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The effect of clemastine fumarate, a histamine H1-antagonist, on the potentiation of itch by prostaglandin E1 (PGE1) was studied in normal humans. The antihistamine drug did not abolish the potentiation, which suggests that the effect of PGE1 on itch does not depend on the liberation of endogenous histamine.
The mechanisms of histamine release due to d-tubocurarine from rat mast cells have long been known to anesthesiologists, such as degranulatory process, Ca++ dependent process and energy coupled process. However, not much is known about histamine release due to some drugs such as trimethaphan and muscle relaxants other than d-tubocurarine, like alcuronium, pancuronium or succinylcholine, although many clinical reports related to hypersensitivity reactions due to muscle relaxants can be found. In this experiment, the histamine releasing activities of trimethaphan and muscle relaxants were examined using the laboratory model created by Ellis (1970) who reported the selective release of histamine due to d-tubocurarine. Also observed the effects of autonomic neuro-effective drugs such as theophylline, isoproterenol or carbamylcholine on histamine release due to d-tubocurarine. From this experiment, it is suggested that trimethaphan releases histamine through nonselective process but muscle relaxants release histamine selectively. It is also found that pancuronium had little effects on rat mast cells and its histamine releasing activity was selective, if any. Histamine release from rat mast cells due to d-tubocurarine was clearly depressed by pretreatment of theophylline or isoproterenol. In the case of carbamylcholine, low doses inhibited histamine release, but higher doses allowed histamine to be liberated from mast cells. From these findings, it is concluded that some drugs like theophylline or isoproterenol may diminish the side effects of d-tubocurarine and perhaps some other muscle relaxants. Also, as theophylline and isoproterenol are concerned, increase of cyclic AMP may play a role in the inhibition of histamine release. The data using carbamylcholine suggested that the cholinergic receptors on the rat mast cells may be involved through the process of histamine release.
The aim of our study was to determine whether patients suffering from food allergy show any pathologic reactions on the mucosa of the gastrointestinal (GI) tract after allergen contact. For this reason, we included in the study 30 patients whose food-allergic history had been proven through double-blind challenge tests; 20 healthy volunteers also were included as controls. The patients and volunteers underwent standard laboratory investigations and allergy tests with PRICK and RAST. To observe possible mucosal reactions, we applied the proposed allergens via endoscope to the gastric mucosa. Macroscopic reactions were observed blindly by two independent physicians. Biopsies were taken from the challenged areas for histological and histochemical analysis. The examinations included the estimations of tissue histamine concentrations and of mast cell and lymphocyte counts. In all 30 patients, macroscopic reactions (swelling, erosions, bleedings) were observed. Patients with food allergy had, in contrast to healthy volunteers, elevated lymphocyte counts, tissue histamine concentrations, and mast cell counts. After provocation, tissue histamine concentrations and mast cell counts fell significantly. Skin and RAST tests showed positive results in only 46.7% and 50.0%, respectively, of food-allergic patients. We conclude, first, that through intragastric provocation under endoscopic control (IPEC), food-allergic reactions on the mucosa of the GI tract can be verified and, second, that the liberation of tissue histamine seems to play an important role in the establishment of food-allergic reactions on the mucosa.
Urinary excretion of histamine, as well as histaminuria following intravenous L-histidine loading, were studied in patients with so-called vascular headache. It was found that urinary excretion of histamine was increased on one or more occasions in 7 of 22 patients with cluster headache. The excretion was significantly higher on attack days than on attack free days. With migraine, increased excretion was found in 5 of 31 patients on days of an attack, whereas the corresponding figure for headache free days was 7 of 24 patients. Three patients showed increased histamine excretion during, as well as between, attacks. The excretion on attack days was not significantly different from that on attack free days. In cluster headache patients, L-histdine administration on attack days did not indicate that an increased histamine formation took place under such circumstances. The underlying mechanism behind the increased histamine output with cluster headache may be increased formation or liberation or altered catabolism. Histamine is more likely to be a consequence than the cause of an attack of cluster headache.
We investigated whether production of histamine by bacteria isolated from sputum of patients with infective lung diseases could be attributed to the presence of histidine decarboxylase (HD). Twenty gram-positive and 20 gram-negative organisms were studied for their ability to decarboxylate 14C-histidine in vitro over the pH range 4.5-7.5. Of the bacteria investigated, lysates from the gram-negative species Haemophilus influenzae, H. parainfluenzae, Moraxella (Branhamella) catarrhalis and Pseudomonas aeruginosa liberated 14CO2 and histamine from 14C-histidine in the presence of the cofactor pyridoxal phosphate. In contrast, results obtained in the absence of cofactor were similar to those of negative (lysate-free) controls suggesting that the HD enzymes of these species resembled those previously described in other gram-negative bacteria. No HD activity was detected over this pH range in lysates from gram-positive species. This finding correlated with earlier observations that these gram-positive organisms did not produce histamine in vitro.
