PubMed Health⌕ Search

Biomedical subjects

G Ricevuti

Publications and source records attributed to G Ricevuti.

At least 19 recordsLinked to original sources
PubMed1992

Correlation between CD11b/CD18 and increase of aggregability of granulocytes in coronary artery disease.

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial 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 infarcts. Experience in humans shows the modification of PMN function in angina and during myocardial ischemia. In our studies, patients affected by coronary artery disease presented an increase in granulocyte aggregability in coronary sinus and showed a related higher expression of CD11b/CD18 in coronary sinus with respect to aorta leukocytes. The potential role of this modification of PMNs was analyzed.

Adult↗
PubMed1992

Phagocyte activation in coronary artery disease.

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 molecules mediating tissue injury which act synergistically with other molecules and cells. The aim of our investigation was to evaluate the granulocyte function in patients affected by coronary artery disease (CAD) and during coronary angioplasty (PTCA). We studied 20 patients suffering from CAD. The PMN's aggregating activity was greater in the coronary sinus than in the aorta (P < 0.01). The increase in aggregating activity was evident in patients who were smokers: their cells release significantly lower quantities of leukotriene C4 (P < 0.025). In the 20 patients who underwent coronary angioplasty we analyzed superoxide release after stimulation with phorbol-myristate-acetate (PMA). The results showed a greater decrease of PMN's superoxide production in the coronary sinus than in the aorta (P < 0.05). In all patients affected by CAD we evaluated the PMN's expression of CD11b/CD18 membrane integrins. In these patients the increase in expression of CD11b/CD18 was statistically significant in comparison with the controls (P < 0.01). This increase in expression correlates with a higher aggregation (r = 0.87, P < 0.001). 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 paper presents studies carried out in vivo which have been instrumental in demonstrating the role of granulocytes as mediators of myocardial ischemia.

Angioplasty, Balloon, Coronary↗
PubMed1992

Interaction between (-)naloxone and morphine in modifying superoxide generation from human granulocytes.

The effect of the opioid agonist morphine and of the (-) and (+) stereoisomers of the antagonist naloxone were studied on superoxide generation from human granulocytes. Morphine or naloxone had no effect on basal or phorbol 12-myristate 13-acetate (PMA)-stimulated superoxide generation. Combined equimolar (-)naloxone and morphine concentrations (0.1 pM-0.1 microM) inhibited PMA-stimulated superoxide generation, while combined (+)naloxone and morphine had no effect. The stereospecific effect of naloxone suggests the involvement of opioid receptors. Thus, inhibition of superoxide generation by combined (-)naloxone and morphine could result from the unmasking of non opioid effects of morphine. It is suggested that the opioid control of oxidative metabolism in human granulocytes could involve multiple receptors mediating opposite effects.

Adult↗
PubMed1992

[An in-vivo and in-vitro study of phagocyte migration in patients with AIDS].

Polymorphonuclear leukocytes (PMN), are considered the first line of host defense. The PMN defects were related with an increase susceptibility to infections. We studied the neutrophil chemotactic function in 20 patients suffering from AIDS. The results of in vivo study demonstrated the decrease of chemotactic activity at 6 hour (p < 0.001) in the patients respect to control. The data of in vitro studies confirmed the granulocyte chemotactic defects, statistically significant, in the patients compared to the control subjects, when we used all chemotactic factors. These results showing the profound immune disturbances characteristic of the disease can favour infective susceptibility and complicate follow-up of AIDS.

AIDS-Related Opportunistic Infections↗
PubMed1991

Granulocyte function in coronary artery disease.

Granulocytes defend the body against invading microbes by producing a complex armamentarium of toxic substances, such as proteolytic enzymes, oxygen radicals and arachidonic acid metabolites. Under certain circumstances, however, such compounds may be released in the absence of phagocytosable particles, resulting in injury to normal cell and connective tissue degradation. Recent experimental studies have emphasized the potential role of granulocytes in the pathogenesis of myocardial ischemia. Clinical investigations have also shown alterations in neutrophil function in stable and unstable clinical manifestations of ischemic heart disease. "Priming" of granulocytes in stable forms of coronary disease may predispose to the subsequent development of acute coronary events, whereas activation of neutrophils may lead to alterations in vascular permeability and coronary flow regulation, leading to further myocardial and endothelial injury in acute myocardial infarction, unstable angina and coronary angioplasty.

Coronary Disease↗
PubMed1991

Role of granulocytes in endothelial injury in coronary heart disease in humans.

