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Biomedical subjects

E Masini

Publications and source records attributed to E Masini.

At least 109 records · Page 6Linked to original sources

Biological markers and therapeutic outcome in alcoholic disease: a twelve-year survey.

The early diagnosis and evaluation of the biological consequences of alcohol abuse are reviewed in a population of 401 chronic alcoholics admitted to our Toxicological Unit from January 1973 to the end of December 1984; selected cases were treated with disulfiram implantation. The results of the study indicate that anemia with increased globular volume of erythrocytes, elevated serum gamma-glutamyl-transferase activity, increased postprandial cholalemia, and increased elimination of pentane in the breath can be considered suitable markers for the early diagnosis of alcohol abuse. Disulfiram implantation significantly prolonged the abstinence duration in the treated patients.

Adult↗

Histamine release from serosal mast cells by intermediate products of arachidonic acid metabolism.

In the present paper we report the results of experiments carried out to measure the release of histamine from isolated rat mast cells during the metabolic activation of arachidonic acid. Arachidonic acid (10(-8)-10(-4) M) and the terminal products (10(-6) M) of the arachidonic acid pathways were devoid of any significant histamine releasing properties. A substantial amount of histamine was released from rat mast cells by low concentrations of arachidonic acid during incubation with prostanoid generating systems, such as guinea-pig lung microsomes, rat serosal macrophages and polymorphonuclear cells and prostaglandin-H-synthase from calf seminal vesicles. The release of histamine was not accompanied by a leakage of lactate dehydrogenase and was blocked by D-mannitol and by lipoxygenase and cyclooxygenase pathway inhibitors. The data are consistent with the hypothesis that free radical derivatives of arachidonic acid, originating from hydroperoxy fatty acids, are generated during catalysis, causing mast cell histamine release.

Animals↗

Histamine and lactate dehydrogenase (LDH) release in ischemic myocardium of the guinea-pig.

Histamine has been proved to be released during myocardial infarction and ischemic arrhythmias in dogs. The aim of the present experiments was to evaluate if ischemia and reperfusion modify histamine and lactate dehydrogenase (LDH) release in isolated guinea-pig heart. The results obtained show a steady increase of LDH release both in the ischemic and reperfusion phases. The release of histamine was reduced during the ischemic phase and increased significantly during reperfusion. A significant diminution of mast cell granule metachromasia was observed in the right auricles at the end of the reperfusion period. D-mannitol and reduced glutathione (GSH) modified the kinetics of histamine and LDH release. Cimetidine was able to decrease significantly the release of histamine during the ischemic and reperfusion phases and also reduced the release of LDH; triprolidine was completely ineffective. The results suggest that oxygen-derived free radicals may be involved in the pathogenesis of myocardial dysfunction after ischemia and reperfusion.

Animals↗

The antianaphylactic action of histamine H2-receptor agonists in the guinea-pig isolated heart.

The effects of histamine and of H1- and H2-receptor agonists on the response to specific antigen were studied in isolated hearts taken from actively sensitized guinea-pigs. Histamine and H2-receptor agonists (dimaprit, impromidine) dose-dependently decrease the positive chronotropic and inotropic effects, and the severity of arrhythmias evoked by the challenge of sensitized hearts with specific antigen. Nordimaprit and the selective H1-receptor agonist 2-pyridyl-ethyl-amine (2-PEA) did not modify the patterns of cardiac anaphylaxis. The positive inotropic and chronotropic responses of the isolated heart to exogenous histamine appear to be partly reduced in the presence of dimaprit. The H2-receptor agonists decrease the amount of histamine released during cardiac anaphylaxis which is increased by cimetidine, while nordimaprit and PEA were ineffective, indicating an inhibitory function afforded by H2-receptors in cardiac anaphylaxis.

Anaphylaxis↗

Mast cell histamine release induced by intermediate products of arachidonic acid metabolism.