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From the assumptions governing the behaviour of primitive cells, a set of corollaries is established and the corollaries are used in coming to an understanding of the growth and differentiation of the pancreas. A case is made out to show that there is a constant replacement of old acini by new throughout the life of the pancreas, and that new acini are derived from primitive cells (fixed reticulum cells) present in the stroma which envelopes the fine ducts. The part played by the mast cells in the process is discussed, and view put forward that circulating thymocytes are mast cell precursors, and that the function of the mast cell is to provide the primitive cells of the pancreas (and the primitive cells of certain other tissues) with Zn in an assimilatable form. The hypothesis is made that Zn can only be assimilated by primitive cells, and, that for organs other than the thymus, it is assimilated in the form of the histamine-Zn complex liberated by the mast cells. The fate of the mast cell is analysed, and the suggestion made that, following degranulation, the mast cell nucleus is transformed into a cell of the eosinophil series. The role of the basophil is also analysed, and the conclusion reached that basophils are mast cells whose development has been modified by plasma.
Rat peritoneal mast cells respond to various secretagogues, such as ionophore A23187, concanavalin A (Ig E receptor cross-bridging) and compound 48/80 (membrane perturbing), to secrete histamine and to liberate arachidonic acid. Arachidonic acid release was made identifiable by pretreatment with BW755C, an inhibitor of both lipoxygenase and cyclo-oxygenase. The extent of arachidonic acid release varied among these three secretagogues. A23187 appeared to be most potent, whereas compound 48/80 was weakest. The sources of released arachidonic acids may be different depending on the types of stimulants. The stimulation with A23187 released arachidonic acid mainly from phosphatidylcholine and triacylglycerol. After treatment with concanavalin A and compound 48/80, in addition to phosphatidylcholine, phosphatidylinositol also appeared to serve as a donor of arachidonic acid.
The contractile activity and mobilisation of arachidonic acid metabolites in response to the antigen challenge were studied in isolated lung parenchymal tissue from the actively sensitised guinea pig. The sustained constriction of the lung tissue was evoked by the antigen, associated with significant liberation of TXB2, histamine and p-LTs. Other prostanoids (PGF2 alpha, PGD2, PGE2 and 6-keto-PGF1 alpha) were also released by the antigen challenge. DP-1904, an inhibitor of TX synthetase, significantly suppressed the late phase of the antigen-induced constriction. DP-1904 was potent to inhibit the production of TXB2, while DP-1904 accelerated the formation of PGF2 alpha, PGE2 and 6-keto-PGF1 alpha, presumably indicating the alternative changes of dilatory metabolites to the spasmogenic component. Mepyramine and FPL-77512 augmented the effect of DP-1904. AA-861 inhibited the antigen-induced constriction of the lung parenchymal tissue by inhibiting the release of p-LTs and TXB2. Pretreatment of the lung parenchymes with anti-guinea pig platelet serum, in order to deplete the platelets, did not affect the generation of TXB2 both in resting and also in the antigen-stimulated status, indicating that TXA2 is produced in the topical pulmonary tissue. It is concluded that DP-1904 inhibits the parenchymal contraction through potent inhibition of TXA2 generation, associated with significant elevation in PGE2 and PGI2.
It is more than a century ago that Moraxella catarrhalis was discovered and described in some detail. However, it was not until the last decade that M. catarrhalis was recognized as a facultative pathogen, namely in otitis media (predominantly in children), sinusitis and nosocomial pneumonia in the group of elderly, debilitated patients. Liberation of endotoxin, histamine, and chemotactically active factors can be considered the major pathogenicity factors. The pathogen can protect itself, on the one hand by binding of the Clq subcomponent of the complement system followed by subsequent formation of a functionally inactive complex with Cl, and on the other hand by inactivation of the terminal (lytic) complement complexes by means of a specific protein on the surface of the outer cell wall. Routine diagnostic procedures require, above all, culture of the pathogen: up to now the detection of specific IgA-antibodies has not been routinely available. More than half of the clinical isolates are known to exhibit beta-lactamase production (BRO-enzymes). This is the reason why combinations of a penicillin compound with a beta-lactamase inhibitor, the group of the newer cephalosporins (including the orally active ones), doxycycline and the macrolides are therapeutically effective.
