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Biomedical subjects

M A Lazzari

Publications and source records attributed to M A Lazzari.

At least 19 recordsLinked to original sources
PubMed1994

Platelet aggregation inhibition by mononuclear leukocytes.

In this study we have investigated the effect of human mononuclear leukocytes (ML) on platelet aggregation. The results obtained demonstrated that coincubation of platelets with nonstimulated ML decreased platelet aggregation induced by collagen or thrombin in a concentration-dependent manner. The inhibitory effect increased with the incubation period of the cells, reaching a plateau at 5 minutes. T and non-T enriched ML suspensions exerted an inhibitory effect similar to the total population of ML. Supernatants from ML or mixed cell suspensions also diminished platelet aggregation. 6-keto PGF1 alpha concentration in the supernatants was less than 10 pg/ml. Hemoglobin, L-arginine and cytochrome C did not modify the antiaggregating activity of ML, whereas superoxide dismutase potentiated the inhibition of aggregation mediated by ML. The inhibitory effect was not modified by monoclonal antibody (MoAb) against the lymphocyte function-associated antigen 1, alpha subunit (LFA-1 alpha) or by a MoAb directed against P-selectin. Our results demonstrated that ML inhibited platelet aggregation, at least partially, by the release of a soluble factor(s) distinct of prostacyclin or nitric oxide. Surface adhesion molecules seem also not to be involved.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Behavior of diluted activated partial thromboplastin time in pregnant women with a lupus anticoagulant.

The present study was developed to verify whether a reduction in phospholipid concentration could increase the activated partial thromboplastin time (APTT) sensitivity to detect lupus anticoagulant (LA) during pregnancy. The authors studied 38 pregnant women (10 normal subjects and 28 patients with associated clinical complications) and 40 nonpregnant control subjects. Tests to detect LA, including APTT, platelet neutralization procedure (standard APTT), the kaolin clotting time, the diluted Russell viper venom test neutralized by lysed platelets, and factor assays, were performed. Positive results were found in 5 of 28 pregnant women with associated clinical complications. The APTT, using three different phospholipid concentrations (standard and more diluted cephalin), was performed on plasma samples and on its 1:1 mixture with normal plasma. The behavior of standard and diluted APTT was similar in negative LA pregnant women and nonpregnant control subjects. The mean values showed nonsignificant differences. Four of five pregnant women with positive LA findings had a prolonged APTT, which was not corrected by the addition of normal plasma using standard conditions. When diluted phospholipids were used, only one of them had a prolonged APTT that was corrected by the addition of normal plasma. Therefore, the highest sensitivity (80%) and specificity (100%) of the APTT to detect LA in pregnant women were obtained using the standard conditions.

Female↗
PubMed1992

A simple enzyme-immunoassay test for von Willebrand factor binding in human arterial subendothelium.

In order to determine the binding of vWF, subendothelium from everted human umbilical arteries was perfused with dialysed serum containing different concentrations of purified vWF using an annular perfusion chamber at a wall shear rate of 1100 sec-1 for 30 min. After perfusion, control (not perfused) and perfused vessel segments were washed and incubated with a diluted rabbit antibody against human vWF. Then the nonbound anti-vWF from both samples were used to determine indirectly vWF by EIA. Although in our experiments normal vWF serum concentrations were not enough to exert vWF binding, a substantial binding could be attained with vWF levels around 2.5 U/ml. To estimate the pre-existing subendothelial vWF amount, three different experiments were developed: a) diluted IgG from a nonimmunized rabbit, b) a diluted rabbit antibody to human vWF, c) PBS-BSA. After washing, vessel segments were incubated with rabbit antibody to human vWF. After incubation, the nonbound anti-vWF was used to determine indirectly vWF by EIA. The results obtained showed that the amount of pre-existing vWF was approximately 1.1x10(-3) U vWF/cm2 subendothelium.

Endothelium, Vascular↗
PubMed1991

Visualization of platelet glycoproteins Ib and IIIa by immunoenzymatic stain using avidin-biotin peroxidase complex.

A method is described here for the identification and quantitation of antigens by monoclonal antibodies. This method is based upon 1) separation (crossed-immunoelectrophoresis) and immunoprecipitation (rocket immunoelectrophoresis and crossed immunoelectrophoresis) of glycoproteins Ib and IIIa with a polyspecific antiserum; 2) binding of the non precipitating monoclonal antibody to glycoproteins precipitated by the rabbit antibody; 3) visualization of the monoclonal antibody with secondary biotinylated antibody and after addition of avidin biotin peroxidase complex, the peroxidase activity is detected by 4-Cl-1-naphtol. By this technique, the agarose gel plate could be stained directly and this allowed us to eliminate electrophoretic transblotting and radioactive compounds.

Animals↗
PubMed1991

Interferon-gamma enhances PAF-acether production by stimulated human polymorphonuclear leucocytes.

