Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where B. Palmerani is active.

Publication


Featured researches published by B. Palmerani.


Biochemical Pharmacology | 1990

Histamine release from rat mast cells induced by metabolic activation of polyunsaturated fatty acids into free radicals

Emanuela Masini; B. Palmerani; F. Gambassi; A. Pistelli; E. Giannella; Brunella Occupati; M. Ciuffi; Tatiana Bani Sacchi; Pier Francesco Mannaioni

Polyunsaturated fatty acids (PUFA: arachidonic and linoleic acid) release histamine from isolated purified rat serosal mast cells only in the presence of oxidizing systems such as phenobarbital-induced rat liver microsomes, prostaglandin-H-synthetase (PHS) or soybean lipoxygenase. The release of mast cell histamine by activated PUFA has a long time-course and the electron microscopical features are consistent with an exocytotic secretion in the case of arachidonic acid and cell lysis in the case of linoleic acid. The phenomenon is associated with a significant increase in malonyldialdehyde (MDA) and conjugated diene generation, suggesting a relationship between histamine release and membrane lipid peroxidation. The secretion of histamine was inhibited by anti-free radical interventions such as D-mannitol, reduced glutathione and alpha-tocopherol. Some cyclooxygenase and lipoxygenase inhibitors, cimetidine and carnitine derivatives, are differentially active in the inhibition of mast cell histamine release by activated arachidonic acid. These results suggest that free radical derivatives of PUFA, generated by metabolic activation, trigger mast cell histamine release.


Inflammation Research | 1990

Ischemia reperfusion injury and histamine release in isolated and perfused guinea-pig heart: Pharmacological interventions

Emanuela Masini; Stefano Bianchi; F. Gambassi; B. Palmerani; A. Pistelli; L. Carlomagno; P. F. Mannaioni

Experiments were carried out to provide further information on the biochemical and morphological changes occurring in the guinea-pig heart after multiple ligature and reopening of the left anterior descending (LAD) coronary artery. In isolated perfused guinea-pig heart the reopening of LAD coronary artery leads to a release of histamine related to a loss of metachromasia by cardiac mast cells. The process is associated with malonyldialdehyde (MDA) production, cellular overload of calcium and ventricular arrhythmias which can be modulated by pharmacological interventions.


Inflammation Research | 1989

Ischemia-reperfusion injury and histamine release in isolated guinea-pig heart: the role of free radicals.

Emanuela Masini; F. Gambassi; E. Giannella; B. Palmerani; A. Pistelli; L. Carlomagno; P. F. Mannaioni

Free radicals produced by the occlusion and opening of the left anterior descending coronary artery and/or by perfusion of isolated guinea-pig heart with FeCl3/ADP (10 μM/100 μM) induce a differential release of histamine and lactate dehydrogenase (LDH) in the perfusates with a preferential liberation of histamine in the reperfusion phase, associated with an increase of ventricular arrhythmias. The release of histamine has been correlated with malonyldialdehyde (MDA) production and tissue calcium content in left ventricular tissue. MDA increased during ischemia, while the calcium content increased when the tissue was reperfused. Under these conditions, N-t-butyl-α-phenylnitrone (BPN), a molecule capable of forming spin adducts with free radicals, andd-mannitol are active in preventing reperfusion-induced arrhythmias.


Inflammation Research | 1990

Histamine release by platelet aggregation.

P. F. Mannaioni; B. Palmerani; A. Pistelli; F. Gambassi; E. Giannella; T. Bani Sacchi; Emanuela Masini

Coincubation of rat serosal mast cells with human platelets leads to a significant release of histamine, which dose-dependently increases when platelet aggregation is induced by various concentrations of arachidonic acid. In turn, histamine enhances platelet aggregation induced by different agonists, this effect being mimicked by pyridyl-ethyl-amine (PEA), blocked by mepyramine and amplified by ranitidine. The data suggest the existence of a platelet-derived histamine releasing factor (PDHRF) and indicate the presence of platelet H1 and H2 receptors, capable of modulating platelet aggregation.


International Archives of Allergy and Immunology | 1987

Mast Cell Histamine Release Induced by Intermediate Products of Arachidonic Acid Metabolism

Emanuela Masini; B. Palmerani; Tatiana Bani-Sacchi; E. Giannella; Roberto Fantozzi; Pier Francesco Mannaioni

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.


Inflammation Research | 1987

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

Emanuela Masini; E. Giannella; Tatiana Bani-Sacchi; R. Fantozzi; B. Palmerani; P. F. Mannaioni

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 (10−8−10−4M) and the terminal products (10−6M) 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 byd-mannitol and by lipoxygenase and cyclo-oxygenase 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.


