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Biomedical subjects

D Pasotti

Publications and source records attributed to D Pasotti.

36 records · Page 2Linked to original sources
PubMed1989

[In vitro effects of morphine and opioid peptides on neutrophil granulocyte aggregation and ATP release].

The effects of morphine and opioid peptides on neutrophil aggregation and ATP release were studied. Inhibition of human granulocyte aggregation and ATP release was observed in the presence of morphine in a naloxone stereoselective manner, whereas the opioid peptides were ineffective. The effects of DAGO, DADL and Dynorphin 1-9 on the granulocyte aggregation and ATP release were also evaluated, but these opioids peptides are unable to modify neutrophil function. Our studies confirm the role of mu receptors on modulation of polymorphonuclear granulocyte aggregation and suggest a key role of opioid peptides in the regulation of some immune system functions.

Adenosine Triphosphate↗
PubMed1989

[Granulocyte disease caused by glycoprotein complex deficiency correlated with leukocyte adhesion].

This report summarizes the clinical and laboratory findings from a group of our patients and literature reviews from several families who have a genetic deficiency in three related leukocyte membrane surface antigens known as CR3,LFA-1, and p150,95. Each surface antigen has an identical beta-chain noncovalenty linked to one of three distinct alpha-chain types. Patients affected by this autosomal recessive disease have now been identified by several investigators. The patients have an increased susceptibility to bacterial infections that is similar to patients who have other types of neutrophil functional deficiencies or neutropenia. Laboratory tests have indicated that isolated neutrophils from these patients have two major types of functional deficiencies that probably contribute to their reduced ability to overcome bacterial infections. This review focuses exclusively on the phagocytic and cytotoxic abnormalities of neutrophils from these patients.

Antibodies, Monoclonal↗
PubMed1988

Serum, sputum and bronchial concentrations of erythromycin in chronic bronchitis after single and multiple treatments with either propionate-N-acetylcysteinate or stearate erythromycin.

Serum and bronchial concentrations of erythromycin were determined in 30 chronic bronchitic patients during an exacerbation phase of bacterial infections. The levels were measured after single and multiple oral treatments with erythromycin-propionate-N-acetylcysteinate (EPAC) or erythromycin stearate (ES) in a double-blind design. EPAC showed higher and longer-lasting erythromycin levels in serum, sputum and pure bronchial mucus than ES. It is believed that EPAC is better absorbed because of its greater stability in the gastrointestinal juices. Higher concentrations in bronchial secretions not always depend on the blood levels. It seems to be possible that the N-acetylcysteine moiety in the molecule of EPAC drug can facilitate antibiotic penetration because of its mucolytic activity. The clinical response (disappearance of fever, clearance of bacterial pathogens from sputum, reduction of quantity and viscosity of sputum) also occurred faster in the EPAC than in the ES group.

Acetylcysteine↗
PubMedDate not supplied

Pharmacokinetics of dipyridamole-beta-cyclodextrin complex in healthy volunteers after single and multiple doses.

Dipyridamole is a well known anti-aggregating agent characterized by poor water solubility as well as scant and variable bioavailability. Recently, the compound was complexed with beta-cyclodextrin forming a molecular encapsulation resulting in better oral absorption and stronger biological activities in animals. In the present study, a randomized double blind cross-over comparison between dipyridamole-beta-cyclodextrin complex (dip-beta-CD) and dipyridamole was performed in 12 healthy subjects after single (75mg) and multiple oral treatments (75mg TID). Dip-beta-CD showed better bioavailability and less interindividual variability than dipyridamole either after single or multiple doses. In particular, dip-beta-CD had a greater AUC and Cmax, and a smaller Tmax even at the steady state. In addition, 100% of the subjects receiving a single dose of dip-beta-CD, as compared to 66.7% of those treated with dipyridamole, had plasma levels superior to 1 microgram/ml (which is the supposed anti-aggregating threshold level). In contrast, 0 and 33.03% of the subjects showed plasma levels superior to 2.5 micrograms/ml (which might cause the appearance of side-effects) on the 7th day of the multiple treatment with dip-beta-CD and dipyridamole, respectively. In fact, the subjects presenting higher levels after uncomplexed dipyridamole also complained of headache and/or dizziness on occasion. No adverse side effects were reported for dip-beta-CD.

Administration, Oral↗
PubMedDate not supplied

[The nervous system and the immune system: the role of morphine and opioid peptides in the function of neutrophilic granulocytes].

Inhibition of human granulocyte chemotaxis towards casein was observed in the presence of mu and k receptor agonist, which per se exhibits chemokinetic activity. Naloxone was found to prevent both the opioid and opioid unrelated increase of granulocyte migration. Although opioid agonists with different receptors specificity were capable of strongly modifying human granulocyte migration, no conclusion can be drawn on the role of opioid receptors in regulating migration activity. The effects of morphine and opioid peptide on neutrophil aggregation and ATOP release were studied. Inhibition of human granulocyte aggregation and ATP release was observed in the presence of morphine in a naloxone stereoselective manner, whereas the opioid peptides were ineffective. The effect of DAGO, DADL and dynorphin 1-9 on granulocyte aggregation and ATP release were also evaluated, but these opioid peptides are unable to modify neutrophil function. Our studies confirm the role of mu receptors on modulation of polymorphonuclear granulocyte function and suggest a key role of opioid peptides in the regulation of some immune system functions. In comparative studies Ca++ (A 23,187) and dynorphin 1-9, per se, induced stimulation of arachidonic acid metabolites from granulocytes. In this regard dynorphin 1-9 may function as a mediator between the central nervous system and immunity.

Adenosine Triphosphate↗
PubMedDate not supplied

In vitro effect of opioid agonist and antagonist on superoxide release by granulocytes.

The effect of the opioid agonist morphine and of the (-) and (+) stereoisomers of the antagonist naloxone were studied on the O2-generation from human granulocytes. Morphine or naloxone had no effect on basal or phorbol myristate acetate (PMA) stimulated O2-generation, while equimolar (-) naloxone and morphine concentrations (1 x 10-13 - 1 x 10-7 M) inhibited the stimulated O2-generation. The effect of (-) naloxone was stereospecific, suggesting the involvement of opioid receptors. The unmasking of non opioid effects of morphine could be responsible for the inhibition of O2-generation. It is suggested that the opioid control of oxidative metabolism in human granulocytes could involve multiple receptors mediating opposite effect.

Adult↗
PubMedDate not supplied

[The central nervous system and inflammation: the role of opioid peptides].

Inhibition of human granulocyte aggregation was observed in the presence of morphine in a naloxone stereoselective way, while the opioid peptides were ineffective. In comparative studies Ca(+)+ (A23187) and dynorphin 1-9, per se, induced stimulation of arachidonic acid metabolites from granulocytes. In this regard dynorphin 1-9 may function as a mediator between the central nervous system and the inflammation.

Arachidonic Acids↗
PubMedDate not supplied

[Diphenylhydantoin induces an alteration in immune system cellular functions: an in vitro study of platelet and granulocyte aggregation].

In vitro experiments were performed in order to clarify the influence of phenytoin on human granulocyte and platelet function. Therapeutic anticonvulsant concentrations of the drug significantly reduced the granulocyte aggregation produced by formyl-methionyl-leucyl-phenilalanine; phytoemoaglutinin-induced granulocyte aggregation was unaffected by phenytoin. In the same range of concentrations the drug was able to inhibit ADP-, epinephrine- and collagen-induced platelet aggregation. The possible in vivo implications of these data are discussed.

Cell Aggregation↗
PubMedDate not supplied

[Granulocytes and oxidative metabolism: role of monoclonal antibodies in superoxide anion release from neutrophils].

We studied the effects on the granulocyte oxidative metabolism of some monoclonal antibodies reacting with a membrane surface antigen fundamental for the functions of these cells. The aim of this investigation was to evaluate the role of CD11b/CD18 membrane glycoproteins on superoxide release from granulocytes. The preincubation with MoAbs 60.1, OKM1, 60.3 determined a significant decrease of anion release from granulocytes stimulated by fMLP.

Antibodies, Monoclonal↗
PubMedDate not supplied

[Breast and skin localization of non-Hodgkin's lymphoma. Description of a clinical case].

A clinical case of a patient suffering from non-Hodgkin lymphoma with breast localization and skin infiltration is reported. Skin lesion was the presenting feature: after diagnosis and chemotherapy the relapse of lymphoma was characterized by breast infiltration. These particular localizations are discussed in terms of their unfavourable prognostic significance in lymphoma.

Adult↗
PubMedDate not supplied

[The effect of opioid peptides on peripheral blood granulocytes].

Some neuropeptides may influence various functions of immunocompetent cells. Endogenous opioids have been implicated in the correlation of the immune, endocrine and nervous system. The object of our study was to evaluate the effects induced by some agonist and antagonist endogenous peptides to opioid receptors on granulocytes (PMNs) functions in vitro. We used these drugs: D-Ala2-D-Leu6-enkephalin (DADL-Sigma-Chemical-Usa); D-Ala2-N-ME-Phe4-Gly-ol5-enkephalin (DAGO-Sigma-Chemical-Usa); Dynorphin 1-9 (Sigma Chemical-Usa); naloxone (Sigma Chemical-Usa) and morphine (Sifac-Italy). Morphine was able to inhibiting neutrophil granulocyte chemotaxis induced by serum activated with E. Coli (p < 0.01), by casein (p < 0.01 and <fMLP (p < 0.01). Furthermore morphine and 1-9 dynorphin inhibited spontaneous migration of PMNs both when added to the upper compartment together with cells. Naloxone was able to inhibit PMNs chemotaxis induced by serum, casein and fMLP, this drug was not able to behave on chemokinesis or random migration activity. Morphine was found to inhibit PMNs aggregation induced by PHA (0.01), PMA (0.01), fMLP (0.01) and Ca++ ionophore (p < 0.01), ATP release (p < 0.01), thromboxane B2 (TxB2) and leukotriene B4 (LTB4) secretion during cell aggregation. Dynorphin 1-9, per sé, induced TxB2 and LTB4 secretion from PMNs. Morphine inhibition of both cell aggregation and ATP release, but not arachidonic acid metabolism product secretion, was prevented by naloxone. The naloxone sensitive impairment by morphine of CD 11/CD 18 complex surface expression observed could play a role in opioid inhibition of PMNs activation.

Adult↗
PubMedDate not supplied

[The role of the granulocytes in ischemic cardiopathy].

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. Granulocytes can release a variety of mediators tissue injury and synergize with these different mediators, cytokines and other cells resulting in amplification of neutrophil stimulation and rising to additional products with enhanced endothelial injury. Free radicals released by PMNs during ischemia or reperfusion produce deleterious effects on cell membranes, endothelial cells and myocardium. Experience in humans shows the modification of PMNs function in angina and during myocardial ischemia: upon reperfusion PMNs accumulate and produce an inflammatory response leading to endothelial injury. Rabbit derived antiserum dependent-reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarction. Another aspect of PMNs function is related to leukotriene C4 release; the vasoconstrictor effect of this leukotriene on coronary arteries is synergistic with that induced by platelet-released thromboxane A2, and the decrease in coronary flow produced by the combination of both substances is greater than the sum of changes caused by the two eicosanoids separately administered. The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in the pathophysiology of myocardial injury due to regional ischemia and reperfusion is an area of intense investigation. This overview will not attempt to be exhaustive. Experimental and clinical studies to elucidate these events should not only provide insight into acute and chronic pathologic tissue damage, but may also lead to the identification of important new targets of pharmacologic intervention.

Acute Disease↗