Human polymorphonuclear leucocytes (PMN) stimulated with either immune complexes (IC), phorbol myristate acetate (PMA) or N-formyl-methionyl-leucyl-phenylalanine (FMLP) generate platelet-activating factor (PAF-acether). The present study demonstrates that treatment of PMN with recombinant human interferon-gamma (IFN-gamma) significantly enhanced the production of PAF-acether by stimulated cells, in a concentration-dependent mode. On the contrary, alpha and beta IFN were completely unable to increase PAF-acether synthesis by stimulated PMN. The significance of these results is discussed.

Antigen-Antibody Complex↗
PubMed1990

Inhibition of human platelet activation by polymorphonuclear leukocytes.

1. The effect of unstimulated human polymorphonuclear leukocytes (PMNs) on platelet activation was examined. 2. Human platelet aggregation and adenosine 5'-triphosphate (ATP) release induced by collagen (1-2 micrograms ml-1); thrombin (0.01-0.02 u ml-1) or arachidonic acid (AA) (0.1-0.2 mM) were markedly inhibited when conducted in the presence of unstimulated PMNs. 3. Platelet inhibition induced by PMNs was dependent on the number of PMNs and on the incubation time of the mixed cell suspension. 4. Platelet inhibition was not reversed in time when PMNs were depleted from the mixed-cell suspension. 5. PMN-mediated platelet-inhibition was not mediated by AA metabolites, oxygen reactive intermediates, nitric oxide or proteases. 6. The factor(s) accounting for the platelet inhibition mediated by PMNs are not yet characterized.

Adenosine Triphosphate↗
PubMed1989

Hormonal regulation on bioactive aortic substance (BAS) production.

Rat's vessel wall releases a protein named BAS (Bioactive Aortic Substance) whose antiaggregating effect on platelets and inotropy vascular properties have been already described. In this work we have investigated the effects of pregnancy, gonadectomy and gonadectomy with hormonal treatment on the BAS production from rat aortic rings. BAS production in pregnancy and ovariectomized rats was markedly decreased compared to normal rats. Return to normal values was obtained after estradiol treatment in ovariectomized rats. Castration resulted in an increased of BAS production which was suppressed by testosterone treatment.

Animals↗
PubMed1989

The influence of sex and different segments of thoracic aorta on bioactive aortic substance (BAS) and prostacyclin (PGI2) synthesis.

BAS is a protein generated by aortic rings isolated from rats. Our previous results clearly established that BAS inhibits platelet aggregation and modifies vascular tone. We have now examined the effect of separated segments of thoracic aorta and the effect of sex on the release of the BAS and PGI2. We evaluated three different segments of thoracic aorta: A = aortic arch, B = the upper segment and C = the lowest segment of the thoracic aorta. We measured the release of BAS and PGI2 from them. The BAS production increased in the first segment (A) when compared with the other two (B and C), whilst PGI2 production was the same along the thoracic aorta. On the other hand female and male thoracic aorta produced the same levels of BAS and 6-keto PGF1 cm.

Animals↗
PubMed1989

Effect of acenocoumarine on the breast-fed infant.

Apart from teratogenic phenomena and the potential risk of maternal or neonatal peripartum haemorrhage, the use of oral anticoagulants during pregnancy poses an additional hazard: the risk of transferring some anticoagulant activity to the nursing infant through breast milk. We analysed the coagulation status of seven full term breast-fed neonates whose mothers were under chronic anticoagulant therapy with acenocoumarine as thromboembolic prophylaxis following cardiac valve replacement. Prothrombin Times (PT) observed in neonates were significantly higher than the corresponding maternal values. Data were subsequently compared with those obtained from a control group comprising forty-two full term neonates nursed by non-anticoagulated mothers: coagulation profiles again showed no signs of any noticeable antivitamin K effect. Our results indicate that mothers given acenocoumarine at therapeutic doses may safely breast-feed their infants: anticoagulant activity in breast milk seems to be negligible as assessed by neonates PT.

Acenocoumarol↗
PubMed1988

Aspirin effect on the release of plasminogen activator inhibitors by human platelets.

Intrinsic plasminogen activators (PA) were tested in euglobulins (eug) of platelet poor plasma (PPP) with and without washed platelets (WP), treated or not with urokinase (UK), streptokinase (SK), collagen (Col) and aspirin (ASA) using fibrin plates method. A significant decrease of the fibrinolytic activity related to the presence and number of platelets was observed. We confirm the presence of platelet anti-UK and anti-SK activities. The former appears to be higher than the other activity. Low and high concentrations of Col stimulated the release of plasminogen activator-inhibitors (PA-I) from platelets, and ASA could not modify this release. Besides ASA might inhibit some PA release. The high concentration of Col was capable to release anti-UK and anti-SK activities from platelets and perhaps other intrinsic PA-I. The low concentration of Col was only capable to release intrinsic PA-I, suggesting that anti-UK and anti-SK needed a stronger stimuli to be released than intrinsic PA-I. We must consider the possibility that the PA-I and/or activators could be released by different metabolic pathways other than cyclooxygenase pathway.

Aspirin↗