This study was performed to evaluate the role of intermediate products of arachidonic acid metabolism on histamine release from rat serosal mast cells. Arachidonic acid in concentrations ranging from 10(-9) to 10(-4) M caused no histamine release from purified rat peritoneal mast cells. High concentrations (10(-6)-10(-6) M) of the terminal products of the arachidonic acid metabolism were also devoid of any significant histamine-releasing properties. The metabolic activation of arachidonic acid with prostaglandin-H-(PGH)-synthase isolated from calf seminal vesicles, evoked a significant release of histamine from rat serosal mast cells. The liberation of histamine was not accompanied by a significant leakage of lactic dehydrogenase (LDH) and the electron microscopical features were consistent with an exocytotic release. The phenomenon was blocked by reduced glutathione (GSSH) and by D-mannitol, a hydroxyl free-radical scavenger. These results suggest that free radical derivatives of arachidonic acid are generated during the catalysis which triggers mast cell histamine release.

Animals↗

Clinical findings and follow-up evaluation of an outbreak of mushroom poisoning--survey of Amanita phalloides poisoning.

One hundred and sixty cases of mushroom poisoning during the period July-November 1981 are reported. The survey details 116 observations of short incubation syndromes and 44 cases of delayed syndrome, identified as Amanita Phalloides poisoning. Of the latter, 40 patients were adult (mean age 46 years, range 20-77; 18 females and 22 males) and 4 were children (less than or equal to 12 years old; 3 females and 1 male). All the patients with Amanita Phalloides poisoning were treated according to a therapeutic protocol, based on the infusion of high doses of penicillin G, administration of dexamethasone and thioctic acid, careful correction of water and electrolyte unbalance. The severity of the disease varied in the population of 44 patients: 4 patients died (2 females, 10 and 77 years old; 2 males, 56 and 64 years old); 26 patients were discharged from the hospital as clinically cured; 14 were discharged with persistently abnormal levels of transaminases and they were advised of a follow-up evaluation. The average length of stay in hospital was 2 weeks. Of the patients followed-up, 6 were symptom-free after 6 months, with normal transaminase values and a normal histopathological picture of liver biopsy specimens. In the remaining patients, there was no normalization of transaminase values and liver biopsy specimens showed a picture of chronic active hepatitis. These patients displayed abnormal immunological tests, with presence of immune complexes and of anti-smooth muscle autoantibodies. The results indicate that Amanita Phalloides poisoning represents a threat not only in the high mortality acute phase, but also in the development of chronic active hepatitis in some survivors.

Adolescent↗

Histamine release by free radicals: paracetamol-induced histamine release from rat peritoneal mast cells after in vitro activation by monooxygenase.

The incubation of paracetamol with isolated rat serosal mast cells evokes the release of histamine only in the presence of (S10) liver microsomes obtained from PCB or phenobarbital treated rats. The release of histamine was not accompanied by a leakage of lactate dehydrogenase and was blocked by the antioxidant alpha-tocopherol and by D-mannitol, an hydroxyl free radicals scavenger. The data are consistent with the metabolic oxidation of paracetamol in the generation of reactive intermediates capable of activating the sequential exocytosis.

Acetaminophen↗

FMLP-activated neutrophils evoke histamine release from mast cells.

Human neutrophils, having been activated by the chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (FMLP), evoke histamine release from rat serosal mast cells. The release is dependent on FMLP concentration and it can be inhibited by disodium cromoglycate and by a flavonoid, silymarin, which displays free radical scavenging properties. Silymarin inhibition of neutrophil-mediated histamine release is dose-dependent. These results further stress the concept of a neutrophil-mast cell interaction, which may be involved in inflammatory processes.

Adult↗

Stimulation and resection of Vidian nerve in patients with chronic hypertrophic non-allergic rhinitis: effect on histamine content in nasal mucosa.