Inflammation Research | 1988

Histamine release in acute coronary occlusion-reperfusion in isolated guinea-pig heart.

Emanuela Masini; E. Giannella; Stefano Bianchi; B. Palmerani; A. Pistelli; P. F. Mannaioni

It has been shown that plasma histamine significantly increases during myocardial infarction in the dog. Histamine is also released when the isolated guinea-pig heart is reperfused after 30 minutes of low flow perfusion. The release of histamine and lactate dehydrogenase (LDH) after left anterior descending coronary artery ligation and release were investigated in the present study and related to the changes in electrocardiographic parameters and to a computer-aided analysis of left ventricular mast cell metachromasia.Spontaneous release of histamine was unchanged during ischemia and increased after the release of the ligature, while we observed a steady increase of LDH overflow. In parallel, a significant diminution of mast cell granule metachromasia was observed in left ventricular samples.The perfusion of the heart with FeCl3/ADP (10 μM/100μM), a free radical-generating system, significantly enhanced both the basal and ischemic-reperfusion release of histamine, while perfusion with N-t-butyl-phenyl-nitrone (BPN/100 μM) a “spin-trapper” molecule, significantly decreased histamine and LDH release and the loss in metachromasia of left ventricular mast cells induced by reperfusion. Inhibitors of xanthine oxidase (allopurinol, 10 μM) and of calcium-activated proteases (leupeptin, 10 μM) modified the kinetics of histamine and LDH release.


International Archives of Allergy and Immunology | 1989

Free Radicals Induce Ischemia-Reperfusion Injury and Histamine Release in the Isolated Guinea Pig Heart

Emanuela Masini; E. Giannella; B. Palmerani; A. Pistelli; F. Gambassi; Pier Francesco Mannaioni

Free radicals are produced by perfusion of isolated guinea pig heart with FeCl3/ADP (10 microM/100 microM) and/or occlusion and opening of the left anterior descending coronary artery. Cardiac histopathology was correlated with histamine and lactate dehydrogenase release and with malondialdehyde production. A differential release of histamine and lactate dehydrogenase in the perfusate was detected, showing a preferential liberation of histamine in the reperfusion phase. The increase in lipid peroxidation product in left ventricular tissues after left coronary artery occlusion was maximal at the end of ischemia.


Inflammation Research | 1988

Modulation of anaphylactic histamine release by calcium channel agonists and antagonists.

E. Giannella; Emanuela Masini; B. Palmerani; A. Pistelli; P. F. Mannaioni

Calcium antagonists have been reported to exert protective effects in hypersensitivity reactions in man and animals. However, their effect on anaphylactic histamine release is highly variable and controversial. In the present paper we evaluate the effect of calcium entry blockers and BAY K 8644 on the response to specific antigen in isolated hearts taken from actively sensitized guinea-pigs and from isolated rat and guinea-pig mast cells, actively or passively sensitized. Verapamil, diltiazem, nifedipine and prenylamine dose-dependently decreased anaphylactic histamine release in isolated actively sensitized guinea-pig mast cells. BAY K 8644 was found to be ineffective. In isolated, passively sensitized rat mast cells, verapamil showed a highly signficant inhibitory effect, while prenylamine (10−4M) was able to evoke a histamine releasing effect. In cardiac anaphylaxis verapamil, diltiazem, prenylamine, but not nifedipine, were active in reducing the release of histamine without modifying the antigen-induced arrhythmias and positive chronotropic and inotropic effects.


International Archives of Allergy and Immunology | 1989

Prostaglandin H synthetase activates xenobiotics into free radicals: histamine release and biochemical characteristics.

Emanuela Masini; E. Giannella; B. Palmerani; A. Pistelli; F. Gambassi; Pier Francesco Mannaioni

In isolated rat serosal mast cells, studies with the fluorescent Ca2+ indicator, quin 2, and with [3H]-myoinositol to label endogenous polyphosphoinositides have established that an increase in cytosol Ca2+ levels was obligatory for histamine release by free radicals. No substantial breakdown of phosphatidylinositol and related polyphosphoinositides was associated with generation of the Ca2+ signal and histamine release, suggesting that the release of histamine by free radicals entails different pathways than the calcium-mobilizing receptors linked to polyphosphoinositides as second messengers.

Collaboration


Dive into the B. Palmerani's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar

A. Pistelli

University of Florence

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

F. Gambassi

University of Florence

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge