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Extracellular histamine stimulates accumulation of adenosine 3',5'-monophosphate in human leukocytes and prevents antigenic release of histamine from cells of allergic donors. Both effects occur at histamine concentrations that can be achieved by antigenic release of the amine in vitro.
Cell populations obtained by bronchial lavage from human subjects were examined for the presence of cells related to the mast cell-basophil series. Such bronchial lumen histamine-containing cells (BLHCC) were identified. The BLHCC stained with toluidine blue may be identified by bright field or dark field microscopy. The BLHCC are alive as evidenced by ability to release histamine (H) after exposure to anti-IgE or calcium ionophore. Although H release from peripheral blood leukocytes by these two agents is potentiated by the presence of D2O, H release from BLHCC of the same subjects by anti-IgE or calcium ionophore was not potentiated by D2O. In studies comparing bronchial cell populations of humans and rhesus monkeys with peripheral blood leukocyte populations of the same subjects, the histamine content of the bronchial cell population was much higher in rhesus monkeys. IgE/Alb ratios of respiratory secretions and serum of the same human subjects were of the same order of magnitude in contrast to previous comparisons done on these fluids in rhesus monkeys.
A controlled, randomized, double-blind, cross-over study was performed in 10 healthy volunteers in order to compare changes of cutaneous blood flow values (CBFV, laser Doppler flowmetry, Periflux, Perimed, S) in histamine-challenged skin before and after administration of a capsule containing either 10 mg cetirizine or 60 mg terfenadine. The overall pattern of the basal cutaneous wheal and flare response to the agonists (histamine: aqueous solution: Hsol, or Phazet: Hprick) and control saline solution, showed the expected range of clinical effects, i.e. Hsol greater than Hprick greater than saline. Similarly, the increase of CBFV on the flare area was higher around the histamine injections as compared with saline. Surprisingly, CBFV was decreased at the site of Hsol and Hprick injections as compared with the levels recorded at the control injections. The following changes were noted after intake of H1-blocking agents. (1) There was a reduction of the areas of wheal and flare at all injection sites after administration of the H1 blockers, this reduction being consistently greater under cetirizine than terfenadine. (2) CBFV, measured 1 cm from the site of Hsol injection (i.e., within the area of normal flare response), was decreased only with cetirizine. In the smaller flare area induced by Hprick, CBFV was equally suppressed by both drugs. (3) At the site of agonist injection, along with a reduction of the size of the wheal, we observed significant increases in CBFV after drug intake. Under these experimental conditions, this quantitative pharmacologic in vivo assay of agonist-antagonist interactions suggests that after initial administration of normally prescribed doses, cetirizine may possess more anti-H1 activity than terfenadine.
Immature human T-lymphocytes form rosettes with autologous erythrocytes (A-RFC). Con A induced suppressor cells in fractions of A-RFC. Mature, immunocompetent T-lymphocytes are non-A-RFC. They bear histamine receptors, and in such fractions histamine induced suppressor cells. After activation, both suppressor cells seem to be identical. They bear histamine receptors, Fe-receptors for IgG and the T8-antigen. For the expression of their suppressive effect the presence of monocytes is required.
The authors made a study of the antihistaminic properties of Pipoxizine in 20 subjects with proven histaminic hyperreactivity. The design of the trial consisted in comparing the changes of VC, FEC1, expiratory airway resistance and V50 produced by a histamine aerosol given before and after administration of Pipoxizine. Pipoxizine was given by mouth to 10 patients and intravenously to the other 10 of the group. The statistical analysis of the results demonstrated an antagonist effect of Pipoxizine on the histamine induced bronchoconstriction. The data of this trial are confirmative of the results of other experimenters. It seems therefore reasonable to take into consideration the use of Pipoxizine in the preventive treatment of the paroxystic attacks of the asthmatic disease.
In a control group (n = 12) the histamine content of the liver was 1.42 microgram/g tissue and the activity of the histamine-degradating enzyme, HMT, 421.5 pmol/(min . mg protein). In patients with affections of the biliary tract (n = 12) the histamine content was significantly raised to 3.09 microgram/g tissue and the HMT activity slightly diminished [349 pmol/(min . mg protein)]. The lowest values of HMT activity were found in the livers of those patients with histologically proven damage of liver cells.