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Hypereosinophilia is often linked to the presence of pluricellular parasites in host tissues. Polynuclear eosinophils are sprung from the bone marrow. After multiplying and maturing, they are thrown into the blood flow and from the blood to the tissues where they are found in immediate contact with the parasite. Eosinophils are major components of the parasitic granuloma. Parasitic diseases are a major cause of hypereosinophilia and eosinophilia is mainly due to helminths. Protozoa do not produce hypereosinophilia, except for toxoplasmosis in which a low and discontinuous eosinophilia may be seen. Subsequently, maggots producing myiasis yield to hypereosinophilia too. In helminthiasis, the action of the eosinophil granulocyte is double. In tissues, it destroys the parasite and plays a regulatory role in mastocytes degranulation. Eosinophils which participate in the inflammatory reaction secrete factors which neutralize mediators liberated by mastocytes, histamine mainly, destroyed by histaminase. In a practical point of view, blood hypereosinophilia is a very useful tool for diagnosis. Eosinophilia reach early a high value, this before the parasitic infection becomes detectable by means of resources other than immunological. The eosinophils rates decreases rapidly as an effect of the anthelmintic drug, this confirming the efficacy and specificity of the prescribed treatment.
The reddening of the ears of guinea pigs following the administration of nicotinic acid and its derivatives is regarded as an animal experiment for the human flush-reaction. In agreement with the observations in humans we found that the reddening effects decreased after repeated administration of xantinol nicotinate (Complamin). The results demonstrate that the reddening of the ears of guinea pigs--and presumably flushing in humans as well--is a complex event. The liberation of prostaglandins, histamine and serotonin, and first of all, cholinergic reactions, seem to be involved.
The maintenance of the circulating fluid within the vascular system is a major role of plasma albumin. Besides its role as a protein reservoir the third function of albumin is its ability to bind and transport metabolic products, regulatory mediators, nutrients and proteins and to bind and neutralize endogenous or exogenous toxins. Bilirubin binding was chosen as a method to describe functional quality of albumin preparations. Binding at the high affinity site is well preserved in all commercial albumin-containing plasma substitutes investigated with KA values in the range of 3.2 to 4.8 . 10(7) 1/mol. Presence of absence of conventional stabilizers does not influence binding characteristics since heating of products according to various pharmacopoeia levels out any difference. The importance of ligand binding properties of a plasma substitute is stressed either in intoxications, e.g. hyperbilirubinemia of neonates or in surgical situations were multiple drug applications might disturb a balanced binding situation. Though relatively mild in nature and less frequently observed in comparison with artificial plasma substitutes incidence of adverse reactions in connection with albumin was used to search for causes. Biochemical parameters like residual proteolytic activity in general or specified (prekallikrein activator), content of aggregates, anti-complementary activity and influence on granulocyte activity did not give any clear answer in this task, neither did pharmacological testing designed to detect factors leading to histamine and kinin liberation or to detect pyrogens.
Functional mast cells have been obtained by peritoneal lavage of the rat and hamster. Both cell types released histamine on stimulation with appropriate dilutions of anti-rat IgE and anti-hamster serum. The maximum response evoked by each reagent was significantly greater for the hamster cells. The release was non-cytotoxic and was in each case blocked by the corresponding soluble antigen. The rat and hamster cells responded to concanavalin A and the lectin from lentil. Phosphatidylserine (PS) potentiated the release only from the rat cells. In the absence of the lipid, the hamster cells were more reactive. The lectin from wheat germ, in the presence of PS, evoked histamine secretion only from the rat cells. Both populations were refractory to the lectin from soybean and to protein A. Rat peritoneal cells were more responsive to the basic secretagogues compound 48/80 and peptide 401 (the MCD-peptide from bee venom). These differences were less marked in the case of polylysine and polyarginine. The two cell populations responded to the calcium ionophores A23187, ionomycin and chlortetracycline. The hamster cells were significantly more sensitive to the former two liberators but markedly less reactive to chlortetracycline. Adenosine 5'-triphosphate (ATP) and dextran were potent histamine liberators from the rat cells but were totally ineffective against the hamster. Acetylcholine and carbamylcholine had no effect on either cell type. These results are discussed in terms of the functional heterogeneity of mast cells from different sources.
1) The influence of acids and bases on the development of the early wound reactions in the intact and the mechanically injured skin of guinea pigs was investigated. The cellular and the enzymohistochemical reactions showed to be different: the tissue leucocytosis after mechanical trauma is less restrained by chemical effects than the reactive increase of enzymic activity in the border of wounds, which proved to be affected by acids more than by bases. Changes in activity of structure bound enzymes could not be demonstrated in the skin after mere action of acids and bases, but only after mechanical trauma. The cellular reaction is in the border of the base necrosis more compact, in case of the acid necrosis broader and more diffuse. Characteristic changes in the nucleus were preferentially found after basic reaction. 2) In the mechanically unhurt skin a significant excess of histamine was found after the action of acids, while the liberation of serotonin was distinctly decreased. After incision and addition of acid the histamine level was decreased and the serotonin concentration significantly increased. After exposition of guinea pig skin to chemicals, the concentrations of the so-called tissue hormones showed a contrary course. 3) After postmortal incision and following cauterization a distinct increase of histamine was found in the wound area. Generally the excess of free histamine in comparison to the unhurt skin is considered to be a vital reaction. But because degranulation of mast cells and liberation of histamine can also be caused by chemical influence in the postmortal period, a critical interpretation in cases of skin exposition to acids or bases is necessary.
OBJECTIVE: To investigate whether generation and liberation of bradykinin and histamine contribute to generalized edema formation in pediatric cardiopulmonary bypass surgery. DESIGN: Prospective observational study. SETTING: Pediatric heart surgery of a university hospital. PATIENTS: Forty-one neonates, infants, and children undergoing cardiopulmonary bypass to correct congenital cardiac anomalies. INTERVENTIONS: Plasma concentrations of bradykinin and histamine were determined before, during, and after cardiopulmonary bypass. Fluid balance was evaluated by control of fluid intake and output. MEASUREMENTS AND MAIN RESULTS: The susceptibility to generalized edema formation increased significantly (r = -.457; p <.005) with decreasing age. Approximately three times higher plasma concentrations of bradykinin (p <.001) were found at the onset of anesthesia and during the total observation period in patients with a fluid retention of >6% of body weight compared with patients with a lower retention rate. Plasma bradykinin reached significantly (p <.01) higher peak concentrations of 237.9 +/- 58.6 fmol/mL during cardiopulmonary bypass and of 227.5 +/- 90.7 fmol/mL during the early postoperative period in patients with severe edema formation in contrast to only 86.6 +/- 10.9 and 65.5 +/- 26.8 fmol/mL in patients with minor fluid retention. A tendency (p =.06) to slightly increasing histamine concentrations from 2.07 +/- 0.13 nmol/L at baseline to 3.32 +/- 1.41 nmol/L during 90 mins of cardiopulmonary bypass was only observed in patients with high fluid retention. CONCLUSIONS: Bradykinin seems to be essentially involved in the enhancement of microvascular permeability in pediatric cardiopulmonary bypass surgery, although a dominant causal role cannot be claimed by this study. Histamine, however, doesn't appear to play a major role and may only contribute as a cofactor. To what extent an increased expression of bradykinin-1 and bradykinin-2 receptors or a reduced potential of bradykinin-degrading enzymes is involved is the object of a further clinical study.
A comparison has been made of the histamine-releasing characteristics of rat mast cells of pleural and peritoneal origin in response to a wide variety of immunological and non-immunological stimuli, namely, IgE antibody-antigen interaction; rabbit anti-rat antibody; concanvalin A (Con A); ACTH (1-24) polypeptide (Synacthen); a decapeptide comprising an amino acid sequence (497-506) within the human gamma-chain (Stanworth, Kings, Roy, Moran & Moran, 1979); adenosine triphosphate (ATP) and the calcium ionophore. This has provided valuable information about the relative responsiveness of target cells from two different sources within the same species. Pertioneal cells proved to be more responsive to basic polypeptide liberators, whereas pleural cells were considerably more responsive to stimuli mediated through IgE antibody, and slightly more responsive to challenge with non-immunological liberators. Interestingly, the histamine-release studies using an antiserum raised against mast cell IgE receptors have indicated that pleural mast cell membranes contain a higher density of IgE receptors than peritoneal mast cell membranes. Moreover, it was established that the amount of histamine release from either peritoneal or pleural mast cells effected by the polypeptide liberators was not influenced by the prior occupancy of the mast cell Fc receptors by rat IgE antibody.