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Biomedical subjects

E Masini

Publications and source records attributed to E Masini.

At least 127 records · Page 7Linked to original sources
PubMed1984

Mediator release from isolated rat ileum in response to field stimulation.

The effect of electrical field stimulation on mediator release from the isolated rat ileum was evaluated by recording the muscle responses and by measuring acetylcholine and histamine appearing in the perfusion fluid. In the presence of cholinesterase inhibitors, supramaximal field stimulation (10 Hz) resulted in twitch responses accompanied by an increased release of acetylcholine. The resting output of histamine was measurable also in the absence of inhibition of cholinesterases, and neatly increased during electrical stimulation. Atropine produced a dose-related decrease in the release of histamine from electrically stimulated muscle, while eserine extends the time-course of the contractile response and of the histamine release as well. The results are discussed in the context of the role ascribed to acetylcholine as a physiological modulator of histamine release.

Acetylcholine↗
PubMed1984

Autacoid and beta-adrenergic agonist modulation of N-formylmethionyl-leucyl-phenylalanine evoked lysosomal enzyme release from human neutrophils.

Isoprenaline, histamine and PGE1 inhibit N-formylmethionyl-leucyl-phenylalanine evoked lysosomal enzyme release from human neutrophils. Their effects are dose-dependent and potentiated by 3-isobutyl-1-methylxanthine pretreatment of the cells. The order of activity is PGE1 greater than isoprenaline greater than histamine. The maximum of inhibition afforded by each agonist depends on the amount of the secretory stimulus, since it is higher at lower concentrations of the secretagogue. Isoprenaline effects are competitively antagonized by propranolol and are mimicked by fenoterol and salbutamol. These results suggest that human neutrophil functions are modulated by endogenous control mechanisms, that can also be activated by drugs acting on the same receptors as the endogenous mediators.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Histamine release by vagal stimulation.

The content of acetylcholine and histamine in the effluent of isolated, vagally innerved guinea-pig auricles was determined. Spontaneous or stimulation-induced overflow of acetylcholine was detected only in the presence of acetylcholinesterase inhibitors. The histamine overflow was measurable also in the absence of inhibition of cholinesterase, and neatly increased during vagal stimulation. The vagally evoked histamine overflow was blocked by atropine and potentiated by eserine. The stimulation-induced histamine overflow in the effluent is discussed, presumably assuming that acetylcholine may release histamine from cardiac histamine stores.

Acetylcholine↗
PubMed1983

N-Formylmethionyl-leucyl-phenylalanine: Different releasing effects on human neutrophils and rat mast cells.

N-Formylmethionyl-leucyl-phenylalanine (FMLP) is a synthetic chemotactic peptide which induced beta-glucuronidase and lysozyme release from human neutrophils treated with cytochalasin B. FMLP-releasing effects were rapid and dose dependent. Unlike other secretagogues of neutrophils (e.g., zymosan and immune complexes), FMLP secretory activity was not modulated by acetylcholine, which by itself did not release lysosomal enzymes from human neutrophils. Isolated rat mast cells did not respond to FMLP, which has been demonstrated to release histamine from human neutrophils. Two markers of rat mast cell secretory granules, histamine and beta-glucuronidase, were assayed, but the results were negative for both. In the same experimental conditions, 48/80 released histamine and the enzyme: the ratio of the net percentage release of beta-glucuronidase to the net percentage release of histamine was congruent 0.4.

Acetylcholine↗
PubMed1983

Muscarinic cholinergic receptor binding in rat mast cells.

Specific [3H]-QNB binding was present in isolated, purified, intact rat mast cells and in crude membrane preparations. The binding is saturable, time- and temperature-dependent. Cholinergic agents inhibit selectively the binding: atropine is the most effective of the antagonists while oxotremorine is the most potent of the muscarinic agonists. It is concluded that rat mast cells are provided with muscarinic cholinergic receptors.

Animals↗
PubMed1983

Stimulation of drug-metabolizing enzymes by nitrous oxide in the rat.

Wistar male rats were subchronically (150 h continuously) or chronically (5 h daily for 15 days) exposed to a 50% nitrous oxide/oxygen mixture. As an index of enzyme induction liver N-demethylase and benzo(a)pyrene-hydroxylase activities, serum gamma-glutamyltranspeptidase activity, urinary d-glucaric acid and pentobarbital sleeping time were evaluated in comparison with a control group. No effect was observed after subchronic exposure to the anaesthetic gas. Chronic exposure, on the contrary, decreased pentobarbital sleeping time, increased urinary d-glucaric acid, liver N-demethylase and serum gamma-glutamyltranspeptidase activities. No increase of liver benzo(a)pyrene-hydroxylase was observed. Chronic nitrous oxide exposure under appropriate conditions can modify some enzymes, metabolizing drugs and xenobiotic compounds.

Animals↗
PubMed1983

Overall evaluation of treatment modalities for heroin addiction in a toxicology unit.

A survey of treatment results is presented, using a variety of guidelines for the therapy of different features of heroin addiction in a toxicology unit. Data on 3,211 inpatients under treatment from 1972 are analyzed separately, as well as the follow-up status of 1,262 outpatients who were enrolled in a methadone treatment program. The results are discussed in terms of reliability of the programs and their risk-benefit ratios for the community.