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. A positive correlation was also found between leukocyte count and severity of coronary artery disease. Rabbit derived antiserum dependent-reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarcts. Granulocytes can release a variety of mediators tissue injury and synergize with these different mediators and other cells resulting in amplification of neutrophil stimulation and rising to additional products with enhanced endothelial injury. This paper reviews "in vivo" studies that have been instrumental in demonstrating this role of granulocytes as a mediator of myocardial ischemia. Experience in humans shows the modification of PMNs function in angina and during myocardial ischemia, and data from our group demonstrated that their aggregability is increased in the coronary sinus of patients with angiographically documented coronary disease. Upon re-perfusion PMNs accumulate and produce an inflammatory response resulting in endothelial injury. Free radicals formed during ischemia or re-perfusion produce deleterious effects on cell membranes, endothelial cell and myocardium. On the other hand the PMNs activation occurring during coronary angioplasty (PTCA) by the release of proteolytic enzymes and the generation of oxygen-free radicals, may aggravate the endothelial damage induced by PTCA and further stimulate platelets having potential implications in subsequent development of restenosis. An other 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, as well as 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 pathophysiology of myocardial injury due to a regional ischemia and reperfusion is an area of intense investigation. Experimental and clinical studies to elucidate these events should not only provide insights into acute and chronic pathologic tissue damage, but may also lead to the identification of important new targets of pharmacologic intervention.

Angioplasty, Balloon, Coronary↗
PubMed1991

Transcardiac release of leukotriene C4 by neutrophils in patients with coronary artery disease.

Leukotriene C4 is a potent constrictor of smooth muscle in vitro and may induce coronary vasoconstriction in vivo. To study leukotriene C4 release by neutrophils in patients with coronary artery disease, neutrophils were separated from blood samples taken from the coronary sinus and aorta in 20 patients with stable exertional angina and angiographically documented coronary artery narrowings (group I). Eight patients with normal coronary arteries were also studied (group II). To assess leukotriene C4 generation, neutrophils were incubated with calcium ionophore A 23187 (0.25 microM) and the supernatants obtained after centrifugation were analyzed for leukotriene C4 by radioimmunoassay. Patients in group I had a significantly lower release of leukotriene C4 from neutrophils separated from the coronary sinus blood than from those separated from aortic blood (4.33 +/- 0.69 versus 5.92 +/- 0.54 ng/ml, p less than 0.025), whereas patients in group II had a similar release of leukotriene C4 by the neutrophils separated from coronary sinus blood and from aortic blood (6.0 +/- 0.72 versus 6.4 +/- 0.66 ng/ml, p = NS). Moreover, in group I patients, a significant correlation was found (p less than 0.01) between the extent of coronary artery disease (expressed by the Leaman coronary score) and the percent reduction in leukotriene C4 released from neutrophils separated from coronary sinus blood as compared with leukotriene C4 produced by neutrophils separated from aortic blood. These data show that neutrophils from patients with coronary artery disease have a reduced ability to produce leukotriene C4 after stimulation by calcium ionophore A 23187.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Flow cytometry analysis of T cell subsets in skin of patients with specific cutaneous manifestation of B non-Hodgkin lymphoma.

Cutaneous lesions may be the atypical initial manifestation of blood disorder. Monoclonal antibodies identify surface phenotype of lymphocytes present in specific cutaneous lesions. We studied cutaneous infiltrates with flow cytometry in 10 cases of non-Hodgkin lymphoma. We characterized T cell subset in skin immune system. The percentage of T cells was compared to percentage observed in healthy specimens from same patient. T4 cells predominate in cutaneous infiltrates, with an increase in T4/T8 ratio. There was also an increase in T6+ cells, Langerhans cell markers in the skin. HLA-Dr+, T6 cells increased in all cases tested, indicative of dendritic cells. These data showed a modification of T lymphocytes only in skin infiltrate of lymphoma.

CD4-Positive T-Lymphocytes↗
PubMed1990

Peptide opioids and morphine effects on inflammatory process.

Morphine was found to inhibit human granulocyte aggregation and ATP, thromboxane B2 (TxB2), and leukotriene B4 (LTB4) secretion during cell aggregation. None of the opioid peptides tested [(D-Ala2, D-Leu5)-enkephalin (DADL), (D-Ala2, N-Me-Phe4, Gly-ol5)-enkephalin (DAGO) or dynorphin 1-9 (Dyn 1-9)] was capable of mimicking morphine effects, while Dyn 1-9 per se induced TxB2 and LTB4 secretion from granulocytes. Morphine inhibition of both cell aggregation and ATP, but not of arachidonic acid metabolism product secretion, was prevented by naloxone. The naloxone-sensitive impairment by morphine of CD11b-CD18 complex surface expression observed could play a role in opioid inhibition of granulocyte activation.

