[RECENT ACQUISITIONS CONCERNING THE BLOOD PLATELETS].
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Blood Platelet Disorders↗
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[Morphologic parameters of blood platelets and dysmorphic erythrocyturia in chronic glomerulonephritis].
Dysmorphic erythrocyturia is known as an attribute of glomerular bleeding. During chronic glomerulonephritis the morphological changes of blood platelets were also observed. The subject of our study was to indicate if the common mechanism leading to blood platelets polymorphology and dysmorphic erythrocytes origination in chronic glomerulonephritis is possible. We estimate the count of blood platelets (PLT), mean platelets volume (MPV), platelet distribution weight (PDW) and platelets crit (PCT) in peripheral blood of 46 patients with chronic glomerulonephritis with dysmorphic erythrocyturia (26 with renal sufficiency and 20 with renal insufficiency) and 32 healthy volunteers. The dysmorphic erythrocyturic erythrocytes were examined in first morning urine. We have not demonstrated the correlation of changes in blood platelets morphology with percent dysmorphic erythrocytes in urine. The results of our investigations do not confirm exactly the common mechanism of the morphological changes which were observed. Minimal changes of the blood platelets parameters may be the results of changes in structure of phospholipids platelets membrane as well as less activation of platelets membrane receptors-GP Ia/IIb and GP Ic/IIa.
Adult↗
The effects of aspirin and paracetamol on the aggregation of equine blood platelets.
The responses of equine blood platelets in citrated platelet-rich plasma to arachidonic acid, U44069 (prostaglandin endoperoxide analogue), adenosine 5'-diphosphate, platelet-activating factor or collagen were investigated by turbidimetric aggregometry. Pre-treatment of the platelets with aspirin (1 mmol/l) or paracetamol (1.3 mmol/l) abolished shape change and aggregation in response to arachidonic acid; decreased the rate of aggregation in response to collagen, with no separate effect on shape change; had no marked effect on aggregation caused by the other agonists; but in no case transformed irreversible aggregation to reversible aggregation. We conclude that thromboxane A2 generation is of minor importance in the aggregation of equine platelets, and in particular that thromboxane A2 is not a significant mediator of irreversible aggregation.
Acetaminophen↗
Reassessment of elevated serotonin levels in blood platelets in early infantile autism.
Blood platelet serotonin content was measured in 30 children with early infantile autism, as defined by Kanner, 30 age-matched normal subjects, and 45 children with various neurological and psychiatric disorders. Serotonin content in the autistic group was 980 +/- 357 ng/mg platelet protein (mean +/- standard deviation), a value significantly higher than that for normal children, 807 +/- 202 ng/mg (p less than .025). Autistic children under school age had higher platelet serotonin concentrations than other older autistic individuals. There was little correlation between age and serotonin levels in the normal children. Elevated serotonin was also seen in some of the non-autistic pathological group, who were disturbed and hyperactive. Elevated serotonin levels are not necessarily a specific biochemical finding for autistic children, but seem to be due to their behavioral distinction.
Autistic Disorder↗
Antioxidative enzymes activities and lipid peroxidation indicators in blood platelets during bed rest.
Our investigations were carried out on blood platelets obtained from 52 males, aged 25-48, free from any systemic disease, hospitalized because of extremities inferioris fractures without clinical complications. The effect of immobilization on oxygen metabolism and function of human blood platelets was studied. Blood was taken from patients after 14, 28 and 90 days of bed rest and platelets were isolated by a differential centrifugation technique. The comparative control group consisted of 41 healthy individuals at their normal physical activity. Short and long term bed rest had different effect on estimated enzymes activities: SOD-1, GPx-SH, Ct (and lipid peroxidation indicators) (MDA-and TXA2). After 14 and 28 days, the enzyme activities significantly decreased, whereas MDA and TXA2 concentrations increased. It was also found that a 14 and 28-day immobilization increased the blood platelets aggregation. However, after 90 days the tendency towards normalization of all the estimated parameters was observed.
Adult↗
Inhibition of prostaglandin E1-induced activation of adenylate cyclase in human blood platelet membrane.
Activation of human blood platelet adenylate cyclase is initiated through the binding of prostaglandin E1 to the membrane receptors. Incubation of platelet membrane with [3H]prostaglandin E1 at pH 7.5 in the presence of 5 mM MgCl2 showed that the binding of the autacoid was rapid, reversible and highly specific. The binding was linearly proportional to the activation of adenylate cyclase. Although the membrane-bound radioligand could not be removed either by GTP or its stable analogue 5'-guanylylimido diphosphate, 150 nM cyclic AMP displaced about 40% of the bound agonist from the membrane. Scatchard analyses of the binding of the prostanoid to the membrane in the presence or absence of cyclic AMP showed that the nucleotide specifically inhibited the high-affinity binding sites without affecting the low-affinity binding sites. Incubation of the membrane with 150 mM cyclic AMP and varying amounts of prostaglandin E1 (25 nM to 1.0 microM) showed that the percent removal of the membrane-bound autacoid was similar to the percent inhibition of adenylate cyclase at each concentration of the agonist. At a concentration of 25 nM prostaglandin E1, both the binding of the agonist and the activity of adenylate cyclase were maximally inhibited by 40%. With the increase of the agonist concentration in the assay mixture, the inhibitory effects of the nucleotide gradually decreased and at a concentration of 1.0 microM prostaglandin E1 the effect of the nucleotide became negligible. These results show that cyclic AMP inhibits the activation of adenylate cyclase by low concentrations of prostaglandin E1 through the inhibition of the binding of the agonist to high-affinity binding sites.
