisms of the depressor phases of action have been studied on cardiac and vascular preparations both in situ and in vitro.3. While in the whole animal, catecholamine release from the adrenal medulla and histamine liberation may be implicated in the responses, the vasodilator and vascular relaxant actions of morphine and, probably, pethidine, nalorphine and diamorphine on the isolated preparations are not mediated by the liberation of known peripheral transmitters or autacoids or by interaction with their specific receptors.
Compound 48/80 inhibited the growth of protozoa, bacteria, and fungi but had no effect on the multiplication of viruses. All susceptible organisms were inhibited by 10 microgram/ml of crude compound 48/80, and some were inhibited by as little as 0.1 microgram/ml. Against Tetrahymena pyriformis, this drug was seven times more potent than quinine. Separation of compound 48/80 into different fractions indicated that some antimicrobial activity could be separated from the histamine-liberating activity. It was found that compound 48/80 is not surface active at 500 microgram/ml.
Upon incubation of hamster serum with bacterial endotoxin, a factor is produced which releases histamine and heparin from hamster mast cells and increases capillary permeability in guinea pig skin. The major histamine-releasing activity derived from hamster serum was characterized by gel filtration, found to have a molecular weight of approximately 60,000, and shown by electrophoresis to migrate with alpha-2- or beta-1-globulins. The ability to increase vascular permeability was not reversed by antihistamine. On the basis of these properties, the histamine-liberating factor generated by endotoxin in hamster serum differed significantly from known anaphylatoxins.
The effect of morphine on gastric mucus synthesis was studied in conscious rats, using the method of staining mucus with alcian blue then destaining it with magnesium chloride. It was found that morphine significantly enhanced gastric mucus synthesis, as did fentanyl, a non-histamine-liberating opioid. The effects of the opioids on mucus synthesis were significantly attenuated by pretreatment with naloxone 8 mg/kg or cimetidine 100 mg/kg. Cimetidine itself significantly suppressed gastric mucus production in saline-treated rats. These findings suggest that the increased gastric mucus synthesis caused by morphine is due to activation of opiate receptors and not to histamine release. It appears that cimetidine may counteract rather than block the receptor effects of the opioids by a direct action on the mucus-secreting glands.
The antagonism of histamine secretion from rat peritoneal mast cells by a range of drugs (e.g., antihistamines, local anesthetics, tranquilizers, antidepressants, adrenergics and antiadrenergics) and arylalkylamines was studied. Simple arylalkylamines, those without quaternary ammonium, phenolic or anionic groups, uniformly inhibited histamine secretion induced via three major secretory pathways of mast cells (compound 48/80, A23187 and concanavalin A). That is, each simple arylalkylamine nonselectively inhibited all three secretagogues at about the same concentration (avg. range = 2.2). This nonselective inhibition was rapid in onset (seconds), readily reversible by washing and not related to a decrease in ATP. It is likely that these agents act nonspecifically at a step in the final common pathway in the cell membrane, possibly to inhibit fusion of the secretory granules with the plasma membrane. Other, more complex arylalkylamines were selective in their antagonism of histamine secretion. Quaternary arylalkylammonium compounds selectively antagonized polyamine secretagogues (48/80 and polymyxin B), whereas arylalkylamines, with other hydrophilic groups, selectively inhibited one or another of the secretory pathways. These complex arylalkylamines must act before the final common pathway because of their selective inhibition. At higher concentrations most of the arylalkylamines caused disruption of the mast cells and liberated histamine.
The mercurial compounds are known to be a common cause of allergic contact dermatitis. Immediate hypersensitivity is rarely induced by mercurial organic derivatives. However, none of the published cases showed both immediate and delayed hypersensitivity as was the case of one of our two patients. A boy and a woman experienced urticaria and anaphylaxis, respectively after topical application of Merchromine (Merbromine). We were able to demonstrate immediate hypersensitivity in both patients to mercuric fluorescein compounds by skin test and histamine liberation. In addition, the child but not the woman, showed delayed hypersensitivity to mercurial compounds.
The influence of three compounds of the essential oil of Chamomilla recutita (L.) Rauschert on the protamine sulphate-provoked degranulation of mast cells from Lewis-1a rats was investigated. The effect was determined by measuring histamine liberation fluorometrically. Chamazulene and (-)-alpha-bisabolol had no distinct effects. The en-yne dicycloether partly inhibited the degranulation in concentrations above 10(-4) M.
Eosinophilic colitis is a rare entity of unknown etiology characterized by diarrhea, abdominal pain, and gastrointestinal bleeding. Diagnosis includes histopathological infiltration of more than 20 eosinophils in colon. It is frequently associated with milk hypersensitivity and, less usual, with other foods and increased IgE. Histopthological appearance of eosinophil mediators has been observed in the gut. It is sometimes related to the degree of infiltration of eosinophils in the gut as well as to the disease severity. There is not an established treatment for this entity, although systemic steroids have been used with certain efficacy. However, there is a recurrence of the symptoms when the therapy stops, besides the well known side effects of the long-term use of steroids. Cromolyn inhibits mast cell degranulation and prevents liberation of mediators. It is successful in certain cases, specially the severe ones. However, it is not available for its use in our country. Ketotifen, as last resource in our patients with bad response to habitual treatment and restriction diet, was used. Although its use is controversial, we consider that stabilizing mast cell membrane with subsequent inhibition of degranulation and recruitment of eosinophils to sites of inflammation, would also restrain histamine liberation and blockage of H1 receptors, which would diminish local damage induced by eosinophils. Nonetheless ketotifen mechanism of action is unknown, our patients improved after treatment with this drug.
The incubation of zymosan, endotoxin, or immune aggregates with normal human serum activates a factor which induces release of histamine from autologous basophils. The reaction can be divided into two steps: in the first, complement must be activated and in the second, the histamine-releasing factor interacts with basophils. The generation of histamine-releasing activity in serum occurs at 17 to 37 degrees C but not at 0 degrees C, is inhibited by heating the serum at 56 degrees C for 30 min, or by the addition of EDTA to the serum. Once generated, the histamine-liberating activity is stable to heating at 56 degrees C for 30 min. Gel filtration of the activated serum demonstrated that this factor eluted in the same region as a factor with chemotactic activity. Both factors have a molecular weight of about 16,000 daltons and their activities were inhibited by antibody to human C5. This is therefore a pathway for histamine release by C5a where the activation of the basophil is unrelated to the membrane bound IgE.
Skin tests with histamine, the histamine-liberator, codeine, and various allergens as well as blood basophil degranulation by anti-IgE or anti-IgG4 and total serum IgE levels have been studied in two female populations of different ages (average 23.1 and 73.9 years). All thirty-one patients selected for this study were clinically non-allergic. We observed a trend towards reduced skin reactions to histamine and codeine in the higher age-group; on the other hand, we could not find any decrease of basophil degranulation as a sign of basophil impairment with age. Likewise no difference in total serum IgE levels have been noticed. No correlation between skin tests and basophil degranulation was observed; yet patients with isolated, positive skin tests to house dust and/or Candida albicans showed a statistically significant reduced blood basophil degranulation by anti-IgE or anti-IgG4.
The effect of mepyramine, ketotifen and picumast (3,4-dimethyl-7-[4-(4-chlorobenzyl)piperazine-1-yl]propoxycoumarin dihydrochloride) on anaphylactic histamine release from lungs, heart, stomach, and intestine of guinea pigs in response to antigen was examined in vivo. When sensitized animals were pretreated intraperitoneally with a single dose of these compounds 60 min before i.v. antigen challenge (native ovalbumin 20 mg/kg), a dose related inhibition of immunological histamine release from the lung was established. After pretreatment of the animals with 3 mg/kg of mepyramine, 10 mg/kg of ketotifen, and 6 mg/kg of picumast dihydrochloride, the inhibitory effect on histamine release from the lung was so marked that both the acute and the protracted anaphylactic shock were completely suppressed. The corresponding histamine levels in blood plasma, regularly measured 1.5 min after antigen stimulation, had dropped to about 40%, 50%, and 35%, respectively (p less than 0.05), whereas lung histamine content increased by about 60%, 150%, and 90% compared with unpretreated, shocked controls. According to these findings the number of lung mast cells in protected animals was significantly increased. In addition, ketotifen significantly reduced histamine release from heart and intestine. In contrast the compound injected intravenously 1 min before antigen challenge had no effect on mast cell degranulation and on histamine liberation, thus only decreasing the acute anaphylactic bronchospasm. These data suggest that all three drugs were acting as H1-antagonists when administered immediately prior to the antigen-provoked anaphylactic reaction. The property of these drugs to inhibit mast cell degranulation and the reduction of mediator release, however, appears to depend on their prolonged action on these cells. Together with their histamine antagonism anaphylactic death is thus prevented.