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PubMedDate not supplied

[Usefulness of determining conjugated amine catecholamines in blood platelets for diagnosis of pheochromocytoma].

The studies included 14 patients with pheochromocytoma (mean age 39.5 years), 32 patients with arterial hypertension (mean age 39.5 years), and 9 healthy volunteers (mean age 39.5 years). Free and conjugated noradrenaline and adrenaline in blood platelets have been assayed with RIA technique. It was shown that mean concentrations of conjugated noradrenaline and adrenaline in blood platelets are significantly higher in patients with pheochromocytoma than those in hypertensive patients and healthy individuals. However, such test may be used with limitations as there is high percentage of increased values in patients with the primary arterial hypertension. A decreased noradrenaline inactivation in blood platelets of patients with pheochromocytoma has also been observed. This may exert some effect on the diversified clinical course of this type of arterial hypertension.

Adrenal Gland Neoplasms↗
PubMed1983

Opsonized-zymosan induces a respiratory burst in human blood platelets.

Opsonized-zymosan-stimulated polymorphonuclear cells show a cyanide-insensitive oxygen consumption. We have investigated whether opsonized-zymosan could induce similar metabolic change in human blood platelets. Preparation of intact human blood platelets, obtained by separation through a Ficoll layer (23% w/v) were challenged with opsonized-zymosan. The polymorphonuclear cell contamination was less than 1/10(8) platelets. The opsonized-zymosan-stimulated platelets showed an increase of oxygen consumption. The mean of oxygen burst measured by a polarographic method with a Clark electrode was 11 nmole/10(9) platelets/min (S.E.M. 4; n = 15). The duration of the burst was 2 min. Unstimulated platelets did not show the oxygen burst. The inhibitors of respiratory chain and prostaglandin synthesis completely abolished the oxygen consumption by opsonized-zymosan-stimulated platelets. The simultaneous addition of NADH (1 mM) and opsonized-zymosan induced a burst of oxygen consumption, which occurred after a variable lag phase (10-12 min) from the stimulation, also in the presence of inhibitors. This burst, which lasted about 1 min, amounted to 10 nmole/10(9) platelets/min (S.E.M. 2; n = 15) and it was higher in the presence of NAN3, a catalase inhibitor. Zymosan treated with hydrazine or heated plasma (56 degrees C) did not cause increased oxygen consumption. Inulin or inulin-treated serum did not stimulate platelets. In these experimental conditions some NADH disappeared, as shown by isotachophoresis. The results demonstrated that an immunological stimulus may activate a membrane-linked cyanide-insensitive oxygen metabolizing system.

Blood Platelets↗
PubMed1999

Morphological parameters of blood platelets before and after renal artery embolization in patients with renal cancer.

Embolization consists in the occlusion of renal artery and its ramifications, which induces acute renal infarction. Renal artery embolization, causing necrosis, stimulates cellular reactions within and around the neoplasm. The interaction of neoplastic cells with blood platelets is of great importance in the development of neoplastic disease. Neoplastic cells exert a stimulatory effect on blood platelets. During activation, platelets change in shape and secrete certain substances. The aim of the present study was to evaluate morphological parameters of blood platelets in renal cancer patients before and after renal artery embolization. 45 patients suffering from renal cancer were examined (22 women and 23 men) before and after embolization. Diagnosis was established basing on the patients' history, clinical picture, and ultrasonographic, urographic and angiographic examinations. Tumour advancement was defined as T2 and T3. The study has demonstrated that embolization leads to an increase in platelet count and in the percentage of "megathrombocytes". The changes observed in the study may indirectly testify to the involvement of the thrombopoietic system in the course of neoplastic disease.

Adult↗
PubMed1987

An in vitro study of the adhesion of blood platelets onto vascular catheters. Part I.

The adhesion of human blood platelets onto vascular catheters was studied using a specially designed perfusion chamber. Polyurethane catheters were exposed to citrated human blood for different periods (up to 20 min) and at different wall shear rates (190, 260, 330 sec-1). The rate of platelet adhesion was determined using 111In-labeled platelets, while the morphology of adhering platelets was investigated using scanning electron microscopy. A linear increase in platelet adhesion was found within the first 10 min of perfusion, after which a plateau value was reached. The number of adhering platelets did not vary significantly with the shear rates applied, which may indicate that within the range of shear rates studied, the adhesion of platelets onto the catheter surface is mainly determined by the rate of the reaction between the platelets and the material surface. Catheters coated with a conjugate of heparin and albumin showed a four- to five-fold reduction in platelet adhesion as compared to uncoated catheters. This reduction in platelet adhesion was not only due to the presence of albumin moieties at the surface but also to the presence of heparin residues in the adsorbed albumin-heparin conjugate.