Adenosine Triphosphate↗
PubMed1990

Increased neutrophil aggregability in coronary artery disease.

The purpose of this investigation was to study neutrophil (PMN) aggregation in the aorta and coronary sinus of 20 patients with angiographically documented coronary artery disease (group I) compared with eight patients with normal coronary arteries (group II). PMNs were separated from the other blood components and their aggregation response to Ca2+ ionophore A 23187 l x 10(-5) M (final concentration) was measured. Group I patients had higher aggregating activity in the coronary sinus than in the aorta (24.9 +/- 3.7 vs 18.7 +/- 3.4 average maximum delta T, P less than 0.01), while no difference was found in group II (coronary sinus 16.7 +/- 3.5; aorta 16.3 +/- 2.4 average maximum delta T P = NS). Among group I patients, smokers had a significantly higher aggregating activity than non-smokers, whereas no correlation was found between aggregation response and blood cholesterol values. These data suggest that the presence of atherosclerotic plaques in coronary vessels may prime PMNs so that they show greater aggregating response to subsequent stimulation.

Aorta↗
PubMed1990

Surface expression of CD11b/CD18 of pseudo-Pelger granulocytes in chronic myeloid leukaemia.

The aim of the present study was to evaluate the surface membrane glycoproteins of pseudo-Pelger granulocytes in six patients suffering from chronic myeloid leukaemia (CML). We studied the functional and immunochemical activities of five monoclonal antibodies (MoAb) minimally reactive with integrin familial antigens of pseudo-Pelger granulocytes. The study conducted with cytofluorimetric and immunological alkaline phosphatase anti-alkaline phosphatase (APAAP) analysis showed a decreased expression of CD11b/CD18 detected by antibodies OKM1, 60.1 and 60.3 (P less than 0.001). Lymphocyte function associated antigen (LFA-1) was expressed in normal amounts in pseudo-Pelger granulocytes. There was decreased expression of CD11b/CD18 in pseudo-Pelger granulocytes with respect to controls (P less than 0.001) after stimulation with formyl-met-leu-phe (FMLP). We conclude that acquired pseudo-Pelger granulocyte dysfunction may be correlated to decrease of surface glycoprotein expression of CD11b/CD18.

Aged↗
PubMed1990

Granulocyte activation after coronary angioplasty in humans.

To determine whether percutaneous transluminal coronary angioplasty (PTCA) would lead to neutrophil activation with subsequent discharge of proteolytic enzymes, like elastase, and oxygen free radicals, like superoxide anion, blood samples were taken from the coronary sinus and aorta in 14 patients with stable angina and one-vessel disease who underwent PTCA. Neutrophils were separated by means of the Ficoll-Hypaque system and were stimulated to detect release of elastase and generation of superoxide anion. Plasma levels of elastase were also measured by an immunoenzymatic method. PTCA was successful in all patients. Plasma elastase levels increased significantly at the end of the procedure compared with pre-PTCA values both in the coronary sinus (from 129.2 +/- 16.6 to 286.6 +/- 39.7 micrograms/l, p less than 0.005) and in the aorta (from 117.4 +/- 13.6 to 258.1 +/- 41.3 micrograms/l, p less than 0.005). On the other hand, superoxide anion released in the supernatants after neutrophil stimulation by phorbol-myristate-acetate decreased after PTCA in the coronary sinus (before PTCA, 60.1 +/- 7.1; after PTCA, 40.7 +/- 6.8 nmol 1 x 10(7) granulocytes/ml/15 min, p less than 0.05), whereas a mild but not significant decrease was observed in the aorta (from 58.3 +/- 10.9 to 55.3 +/- 8.6 nmol 1 x 10(7) granulocytes/ml/15 min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

In vivo and in vitro HeNe laser effects on phagocyte functions.

The goal of this work was to evaluate the effect of helium-neon (HeNe) laser irradiation on immunocompetent cells. We used the in vivo skin window method and in vitro granulocyte function tests. The study of cellular migration showed a marked decrease in vitro and in vivo in a dose-independent manner. Superoxide release was not modified by laser irradiation. The granulocyte's aggregation, when using PHA and PMA, presented a reduction that was statistically very significant, not as a subordinate dose. An increase of the release of ATP was demonstrated only at 4 joules and precedes granulocyte aggregation. When using Ca2+ ionophore A23187 as stimulus, laser irradiation at 1, 2 or 4J did not show any modification of granulocyte aggregation. The monoclonal antibody 60.1, which identifies a membrane antigen fundamental for aggregation and chemotaxis, is expressed in normal amounts on granulocyte membranes both before and after irradiation with a HeNe laser. In fact, Laser irradiation preferentially attacks the area of the cellular centrosome that determines a modification of cellular morphology. The electron microscope and immunofluorescence study with a monoclonal antibody have pointed out a disorganization of the microtubules. The alteration of some of the granulocyte functions is correlated to the damage in the centrioles. The granulocyte mitochondrial system and surface membrane remain intact, and this explains the normal production and release of free radicals. Further experiments are necessary to evaluate the clinical application of lasers in various diseases with immunophagocytic pathogenesis.