Adenylyl Cyclases↗
[The blood platelets in parasitic diseases].
Parasitic invasions are the source of foreign antigens and exotoxins which trigger local or systemic inflammatory processes. Antibody-dependent cellular toxicity is the major antiparasitic defensive mechanism, with eosinophils as the effector cells. Macrophages, neutrophils and platelets develop the cytotoxic activity against antibody-coated parasites. Blood platelets participate in various stages of blood clotting, in sclerosis, coronary disease, neoplasms, inflammatory processes and in allergic and immune reactions. Blood platelets actively participate in defense mechanisms of the organism, e.g. in antiparasitic immunology. Platelet stimulation may be a result of direct contact with parasite, increase IgG and/or IgE concentration, the presence of complement components, CRP or lymphokins. Blood platelets reveal cytotoxic activity through release various inflammatory mediators, phagocytic activity and cooperation with other cells of immunologic system.
Animals↗
Fibrin-blood platelet interaction in a contracting clot.
The interaction of fibrin and blood platelets was studied by measuring tension development in clots containing different ratios of these two components. Isometric tension attained a saturation value (MT) when plotted as a function of the concentration of either component at a constant concentration of the other. The value of MT increases linearly with the minimal platelet concentration (Ps) required in order to reach saturation at various different fibrin concentrations. A linear relationship also holds in a plot of Ps versus the logarithm of the corresponding fibrin concentration. When the cylindrical clots contracted isotonically, the velocity, normalized with respect to the momentary length, was found to be constant. This velocity decreased in an hyperbolic manner with increasing fibrin concentration at a constant concentration of blood platelets. The results are interpreted in terms of a three-dimensional network in which the blood platelets serve as contractile cross-bridges connecting fibrin fibres. Tension development is assumed to be accompanied by the reduction of the angle between fibrin fibres. An attempt was made to calculate the isometric tension developed by a platelet.
Blood Coagulation↗
Monoamine oxidase activity in blood platelets from manic and depressed patients.
To evaluate the possible abnormality in MAO activity in affective disorders, blood platelet samples were obtained from 80 patients with mania and depression. Blood-platelet MAO activity was measured by a newly developed assay procedures using serotonin as substrate. MAO activities in 121 normal adult subjects were in a range of 2.49-12.05 nM/mg protein/hour, with the mean values of 4.91 +/- 1.72 (+/-S.D.) for men and 6.88 +/- 1.99 for women. (p less than 0.001) MAO activities in the manic and depressed patients were in a range of 0.65-13.40 nM/mg protein/hour, and both manic and depressed patients showed the mean value very familiar to that in the normal subjects. Bipolar depressed patients did not exhibited lower MAO activity in the blood platelets than other clinical subtypes of depressive illness, including unipolar, involutional, neurotic and chronic characterological, and first-episode depression. No significant differences were established between these five subcategories of depression, while significant higher values were evident in female than male patients (p less than 0.001). No correlation was found between the MAO activity and serotonin levels in the blood platelets either in the normal subjects or in the depressed patients.
Adolescent↗
Inhibition of activated blood platelets by interferon alpha 2b in chronic hepatitis C.
BACKGROUND/AIMS: Interferon alpha used in treatment of chronic hepatitis C significantly influences the blood platelets. The role of platelets in initiating and developing pathological processes in hepatic diseases is still barely known. We studied the effects of interferon alpha 2b (IFN alpha2b) on blood platelets in chronic hepatitis C. METHODOLOGY: The studies were conducted in 16 patients who underwent IFN alpha2b treatment 3 times a week at 6MU. The examination was carried out before and on the 14th day of the treatment of IFN alpha2b. Morphological parameters of blood platelets were determined by hematological methods and flow cytometry. Expression of receptors on blood platelet surfaces (CD41, CD42a, CD62P) and thrombopoietin, platelet-derived growth factor, soluble form sP-selectin, IL-6, and tumor necrosis factor alpha were also determined. RESULTS: The use of IFN alpha2b in patients with chronic hepatitis C significantly effects blood platelets morphology by causing the decrease in their number, the change in population size, and the increase in large platelet count. Interferon decreases P-selectin expression on platelets, sP-selectin and platelet-derived growth factor concentration in plasma. During interferon therapy we noted increase concentration of thrombopoietin, tumor necrosis factor alpha, IL-6 in chronic hepatitis C. CONCLUSIONS: IFN alpha2b stabilizes activated platelets and probably decreases their participation in inflammatory and fibrotic processes in the liver.