Albumins↗
PubMed2000

Adhesion of blood platelets to collagen and fibrinogen after treatment with cisplatin and its complex with glutathione.

Cisplatin (cis-diamminedichloroplatinum II, CDDP) is one of the most widely used chemotherapy drugs. Unfortunately, it induces serious side effects such as haematological toxicity. The aim of the present study was to evaluate the effect of CDDP on the first step in blood platelet activation-platelet adhesion, induced by thrombin or adenosine diphosphate (ADP), to collagen and fibrinogen. The action of cisplatin was compared with the action of cisplatin glutathione complex (GS-Pt) on platelet adhesion and on free radical generation measured by chemiluminescence. Pretreatment of blood platelets with cisplatin (0.1-20 microM) caused a dose- and time-dependent reduction of platelet adhesion to collagen and fibrinogen (p <0.05). The GS-Pt complex (20 microM, 30 min) had a stronger inhibitory effect on this process. Moreover, the complex (R2 = 0.992; p <0.05) also stimulated the chemiluminescence of blood platelets to a greater extent than CDDP alone (R2 = 0.999; p <0.01). The results suggest that inhibition of platelet adhesion in the presence of cisplatin and its complex with glutathione correlates with the generation of reactive oxygen species in these cells.

Animals↗
PubMed1986

Characterization of two murine monoclonal antibodies (P10, P12) directed against different determinants on human blood platelet thrombospondin.

Thrombospondin, a 450-kDa glycoprotein composed of three disulphide linked chains, is located in human blood platelet alpha-granules and is released from platelets upon stimulation. This glycoprotein is thought to play a major role in platelet aggregation. The aim of this study was to characterize two monoclonal antibodies (P10 and P12) directed against human blood platelet thrombospondin. When the released material obtained after stimulation of platelets with thrombin in the presence of 2 mM calcium was immediately treated with EDTA, labelled with 125I and incubated with monoclonal antibodies P10 and P12, both immunoprecipitated a major labelled protein band with a molecular mass of 160 kDa and a weaker band at 146 kDa, as analysed on reduced dodecyl sulphate/polyacrylamide gels. The major band corresponds in molecular mass to the thrombospondin subunits. If, however, the released material was left in the presence of Ca2+ for 48 h, then the main band was at 130 kDa and in addition one minor protein band (75 kDa) was immunoprecipitated by P10 whereas P12 recognized two minor protein bands (75 and 60 kDa). When P10 and P12 were incubated with 125I-labelled platelet releasates treated for 48 h at 4 degrees C with 10mM EDTA, three major protein bands (160, 146 and 130 kDa) were immunoprecipitated in addition to the minor bands mentioned above. These results indicate that thrombospondin is probably degraded by the endogenous platelet calcium-dependent protease. Investigation of tryptic peptide fragments of thrombospondin isolated by fast protein liquid chromatography showed that 125I-labelled antibody P10 bound to 400-kDa and 120-kDa fragments whereas 125I-labelled P12 only recognized a 400-kDa fragment. Competition studies involving solid-phase antibody binding and double antibody sandwich assays showed that P10 and P12 were directed against different determinants of thrombospondin. Purified thrombospondin, isolated in the presence of calcium, either directly or after treatment with EDTA, haemagglutinated trypsinized, formaldehyde-fixed sheep erythrocytes identically. The haemagglutination activity of EDTA-treated thrombospondin was inhibited by P10 and enhanced by P12. On the other hand, P10 and P12, despite their binding to calcium-treated thrombospondin, had no effect on its haemagglutination activity. Monoclonal antibodies P10 and P12 could be useful tools to investigate the role of thrombospondin in platelet aggregation.

Antibodies, Monoclonal↗
PubMed1993

Characterization of an ATP diphosphohydrolase activity (APYRASE, EC 3.6.1.5) in rat blood platelets.