Clonidine↗
PubMed1982

Mast cell receptors controlling histamine release: influences on the mode of action of drugs used in the treatment of adverse drug reactions.

In drug-induced allergic diseases of the immediate type (anaphylactic and anaphylactoid reactions), the primary target cells are tissue mast cells, which discharge their granular content upon interaction with different secretagogues (immunological releasers; histamine liberators) on specific plasma membrane receptors. Experiments are reviewed here which report that IgE-mediated histamine release from mast cells, and the secretion of histamine induced by non-immunological secretagogues (dextran; compound 48/80; acetylcholine) are blocked by beta-adrenoceptor and H2-receptor agonists, their inhibiting effect being surmountable by beta-adrenoceptor blocking drugs and by anti-H2-antihistamines. Specific radioligands ([3H]-dihydroalprenolol; [3H]-cimetidine) binding to rat mast cell membranes points to the possibility that inhibition of histamine release is brought about by the activation of mast cell beta-adrenoceptors and H2-receptors. Drugs used in therapy of anaphylactic or anaphylactoid reactions may act either on tissue receptors, competing with released mediators, or by inhibiting the release of allergic mediators from mast cells, on activation of specific receptors located in mast cell plasma membranes.

Acetylcholine↗
PubMed1982

Presence of functionally active beta-adrenoceptors in rat mast cells. Correlation between (--)[3H]-dihydroalprenolol binding and inhibition of histamine release.

The correlation between the binding of a beta-adrenoceptor antagonist, (--)[3H]-dihydroalprenolol (DHAP), and the adrenergic inhibition of histamine release by acetylcholine and by compound 48/80 was studied with isolated purified rat mast cells and in rat mast cell crude membrane fractions. Acetylcholine-evoked histamine release was inhibited by catecholamines, in the order isoprenaline greater than adrenaline greater than noradrenaline. Pretreatment of cells with (--)alprenolol antagonized the inhibitory effect of isoprenaline on acetylcholine-induced histamine release. 40/80-evoked histamine release was blocked by isoprenaline at significantly higher concentrations than those required to inhibit cholinergic histamine release. The inhibitory effect of isoprenaline was equally antagonized by preincubating mast cells with (--)alprenolol. Specific binding sites for DHAP have been demonstrated in rat mast cell membranes. The specific binding of DHAP was inhibited by adrenoceptor agonists and antagonists according to the stereospecificity of these compounds. A close correlation between the binding-inhibitory potency of various adrenergic compounds and the data obtained in the pharmacological experiments was found, thus indicating the presence of beta-adrenoceptors in rat mast cells.

Acetylcholine↗
PubMed1982

Evidence for H2-receptor-mediated inhibition of histamine release from isolated rat mast cells.

Impromidine, an H2-receptor agonist, inhibited the release of histamine from isolated purified rat mast cells evoked by compound 48/80 and acetylcholine. Pyridilethyl-amine (PEA), and H1-receptor agonist, on the other hand, was only slightly effective at very high concentrations. The inhibitory effect of impromidine was blocked by preincubating the cells with cimetidine, but not by chlorpheniramine. The existence of an H2-mediated inhibitory feed-back regulation of histamine release was also suggested by the demonstration of specific binding sites for [3H]-cimetidine in rat mast cell membranes.

Acetylcholine↗
PubMed1982

Removal of alpha-amanitin from blood by hemoperfusion over uncoated charcoal. Experimental results.

The sorbent capacity of uncoated charcoal column (Detoxyl 2, Sorin Biomedica) on alpha-amanitin was studied by adding known amounts of alpha-amanitin to fresh human blood, which was recirculated through a clinical hemoperfusion circuit over a period of 30 min. The column was washed with saline to remove loosely bound alpha-amanitin, and eluted with 0.1 N HCl to detach absorbed alpha-amanitin. Alpha-amanitin concentration was measured in the saline washings and in the acid eluates by means of a radioimmunoassay. Only negligible amounts of amanitin were recovered in the saline washings. Suitable amounts of alpha-amanitin were present in the acid eluates, showing an adsorption optimum for blood concentrations ranging from 50 to 200 ng . ml-1. The results were discussed as predictable of the clinical usefulness of charcoal hemoperfusion in A. phalloides poisoning.

Adsorption↗
PubMed1981

Correlation between cholinergic histamine release and quinuclidinyl-benzilate ([3H]-QNB) binding in mast cell membranes.

Isolated purified rat mast cells release histamine when exposed to acetylcholine according to a different pattern of sensitivity. No correlation was found between the release of histamine evoked by acetylcholine and the high affinity binding of [3H]-quinuclidinyl-benzilate (QNB), a specific cholinergic muscarinic ligand, to rat mast cell membranes, since QNB binding was the same in membrane isolated from cells which were sensitive or insensitive to acetylcholine. In murine neoplastic mast cells, a negative correlation was found between histamine release and [3H]-QNB binding, as no evidence of specific [3H]-QNB binding was present in murine neoplastic mast cell membranes which, accordingly, do not release histamine when exposed to acetylcholine. It is concluded that murine neoplastic mast cells are not provided with muscarinic cholinergic receptors. In rat mast cells, muscarinic cholinergic receptors are always present, but not always coupled with the effector mechanisms triggering the exocytosis.

Acetylcholine↗