Parasympathetic innervation of nasal mucosa plays an important role in the pathogenesis of chronic hypertrophic non-allergic rhinitis (C.H.N.A.R.). The present study investigated the effect of Vidian nerve stimulation and resection on the histamine contents and on the morphological pattern in mucosal samples of patients with C.H.N.A.R. Vidian nerve stimulation determines a significant decrease in histamine content in the samples examined; microscopical observations showed significant variations in the glandular, stromal and vascular components. The changes indicate an enhanced secretory activity, intensive vasodilatation and active degranulation of mast cells, which were significantly decreased in number in the samples obtained after 90 sec of stimulation. The neurectomy of the Vidian nerve resolves quite completely the clinical symptomatology and in parallel decreases the mucosal histamine contents, which are increased in patients with C.H.N.A.R. before the operation in comparison with the normal controls.

Chronic Disease↗

Liver function following hypovolemic hypotension in rats anaesthetized with halothane or enflurane.

Rats which had approximately 25-30% of their calculated blood volume removed were exposed to halothane (1%) or enflurane (2%) in 33% oxygen for 30 min. Hepatic function was evaluated by determining, at various time intervals, serum activities of glutamic-oxalacetic and glutamic-pyruvic transaminase, acid phosphatase and gamma-glutamyl-transpeptidase. In this model serum enzyme activities and animal mortality were significantly increased when hypovolemic hypotension was induced during halothane anaesthesia. The same events did not occur in bleeding animals anaesthetized with enflurane. The marked disparity in hepatic dysfunction and mortality between halothane and enflurane-anaesthetized rats during hypovolemic hypotension may be explained by the more pronounced decrease of oxygen available for the liver and production of reductive toxic intermediates in animals exposed to halothane.

Anesthesia↗

The release of histamine by parasympathetic stimulation in guinea-pig auricle and rat ileum.

Two preparations, a segment of rat ileum and the vagally innerved guinea-pig auricles, have been used in an analysis of the responses to vagal or to electrical field stimulation. The responses to parasympathetic stimulation were depressed by atropine and by tetrodotoxin, and potentiated by eserine. Supramaximal stimulation (10-20 Hz) resulted in increased release of acetylcholine and histamine, both in rat ileum and guinea-pig auricles. The release of histamine after parasympathetic stimulation did not exhibit tachyphylaxis, and it was not reproduced by non-parasympathetic stimuli. In both preparations, atropine produced a significant, dose-related reduction of histamine measured in the bath fluid after stimulation, while eserine increased histamine output. A significant diminution of mast cell granules metachromasia was observed in guinea-pig auricles and in rat intestine after parasympathetic stimulation. The possibility is discussed that acetylcholine released by parasympathetic stimulation would in turn evoke the secretion of histamine from tissue mast cells.

Acetylcholine↗

Immunological modulation of cholinergic histamine release in isolated rat mast cells.

Isolated purified rat mast cells release histamine when exposed to acetylcholine according to different patterns of sensitivity. The degree of histamine release is correlated with the levels of reaginic antibodies presumably bound to the mast cell membrane. In fact, mast cells passively sensitized with mouse myeloma IgE against egg albumin or DNP2-lysine, react to acetylcholine with a release of histamine, which is proportional to the IgE concentration in the incubation medium. The histamine release induced by acetylcholine is due to the stimulation of a muscarinic receptor. Accordingly, acetylthiocholine is unable to evoke histamine release and preincubation of sensitized cells with atropine fully inhibits the cholinergic histamine release. The histamine release evoked by acetylcholine is potentiated by the exposure of sensitized cells to the specific antigen. The present results suggest that sensitization of mast cells is a crucial factor in modulating their sensitivity to acetylcholine.

Acetylcholine↗

Histamine release during an experimental coronary thrombosis in awake dog.

Histamine is released into the systemic circulation during anaphylaxis, by drugs and surgical procedures. Studies in animal models have shown that released histamine is one of the major mediators of arrhythmia occurring during anaphylaxis or the administration of histamine-releasing drugs. The variations in plasma histamine levels in dogs with a subacute coronary thrombosis were investigated and the effects of dimaprit and cimetidine on the electrocardiographic consequence of this thrombosis and on histamine release were assessed. During the first day after the myocardial infarction a ventricular arrhythmia developed and plasma histamine levels were found significantly increased, returning to the basal values when the sinusal rhythm was restored. Dimaprit was able to decrease the number of ventricular extrasystoles and to modulate plasma histamine levels. The action of dimaprit on ECG was not reversed by pretreatment with cimetidine, which on the contrary was able to antagonize the decrease in plasma histamine concentrations induced by dimaprit perfusion.

