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Biomedical subjects

R Fantozzi

Publications and source records attributed to R Fantozzi.

At least 73 records · Page 4Linked to original sources
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

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↗
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↗
PubMed1980

Inhibition of cholinergic histamine release in rat mast cells.

Adrenaline inhibits the acetylcholine-evoked histamine release from isolated purified rat mast cells, in a dose-dependent fashion. The inhibitory effect of adrenaline is reversed by preincubating the cells with a beta-blocker, aprenolol, but not by preincubating them with an alpha-blocker, phentolamine. These results were confirmed by observations using an electron microscope and they suggest that adrenaline inhibits the cholinergic histamine release from rat mast cells acting upoon beta-receptors.

Acetylcholine↗
PubMed1980

Characteristics of histamine release evoked by acetylcholine in isolated rat mast cells.

1. Histamine secretion from rat mast cells occurs in the presence of nanomolar concentrations of acetylcholine. 2. Intact glycolytic and oxidative metabolism is required for the acetylcholine-induced histamine secretion. Removal of extracellular glucose, hypoxia, cyanide and monoiodoacetate almost completely inhibit the secretion. 3. The secretion of histamine is dependent on the extracellular H ion concentration and is blocked when the cells are exposed to Na-deficient media. 4. The order of potency of cholinrgic agonists in evoking the secretion of histamine is oxotremorine > acetylcholine > choline > carbamycholine > nicotine. 5. Atropine competitively blocks the acetylcholine-induced histamine secretion, indicating the presence of cholinergic muscarinic receptors on mast cells. 6. Dibutyryl cyclic AMP and adrenaline inhibit the acetylcholine-induced histamine secretion, indicating a regulatory function afforded by cyclic nucleotides in the cholinergic histamine release.

Acetylcholine↗
PubMed1978

Modulation of the spontaneous histamine release by adrenergic and cholinergic drugs.

Experiments have been reported on the possible modulation of the spontaneous histamine release by adrenergic and cholinergic drugs. Adrenergic drugs increase the spontaneous histamine release in vivo, and in neoplastic mast cells, in vitro. The mechanism of histamine release appears to be dependent upon the activation of alpha-adrenoceptors. Cholinergic drugs activate the release of histamine in many secretory processes in vivo; in vitro, acetylcholine is one of the most powerful histamine releasers in isolated purified rat mast cells. The release of histamine evoked by acetylcholine in rat mast cells is a calcium-requiring, temperature-dependent exocytosis. The physiological relationship of the sympathetic, parasympathetic and histamine-containing cells are discussed.

Animals↗
PubMed1977

The influence of catecholamines and serotonin on histamine uptake and metabolism by guinea pig atrium.

The influence of serotonin and catecholamines on the uptake and metabolism of 14C-histamine by isolated guinea pig atrium has been investigated. Epinephrine, norepinephrine and serotonin were found to reduce the histamine uptake and the formation of methylhistamine, in a dose-dependent fashion. The order of potency was epinephrine greater than norepinephrine greater than serotonin. Aliphatic diamines, such as spermine, do not affect the accumulation and metabolism of histamine. It is suggested that serotonin and catecholamines, may enhance histamine responses by decreasing the uptake and metabolism of this amine.

Animals↗
PubMed1977

The modulation of histamine release by alpha-adrenoceptors: evidences in murine neoplastic mast cells.

Murine neoplastic mast cells which have been loaded with exogenous labelled histamine, released 14C-histamine when exposed to increasing concentrations of phenylephrine and noradrenaline. Adrenaline was only slightly effective, while isoprenaline and dibutyryl-cyclic-AMP were fully inactive. The release of histamine evoked by alpha-adrenergic agonists was antagonized by phentolamine, and left unchanged by practolol and cocaine. It is concluded that alpha-adrenoceptors may be valuable in evoking histamine release by murine neoplastic mast cells.

Animals↗
PubMed1976

A trend in the therapy of Amanita phalloides poisoning.

Recent experimental evidences have been produced on the protection afforded by penicillin G in rats poisoned by Amanita phalloides extracts. A therapeutic trend which combines penicillin G infusions to the classical supportive measures was applied to 33 cases of severe A. phalloides poisoning, with 100% survival rates. The possible mechanism of the protective effect of penicillin G in A. phalloides poisoning is discussed.

Adult↗
PubMed1975

Studies on the 14C-histamine release induced by noradrenaline in mouse neoplastic mast cells.

Murine neoplastic mast cells incubated with labelled histamine released 14C-histamine when exposed to increasing concentrations of noradrenaline. This process was blocked by low temperature, by inhibiting oxidative metabolism and glycolysis, by calcium deprivation and by cytochalasin B. Electron microscope observations of cells exposed to noradrenaline revealed an increase of the Juxtanuclear Golgi Apparatus, and the appearance of a pronounced peripheral vacuolization. Cells exposed simultaneously to noradrenaline and cytochalasin B were characterized by a further increase of the Golgi apparatus, and by the appearance of many electron dense cytoplasmic granules. The possible mechanisms of the noradrenaline induced histamine release were discussed.

Animals↗