In the present report we describe an apyrase (ATP diphosphohydrolase, EC 3.6.1.5) in rat blood platelets. The enzyme hydrolyses almost identically quite different nucleoside di- and triphosphates. The calcium dependence and pH requirement were the same for the hydrolysis of ATP and ADP and the apparent Km values were similar for both Ca(2+)-ATP and Ca(2+)-ADP as substrates. Ca(2+)-ATP and Ca(2+)-ADP hydrolysis could not be attributed to the combined action of different enzymes because adenylate kinase, inorganic pyrophosphatase and nonspecific phosphatases were not detected under our assay conditions. The Ca(2+)-ATPase and Ca(2+)-ADPase activity was insensitive to ATPase, adenylate kinase and alkaline phosphatase classical inhibitors, thus excluding these enzymes as contaminants. The results demonstrate that rat blood platelets contain an ATP diphosphohydrolase involved in the hydrolysis of ATP and ADP which are vasoactive and platelet active adenine nucleotides.

Adenosine↗
PubMed1982

Hydrogen peroxide release from human blood platelets.

The release of hydrogen peroxide from human blood platelets after stimulation with particulate membrane-perturbing agents has been determined by fluorescence using scopoletin as the detecting agent. Platelet suspensions containing less than 1 polymorphonuclear leukocyte/10(8) platelets showed a significant release of hydrogen peroxide (6.11 nmol/10(9) platelets per 20 min, S.D., 0.26, n = 9) after addition of zymosan or latex particles, compared to unstimulated platelets. The release of hydrogen peroxide was only observed when the scopoletin was added to the platelet suspensions during the stimulation. Any attempt to determine hydrogen peroxide release in the supernatant at the end of the incubation with zymosan or latex failed. A NADH-dependent production of hydrogen peroxide was observed by measuring the difference of oxygen uptake in the presence and absence of catalase (500 units), which was not inhibited by potassium cyanide (1 mM). By this method the NADH-dependent cyanide-insensitive peroxide production and release was 6.0 nmol/10(9) platelets per 20 min from resting platelets (S.D., 2, n = 6) vs 15 nmol/10(9) platelets per 20 min from stimulated platelets (S.D., 2, n = 6).

Blood Platelets↗
PubMed1975

The effect of ADP, calcium and some inhibitors of platelet aggregation on protein phosphokinases from human blood platelets.

A protein phosphokinase (ATP: protein phosphotransferase EC 2.7.1.37) which is stimulated by 3',5'-cyclic adenosine monophosphate (cyclic AMP) has been partially purified from both the cytoplasmic and membrane fractions of human platelets. The kinetics of both enzymes preparations are similar in respect to cyclic AMP, ATP, ADP and AMP. 5-10-minus 7 M cyclic AMP stimulated both preparations by approximately 100%. Both ADP and AMP at a concentration of 5-10-minus 5 M inhibited protein phosphokinase activity of the soluble and membrane preparation by between 50% and 70%. The response of the two enzyme preparations to calcium differed. 10 mM Ca-2+ inhibited soluble protein phosphokinase activity approximately 80% both in the presence and absence of 5-10 minus 7 M cyclic AMP whereas the same concentrations of Ca-2+ inhibited the membrane-bound enzyme by approximately 60% in the presence of 5-10-minus 7 M cyclic AMP and 40% in the absence of cyclic AMP. This observation may be of importance in understanding the mechanism of platelet aggregation.

Adenosine↗
PubMed1979

Decreased uptake of 5-hydroxytryptamine in blood platelets from patients with endogenous depression.

5-Hydroxytryptamine (5-HT) uptake was studied by using blood platelets from 13 patients with endogenous depression (Hamilton rating scale 33 +/- 7) and 13 healthy volunteers. An improved method with a short incubation time and low substrate concentration was used, and the incubation was performed in Krebs-Henseleit buffer (pH 7.4) at 37 degrees C. A clear difference in 5-HT uptake by blood platelets was noted: The Vmax of the reaction in patients was 39, and in controls 71 pmol per 2 x 10(7) platelets in 5 min. There was no significant difference in the Km. After a 4-week treatment with imipramine, a competitive inhibition of 5-HT uptake with an increased Km was seen; after a similar treatment with amoxapine there was little change in 5-HT uptake. Amoxapine was inferior to imipramine as an inhibitor of 5-HT uptake, also in vitro. There was no difference in clinical recovery in these treatment groups. These results may be of importance so as to understand the potential biological differences between depressed patients and normal persons.

