PubMed Health⌕ Search

Biomedical subjects

C L Balduini

Publications and source records attributed to C L Balduini.

At least 19 recordsLinked to original sources
PubMed1995

Ristocetin-induced platelet agglutination stimulates GPIIb/IIIa-dependent calcium influx.

We found that intracellular Ca2+ concentration ([Ca2+]i) increased during ristocetin-induced agglutination of aequorin loaded platelets resuspended in plasma. Chelation of extracellular Ca2+ had no effect on platelet clumping, but delayed and greatly reduced Ca2+ increase, indicating that it derived for the most part from Ca2+ influx. Nine monoclonal antibodies (MA) against glycoprotein (GP) Ib largely prevented ristocetin-induced platelet clumping and [Ca2+]i increase, while three anti-GPIb MA with no effect on platelet clumping did not interfere with Ca2+ movement. In unstirred samples platelet agglutination was greatly reduced and [Ca2+]i increase was abolished, suggesting that close platelet-to-platelet contact, in addition to von Willebrand factor (vWF) binding to GPIb, is necessary for Ca2+ transient. Nine MA against GPIIb/IIIa, the gly-arg-gly-asp-ser (GRGDS) peptide and GPIIb/IIIa complex dissociation had no effect on platelet agglutination, but significantly reduced Ca2+ increase. Our results suggest that platelet clumping induced by vWF binding to GPIb is responsible for GPIIb-IIIa dependent Ca2+ influx.

Blood Platelets↗
PubMed1993

Acquired cyclic thrombocytopenia-thrombocytosis with periodic defect of platelet function.

A periodic fall of platelet number characterizes an acquired pathological condition named cyclic thrombocytopenia. We observed a patient in whom the episodes of thrombocytopenia (platelet number less than 50 x 10(9)/l) were followed regularly by thrombocytosis (700-2300 x 10(9) platelets/l). The period of platelet count fluctuation was about 40 d. Morphological examination of bone marrow showed the cyclic disappearance of mature and immature megakaryocytes; bone marrow cultures revealed a periodic severe defect of both multilineage and single-lineage progenitor cell growth. When platelet count was falling, a mild defect of platelet aggregation and ATP release was observed, while platelet function was normal when platelet count was rising. Prednisone, thymopentin, high-dose intravenous gamma-globulin and splenectomy were without effect. After 4 years of cyclic platelet and megakaryocyte fluctuations, stable amegakaryocytic thrombocytopenia developed and the patient died of haemorrhagic stroke.

Adult↗
PubMed1992

Defect of platelet aggregation and adhesion induced by autoantibodies against platelet glycoprotein IIIa.

A young patient developed chronic idiopathic thrombocytopenic purpura. Prednisone therapy normalized platelet number, but bleeding symptoms did not disappear. Platelet function was severely impaired, since platelet aggregation, ATP release and adhesion to collagen and subendothelial matrix were significantly reduced. Plasma and purified immunoglobulins of the patient reproduced the functional defects in normal platelets. Immunoblotting revealed that patient's plasma contained an antibody reacting with a component of platelets with the same electrophoretic mobility of glycoproteins IIIa of normal platelets. Moreover, patient's plasma inhibited the binding of an anti-GPIIb/IIIa monoclonal antibody to platelet surface. Additional immunosuppressive therapy with prednisone and azathioprine normalized platelet function and induced the disappearance of bleeding symptoms.

Adult↗
PubMed1992

Platelet function after in vivo and in vitro treatment with thrombolytic agents.

Whereas in vitro studies showed that plasmin may induce both inhibition and activation of platelets, in vivo and ex vivo investigations suggested that thrombolytic agents are responsible for platelet stimulation. To gain further information on this topic, ex vivo platelet function was studied in 24 subjects with acute myocardial infarction treated with streptokinase or recombinant tissue-type plasminogen activator (rt-PA). Ten patients with acute myocardial infarction who did not receive thrombolytic treatment were also investigated. The data shows that at the end of thrombolytic infusion, the maximal extent of platelet aggregation and adenosine triphosphate release was reduced in treated patients compared with that in untreated ones. In subjects treated with streptokinase, the defect in platelet aggregation derived from both cellular and plasmatic defects. Plasmatic beta-thromboglobulin concentration was significantly reduced after streptokinase, but unchanged after rt-PA. Three days after thrombolytic treatment, platelet aggregation of patients receiving streptokinase or rt-PA was not significantly different from that of untreated subjects. A similar defect in platelet function was obtained in vitro, incubating normal platelet-rich plasma with pharmacologic concentrations of streptokinase. Again, platelet function defect derived from both cellular and plasmatic damages. It cannot be excluded that platelet activation occurs in patients with acute myocardial infarction during the very early phases of thrombolytic treatment. However, it is suggested that a transient defect in platelet function follows both streptokinase and rt-PA infusion.