Adenosine Triphosphate↗
PubMed1989

Effect of piroxicam therapy on granulocyte function and granulocyte elastase concentration in peripheral blood and synovial fluid of rheumatoid arthritis patients.

The effect of piroxicam therapy (20 mg/day for 15 days) on various polymorphonuclear granulocyte (PMN) responses and on PMN elastase concentration was investigated in nine patients with active rheumatoid arthritis. Peripheral blood and synovial fluid samples were collected before starting therapy and 12 h after the last dose of the drug. All patients were evaluable for peripheral blood analysis and six for synovial fluid analysis. Piroxicam therapy had no effect on PMN random migration and phagocytosis, while it significantly reduced both FMLP-induced aggregation and FMLP-induced chemotaxis. This seems mainly due to an effect on FMLP binding, as no differences were observed after therapy in PMA- and PHA-induced aggregation as well as in serum-induced chemotaxis. In contrast, a marked impairment of NBT test and PMA- and FMLP-induced superoxide anion (O2-) production was found after piroxicam therapy. This effect was as evident in peripheral blood as in synovial fluid PMN. Also, a significant reduction in synovial fluid PMN number and synovial fluid PMN elastase concentration (elastase-alpha 1-proteinase complex) was found after treatment. It is concluded that piroxicam may act at different sites on various PMN responses. Its effect on O2- generation and PMN elastase concentration in synovial fluid may have an important role in reducing destruction of arthritic joint tissue.

Adult↗
PubMed1989

New trends in coronary artery disease: the role of granulocyte activation.

Circulating granulocytes play an important role in microvascular perfusion and organ pathology. Oxygen radicals released by aggregated and activated neutrophils may exacerbate the tissue damage caused by ischemia. We studied neutrophil aggregation and oxygen metabolites release in 16 patients suffering from coronary artery disease and in 6 control subjects in aorta and coronary sinus blood samples. The neutrophil aggregation (P less than 0.01) and oxidase activity (P less than 0.01) are higher in coronary sinus than aorta samples only in the patients with respect to controls. While the superoxide generation is decreased in coronary sinus (P less than 0.05). Our aggregation assay supported the potential role of granulocytes in neutrophil-endothelial interactions and tissue damage, and our results about oxidase activity and superoxide release suggested the potential role for neutrophil-derived oxygen radicals in the pathogenesis of vascular injury in vivo.

Calcimycin↗
PubMed1989

A stereoselective blockade by naloxone of opioid and non-opioid-induced granulocyte activation.

Naloxone was found to prevent both opioid and non-opioid-induced migration of human granulocytes in a stereoselective way. Indeed, besides being able to inhibit morphine-induced migration, (-) but not (+), naloxone isomer proved to abolish either casein, serum of fMLP-induced chemotaxis. It is concluded that opioid-induced modulation of granulocyte migration is likely to be mediated through specific receptors, possibly of the mu type. Moreover, the antichemotactic effect of naloxone suggests an involvement of opioid receptors and/or endogenously released opioids in the mechanism of granulocyte activation by different chemoattractants.

Chemotaxis, Leukocyte↗
PubMed1989

Definition of CD 11a, b, c, and CD 18 glycoproteins on chemotactically deficient granulocyte membranes in patients affected by myeloid disorders.

We studied neutrophil chemotaxis and surface membrane glycoproteins in 12 patients suffering from myeloid disorders with abnormal karyotype using in vitro techniques in all 12. Chromosome studies were also carried out virtually simultaneously. We chose to study only patients showing a deficit of chemotaxis (p less than 0.001). Ten of these patients revealed a clonal chromosome abnormality in most of the leukemic cells. The monoclonal antibody technique using MoAb 60.1, 60.3, 60.5, OKM1, LFA-1 and 9E8 demonstrated normal leukocyte membrane glycoproteins CD 11a, b, c and CD 18 and therefore excludes that an abnormality of these is involved in the pathogenesis of altered leukocyte chemotaxis. No correlation between chemotactic deficit and any specific clonal chromosome abnormality was found.

Anemia, Refractory, with Excess of Blasts↗