Adult↗
PubMedDate not supplied

The effect of verapamil on serotonergic mechanisms in the rat blood platelets.

Verapamil in vitro inhibits the uptake and enhances the release of the labeled serotonin from the rat blood platelets. It also inhibits the facilitating action of serotonin on the aggregation response of platelets stimulated by ADP. The obtained results indicate that verapamil significantly influences serotonergic mechanisms in the blood platelets, at least in the rat.

Animals↗
PubMed1979

A study of assay conditions for palmitoyl-CoA synthetase and carnitine palmitoyltransferase in homogenates of human blood platelets.

The assay conditions for palmitoyl-CoA synthetase (P-CoA S) and carnitine palmitoyltransferase (CPT) in homogenates of human blood platelets have been studied. The assay based on trapping of palmitoyl-CoA by carnitine in the presence of exogenous CPT gave higher activity of P-CoA S than the assay based on direct isolation of the palmitoyl-CoA formed. The activity of CPT was higher on exogenous palmitoyl-CoA than on endogenous palmitoyl-CoA formed from palmitic acid and CoA in the presence of endogenous P-CoA S. The activity of CPT was strongly dependent on the incubation time and the amount of platelets used. The initial activity of this enzyme in human blood platelets was higher than previously assumed.

Acyltransferases↗
PubMed1976

Separation of anti-Ia (I-region associated antigens) from anti-H-2 antibodies in complex sera, by absorption on blood platelets. description of three new Ia specificities.

H-2 antigens are expressed in substantial amounts of murine blood platelets (for H-2 antigenic content 1 lymphocyte approximately 50 platelets) whereas Ia antigens are probably not expressed at all (minimal Ia antigenic content more than 35 times lower than for H-2). This property of blood platelets makes them very useful for the selective absorption of anti-H-2 antibodies from complex sera and for the preparation of specific anti-Ia antibodies from such sera. In 20 sera produced against the complete H-2 complex, 12 sera contained anti-Ia antibodies beside the expected anti-H-2 antibodies. In two sera, separation of the anti-Ia antibodies was easily obtained by absorption of the anti-H--2 antibodies on platelets. The analysis of one serum (C3H.Q X B10.D2) anti-C3H [(q X d) anti-k] showed that, in addition to be expected anti-H--2.23 and anti-Ia.2 antibodies, it contained at least three other Ia antibodies, separable by absorption on lymphocytes, which recognized three antigens--Ia.17, determined by the haplotypes k, f, s, r, j; Ia.18, determined by the haplotypes k, f, s; and Ia.19 determined by the haplotypes k and r. The genes are located in the I--A and/or I--B subregions of the H--2 complex.

Absorption↗
PubMedDate not supplied

Lack of the specific influence of histamine and histamine H1, H2 and H3 receptor ligands on the serotonin uptake and release in rat blood platelets.

This work was designed to investigate the influence of histamine, and H1 receptor agonist 2-(2-thiazolyl)ethylamine, H2 receptor agonist dimaprit and H3 receptor agonist R-(-)-alpha-methylhistamine on the serotonin uptake and release in rat blood platelets. Histamine and R-(-)-alpha-methylhistamine (up to 1 mmol/l), 2-(2-thiazolyl)ethylamine (up to 10 mumol/l) and dimaprit (up to 1 mumol/l) failed to affect the serotonin uptake. The concentration-dependent inhibitory effects of higher concentrations of 2-(2-thiazolyl)ethylamine and dimaprit (up to 1 mmol/l) were not diminished by the H1 receptor antagonist dimetindene and the H2 receptor antagonist ranitidine (1 and 100 mumol/l each), respectively. Histamine, 2-(2-thiazolyl)ethylamine, dimaprit and R-(-)-alpha-methylhistamine (up to 10 mumol/l) did not change the serotonin release from rat blood platelets. Our results demonstrate that histamine and histamine H1, H2 and H3 receptor agonists do not affect in a specific manner the serotonin uptake and release in rat blood platelets.

Animals↗