Animals↗

Mast cell and neutrophil interactions: a role for superoxide anion and histamine.

Histamine inhibits superoxide anion (O-2) production from human neutrophils stimulated by N-formylmethionyl-leucyl-phenylalanine (FMLP). The effects of histamine are dose-dependent and competitively antagonized by cimetidine. When passively sensitized rat serosal mast cells and human neutrophils are mixed together, O-2 production from FMLP-activated granulocytes is significantly reduced, following mast cell degranulation by acetylcholine. These inhibitory effects can be counteracted by cimetidine. Exposure of non-sensitized rat mast cells to FMLP-stimulated human neutrophils causes histamine release. These results suggest bidirectional control mechanisms between mast cells and neutrophils, that further stress the role of histamine in regulating inflammatory processes.

Animals↗

Histamine-releasing properties of Polysorbate 80 in vitro and in vivo: correlation with its hypotensive action in the dog.

The solvent of commercial amiodarone (Polysorbate 80) has been reported to produce haemodynamic responses in humans and in dogs similar to those produced by histamine infusion. We therefore evaluated the correlation between hypotension induced by the solvent of amiodarone and its histamine-releasing properties in the awake dog. The solvent of amiodarone administered to a dog, over 5 min in a dose of 10 mg/kg of Polysorbate 80, produced severe hypotension after the first administration; the second injection (24 h later) caused fewer hypotensive effects. Histamine release in the peripheral tissues was demonstrated by a marked increase in plasma histamine concentrations, with the maximum value 10 min after the solvent administration. H1- and H2-receptor blockade with mepyramine (5 mg/kg) and cimetidine (10 mg/kg) significantly reduced the cardiovascular effects of the solvent. Isolated peritoneal mast cells from rats also released histamine in response to Polysorbate 80. These studies show that Polysorbate 80 releases histamine both in vitro and in isolated mast cells from rats and in vivo in the dog, and that the plasma concentrations are correlated with the haemodynamic responses.

Amiodarone↗

Mast cell heterogeneity in response to cholinergic stimulation.

Mast cell heterogeneity in response to acetylcholine has been evidentiated by the virtual lack of sensitivity or by the full reaction to nanomolar concentrations of acetylcholine, observed in samples of serosal mast cells isolated from the same animal species. The incubation with IgE of isolated rat mast cells renders the originally heterogeneous response homogeneous, the release of histamine evoked by acetylcholine being proportional to the IgE concentration. The histamine release induced by acetylcholine is due to the activation of muscarinic receptors, since it is blocked by atropine, not reproduced by acetylthiocholine and potentiated by exposure of the cells to the specific antigen.

Acetylcholine↗

Vidian nerve resection in chronic hypertrophic non allergic rhinitis: effects on histamine content, number and rate of degranulation processes of mast cells in nasal mucosa.

The effects of Vidian nerve resection on the histamine content, number and rate of degranulation processes of mast cells in the respiratory tract of the nasal mucosa in patients with intractable chronic hypertrophic non-allergic rhinitis (CHNAR) have been investigated at various times after surgery. Preliminary data are also presented on the effects of Vidian nerve stimulation on the same parameters. The Vidian nerve was stimulated during surgery before resection. After neurotomy the histamine content was significantly lower than before but the values became less low with the passing of time. The number of mast cells per microscopic field and their degranulation index were significantly lower after surgery than before it. Stimulation determines a significant reduction in the number of mast cells per microscopic field and a parallel reduction in histamine content. These data establish a relationship between cholinergic activity and secretory response of mast cells and demonstrate a role of the parasympathetic nerve supply in the pathogenesis of CHNAR. The great reduction in the number of mast cells and histamine content also suggests that the parasympathetic nerve supply could play a role in the regulation of histamine synthesis and uptake.

Adolescent↗