Adult↗
[History of blood platelets: from "molecules" to "cell"].
Historical annotations attached to the discovery of platelets as blood cells throughout the 19th century are reported. The so-called "minute molecules" were first connected with the formation of red and white blood cells, or of fibrin as well. The active role of platelets in coagulation was recognized only 30 years later. During that time, it became clear that these "molecules" were "cells", anatomical and physiological entities.
Bibliographies as Topic↗
Phagocytic and bactericidal activity and morphological parameters of blood platelets in patients with Trichinella spiralis infection.
PURPOSE: The production of IgE increases in parasitic invasions, triggering local or systemic inflammatory response with the involvement of blood platelets. The aim of the study was to assess the number and morphological parameters of blood platelets as well as their phagocytic and bactericidal activity in patients with Trichinella spiralis infection. It is interesting to investigate the blood platelet response following Trichinella spiralis in order to elucidate possible effects on non-specific immunity. MATERIAL AND METHODS: Twenty-six patients with Trichinella spiralis (before and after antiparasitic therapy) and forty healthy subjects were examined. The platelet count and morphological parameters were determined using a hematologic analyzer Technicon H-1 System. The platelet phagocytic activity was determined by measuring the percentage of phagocytizing cells and the phagocytic index. The bactericidal activity was assessed measuring the percentage of the bacteria killed by platelets and plasma. The strain Staphylococcus aureus ATCC 6538P was used for this purpose. RESULTS: In patients infected with T. spiralis morphological parameters do not change, except for the percentage of large platelets. In the course of trichinellosis the phagocytic index of platelets is statistically significantly decreased and platelet bactericidal activity is impaired, while the bactericidal activity of the plasma is statistically significantly increased, compared to healthy subjects. CONCLUSIONS: The present study has revealed that due to T. spiralis infection, the percentage of large, young blood platelets is decreased. The parasitic infection causes impairment of non-specific immunity through decreased bactericidal activity of blood platelets.
Adult↗
Anti-inflammatory effects of blood platelets in the rat.
A selective accumulation of blood platelets occurs at the sites of intradermal injection of zymosan and carrageenan in the rat. The inflammatory response to zymosan, assessed by the local accumulation of systemic radioactive human serum albumin, was significantly enhanced in platelet-depleted rats. Similar enhancements of the paw oedemas, caused by the subplantar injection of either carrageenan or zymosan, were also observed in thrombocytopenic animals. It is concluded that blood platelets may exert protective, i.e., anti-inflammatory, effects in some models of acute inflammation in the rat.
Animals↗
The significance of malate dehydrogenase isoenzymes in human blood platelets.
Two MDH isoenzymes were detected in the homogenate of normal human blood platelets. According to their properties the cationic isoenzyme is compartmentalized in the mitochondria, the anionic one belongs to the cytoplasma. In spite of the few mitochondria in human blood platelets the proportion of the cationic enzyme is relatively high. Both of these enzymes could belong to a transfer system for malate transport across the mitochondrial membrane. As human blood platelets do not contain creatine phosphate a system like that could be of significance for platelet function.
Blood↗
Effects of cisplatin and selenite on the level of thiols in pig blood platelets.
The level of free sulfhydryl groups of glutathione and proteins in pig blood platelets after short lasting incubation (30 min.) of these cells with cisplatin (cis-diamminedichloroplatinum II) and sodium selenite was investigated in vitro. The concentration of the platelet thiols after sodium selenite or cisplatin treatment distinctly decreased (p < 0.001). Pretreatment of blood platelets with sodium selenite at the low concentration (0.1 microM) protected platelet glutathione against the reaction with cisplatin (p < 0.001). The present study shows that in blood platelets after the incubation with cisplatin the GS-platinum complex was formed. The results of our experiments demonstrated also that the extracellular GSH (1 mM) had the protective effect against cisplatin-induced peroxidation of platelet lipids.
Animals↗
Effect of selective proteolysis on the accumulation of 5-hydroxytryptamine by intact rat blood platelets.
1 The effect of perturbation of intact blood platelets with proteolytic enzymes was studied with respect to 5-hydroxytryptamine (5-HT) transport, adenine transport and intracellular Na(+) and K(+) levels.2 Leucine aminopeptidase and thrombin reduced 5-HT transport, released 5-HT from pre-labelled platelets and disturbed the gradient to monovalent cations. Leucine amino-peptidase, but not thrombin, inhibited adenine transport.3 alpha-Chymotrypsin and carboxypeptidases A and B were without effect on the parameters studied.4 Trypsin selectively reduced 5-HT transport. It did not release 5-HT from blood platelets or inhibit adenine transport.5 The action of proteolytic enzymes is discussed in terms of proteins localized in the external membrane that may function in part as membrane carriers.
Adenine↗
The role of platelet membrane glycoproteins in the adhesion of blood platelets.
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Binding Sites↗
The transfusion of human blood platelets.
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Blood Platelets↗