Adenosine Triphosphate↗
PubMed1991

Platelet aggregation in platelet-rich plasma and whole blood in 120 patients with myeloproliferative disorders.

In vitro platelet aggregation in platelet-rich plasma (PRP) and in whole blood (WB) was assessed in 31 patients with idiopathic myelofibrosis, 32 with essential thrombocytosis, 23 with polycythemia vera, and 34 with chronic myelogenous leukemia. In PRP most subjects showed normal or reduced platelet aggregation, whereas in WB the majority of patients showed increased platelet function. Spontaneous platelet aggregation (SPA) was observed frequently in WB, whereas it was seldom observed in PRP. SPA in WB was inhibited by in vitro addition of aspirin and apyrase, and SPA was only partially dependent on high platelet count because it also occurred in samples with normal platelet content (at variance with 13 subjects with reactive thrombocytosis, in which SPA was observed only in samples with high platelet concentration). Platelets from patients with idiopathic myelofibrosis had the highest tendency to undergo SPA.

Adenosine Diphosphate↗
PubMed1988

Interrelation of platelet aggregation, release reaction and thromboxane A2 production.

Aggregation of platelets, stimulated by different agonists, was inhibited by omitting sample stirring or by preincubation of platelets with a monoclonal antibody against glycoproteins IIb-IIIa or with a pentapeptide containing the sequence Arg-Gly-Asp-Ser. In platelets stimulated by collagen, ADP and epinephrine, the inhibition of aggregation paralleled a reduction of both release reaction and thromboxane A2 formation. When thrombin was the stimulus, ATP release and thromboxane A2 production were unaffected (or only slightly modified) by the inhibition of platelet aggregation. These data add further evidence to the hypothesis that aggregation supports the activation of platelets stimulated by weak agonists.

Adenosine Diphosphate↗
PubMed1988

Effect of GPIIb-IIIa complex ligands on calcium ion movement and cytoskeleton organization in activated platelets.

We studied the influence of the occupancy of the fibrinogen receptor (GP IIb-IIIa complex) on two early aspects of agonist induced platelet activation: the increase of the intracellular Ca2+ concentration and the cytoskeleton reorganization. A monoclonal antibody, a peptide containing the RGD sequence and fibrinogen purified from human plasma were used as GP IIb-IIIa ligands. The obtained results demonstrated that fibrinogen receptor occupancy inhibits Ca2+ movement and cytoskeleton reorganization caused by low thrombin concentration and ADP.

Adenosine Diphosphate↗
PubMed1988

Platelet aggregation in platelet rich plasma and whole blood in 18 patients affected by idiopathic myelofibrosis.

Platelet aggregation in whole blood (WB) and in platelet rich plasma (PRP) was studied in 18 consecutive patients affected by idiopathic myelofibrosis (IM). On the basis of WB studies, 22% of patients were classified as normo-aggregating and 22% as hypo-aggregating, while 55% had spontaneous platelet aggregation (SPA). SPA was observed also when platelets from patients were stirred in the presence of normal erythrocytes, while it never occurred when normal platelets were stirred in the presence of red cells from patients. PRP studies revealed that 33% and 66% of patients were, respectively, hypo- and normo-aggregating. The most frequent abnormality in PRP was represented by defective or absent aggregation response to epinephrine.

Adenosine Diphosphate↗
PubMed1988

The effect of red cells on platelet aggregation: a study with the electronic whole blood aggregometer.

Platelet aggregation was studied in the same platelet rich plasma (PRP) by the simultaneous use of Born's optical method and Cardinal's electronic method. The maximum rate of impedance change (electronic method) correlated well with both the rate and the extent of aggregation as measured by the optical method. The rate of impedance change was therefore the parameter chosen for the study of the effect of red cells on platelet aggregation. Erythrocytes, both at 40 and 60% haematocrit (Hct.), greatly inhibited platelet aggregation induced by ADP and adrenalin, but only minimally affected platelet aggregation induced by collagen.

Electronics↗
PubMed1987

Severe platelet dysfunction in a patient with autoantibodies against membrane glycoproteins IIb-IIIa.

A young women affected by Hodgkin's disease developed chronic autoimmune thrombocytopenic purpura. Splenectomy induced normalization of her platelet count, but hemorrhagic symptoms did not disappear. The patient's platelets did not aggregate in response to collagen and ADP and the IgG fraction of the patient's plasma induced the same defect in normal platelets. The women's IgG recognized glycoproteins IIb and IIIa of normal platelet membranes. Prednisone therapy induced the disappearance of bleeding symptoms and the normalization of platelet aggregation.

Adult↗