Histamine can be presented as neurotransmitter and immunomodulator beside its direct action as mediator of allergic and pseudoallergic responses. Histamine is involved in inhibition or stimulation of metabolic processes which have important in immunological as well in neural processes. The differentiation between H1- und H2-receptors of histamine extends the therapeutical use of antihistaminics in dependence of their pharmacological affinity.
Platinum and palladium salts were shown to possess either histamine releasing or histamine binding properties. Both these effects were dependent on chemical structures of the tested compounds and might be drawn up in the following sequences; Pd greater than Pt, PtIV greater than PtII, NO2 greater than F greater than Cl greater than SCN greater than J, trans greater than cis. One of the possible mechanisms of anti-tumoral effect of platinum and palladium salts might be their marked histamine binding activity.
The effects of histamine-forming capacity (HFC) stimulation by 48/80 as well as of histamine catabolism inhibition by aminoguanidine on the tensile strength and collagen production were studied in wounds of rats. 48/80 raised the level of collagen in wounds and increased their tensile strength. Aminoguanidine increased the histamine content of the wounds but markedly lowered the tensile strength and collagen content.
OBJECTIVE: To test the hypothesis that an early increase in vascular permeability is correlated with later gastric mucosal protection in the rat. METHODS: Histamine, its agonists (H1, H2, H3) and bradykinin, were either given subcutaneously or intragastrically before the intragastric administration of ethanol. The extravasation of intravenously injected 99mTc-glucoheptonate into the gastric wall and into the gastric contents was used as an indicator of increased permeability. Gastric haemorrhagic lesions where measured by computerized planimetry and ethanol absorption was determined by an ACA Clinical Analyzer. RESULTS: Histamine and bradykinin increased vascular permeability in the glandular stomach and provided significant gastroprotection, similar to H1-, H2- and H3-agonists, against ethanol-induced gastric haemorrhagic lesions. This gastroprotection was accompanied by low blood levels of ethanol, probably indicating decreased ethanol absorption and the creation of a histodilutional barrier in the stomach by histamine. CONCLUSIONS: These data indicate that an increase in vascular permeability dissipates the concentration, and may delay the absorption, of ethanol in gastric mucosa by creating a perivascular histodilutional barrier. Vascular injury, which is an early pathogenetic factor in the development of ethanol-induced gastric haemorrhagic erosions, may thus be prevented.
Cattle with different degrees of resistance to Boophilus microplus have responses to tick allergen which correlate with their resistance level. The total amount of histamine in the skin also correlates with both resistance and the immediate hypersensitivity reactions, but the sensitivity to injected histamine does not. Treatment with the antihistamine drug mepyramine maleate suppresses the cutaneous hypersensitivity reactions. The results suggest that the main pharmacologically active agent in these reactions is histamine, and that the total amount of it available locally in the skin may have a role in the resistance to this parasite.
Histamine methyltransferase (HMT) activity was determined by a modified isotope assay in biopsy specimens from gastric mucosa of control subjects, duodenal ulcer patients and after various gastric operations. Enzymic activity of male control subjects who were 'healthy' with respect to their upper gastrointestinal tract was 70.4 +/- 12.8 pmol/(min x mg protein). In male duodenal ulcer patients HMT-activity was significantly lowered by 15%; following selective vagotomy with pyloroplasty a significant increase of 14% was observed as compared to controls. The difference between values before (59.9 +/- 13.3) and after (80.4 +/- 11.7) this operation was highly significant (p less than 0.001). Experiments in a small number of patients showed that after other modifications of vagotomy elevated HMT-activities were also found, whereas after resection procedures such changes of enzymic activity did not occur. According to these results the low gastric HMT-activity of duodenal ulcer patients could play a role in the pathogenesis of a chronic peptic ulcer by being responsible for reduced histamine inactivation and - as a consequence - enhanced acid secretion. Furthermore, vagotomy seemed to influence acid secretion in human subjects not only by direct effects on the parietal cells, but also by an activation of histamine catabolism. One patient, who despite complete vagotomy showed both no reduction in acid secretion and a low gastric HMT-activity, may be the representative of a new population of peptic ulcer patients.
Histamine inhibits the chemiluminescence response of human lymphocytes to Concanavalin A by interfering with early triggering events. The inhibition seems to be mediated via H2 receptors, acts immediately, and is reversible by washing. A longer incubation in a histamine-containing medium induces a refractory state of the cells. The inhibitory effect described here is compared with the inhibitory action of histamine in the lymphocyte transformation test.
In concentrations above 0.1 mM Ketotifen (KT) induced secretion of histamine from rat and mouse mast cells, but not from human basophils. In the same concentrations KT inhibited histamine release from rat mast cells, induced by compound 48/80 and histamine release from basophils, induced by anti-IgE-antibodies and concanavalin A. At low concentration (0.05-0.005 mM) KT enhanced in vitro phytohemagglutinin-induced proliferative response of human lymphocytes. The immunostimulating effect of KT was confirmed in vivo. In doses 0.18-1.4 micrograms/mouse KT significantly increased the number of antibody-producing cells (APC) in spleens of mice immunized by sheep red blood cells (SRBC). KT stimulated both IgM- and IgG-immune response to SRBC.
From a methodological point of view the relevance of clinical-biochemical trials depends on the answers to mainly four complexes of questions: (1) the reliability of the assays in the clinical situation to be tested, (2) the precision and accuracy of sample-taking, (3) the qualification of the design and the protocols in the clinical part of the trial and (4) the usefulness of the time concepts in the trial concerning biorhythms, seasonal influences, psychological trauma of diagnostic procedures and treatment. In this study mainly the second complex of questions was studied intensely. The precision of the fluorometric histamine assay in biopsy specimens from human gastric mucosa depended on several conditions: Biochemical technique, sample preparation and removal of biopsies from gastric mucosa via endoscopy. The CV% of the whole procedure was about 8-times higher than that of the biochemical technique. In clinical-biochemical studies on the significance of histamine or any other hormone (such as gastrin) in any disease (uch as duodenal ulcer) it seems therefore useless to describe the precision of an assay only by the variance of the biochemical technique. Calculation of the histamine content as mean of 3 samples reduced the CV% from 27.2 to 14.9% and should therefore be recommended.
The mechanism of the histamine-liberating action of the synthetic polypeptide C 44 680-Ba, an alkyl-prolyl derivative of beta 1-19 corticotrophin, was investigated and compared with those of Compound 48/80, dextran, Melittin and Triton X-100. It was found that the release of histamine from rat peritoneal cells induced by the polypeptide is dependent on temperature, pH, calcium ions and energy-providing processes. In regard to these criteria, the mode of action of this histamine liberator resembles that of Compound 48/80 but is quite distinct from that of the unspecific substance Triton X-100.
Amines and amino acids are able to form cyclic compounds with pyridoxal 5'-phosphate (PLP). The quantitative relationship between histamine and PLP in the cyclization reaction were examined. It was found that one mole of amine reacts with one mole of coenzyme. The velocity of complex formation increased with an excess of either histamine or PLP, without any change in molar ratios. The formation of cyclic compound was confirmed by the use of isotopic method. The separation of cyclic compound from histamine, but not from PLP, was achieved by paper chromatography.
When the tridecamer component of compound 48/80 (Fraction D, Fr.D), a Ca2+-dependent histamine releaser, was incubated with rat mast cells that had been prelabeled with [32P]phosphate, [3H]inositol or [3H]glycerol, it induced a rapid decrease in [32P]phosphatidylinositol-4,5-bisphosphate (PIP2) followed by increases of [3H]inositol-1,4,5-trisphosphate (Ins P3) and [3H]diacylglycerol during the 10 sec prior to detectable histamine release. Fr.D-induced changes of the metabolism of these compounds occurred even in the absence of Ca2+, but to a lesser extent than in the presence of Ca2+. In contrast, the accumulation of [3H]arachidonic acid into phosphatidylcholine (PC), phosphatidylinositol (PI) and phosphatidic acid (PA) in [3H]arachidonic acid-prelabeled mast cells was Ca2+-dependently stimulated by Fr.D with a concomitant decrease in [3H]phosphatidylethanolamine (PE). These Ca2+-dependent changes in PC and PE were not observed in mast cells preloaded with [32P]phosphate, while [32P]PI and [32P]PA increased Ca2+ independently. Fr.D also increased 45Ca2+ uptake by mast cells within 5 sec after the stimulation. These results indicate that Fr.D binding to mast cell Ca2+ independently induces rapid changes of PI cycle-related metabolism of plasma membrane components, while it also induces Ca2+-dependent accumulation of arachidonic acid into PC, PI and PA in association with the decrease of PE, which may be important during the latent period prior to the Ca2+-dependent release of histamine from Fr.D-stimulated mast cells.