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PubMed1995

[Decreased activity of oxidoreductases in erythrocytes and blood platelets from venous and umbilical blood of women with pregnancy-induced hypertension].

Thirty two pregnancies with pregnancy-induced hypertension (PIH) and twenty seven control normal pregnancies were analysed with regard to maternal and fetal blood enzymatic antioxidants. In PIH maternal erythrocyte, platelet and serum blood and in umbilical cord blood levels of lipid peroxides were higher than in normal pregnancy. Also the activities of platelet and erythrocyte superoxide dismutase and glutathione peroxidase were lower in PIH women. The concentration of lipid peroxides was higher, and the activity of glutathione peroxidase were lower in umbilical cord elements of women with PIH, than corresponding values of women with normal pregnancy. We suggest that disturbances in antioxidant enzymatic system are involved in the pathogenesis of maternal PIH, and it may also have effects on the function of antioxidant status of the fetus.

Adult↗
PubMedDate not supplied

The effect of ethanol on some serotonergic mechanisms in rat blood platelets.

Under in vitro conditions ethanol inhibits the uptake and enhances release of [14C]-5HT from rat blood platelets. Similar results were obtained in blood platelets isolated from the blood rats receiving 2 g/kg ethanol. Ethanol decreased also the 5-HT content in the blood platelets. It inhibited the aggregation of blood platelets but did not change the potentiating action of 5-HT on ADP-induced aggregation. The results indicate that ethanol by its action on the transport mechanisms in blood platelets may elevate the level of free 5-HT in the blood plasma, in this manner potentiating the action of the amine in the circulatory system.

Adenosine Diphosphate↗
PubMed1989

Identical subcellular distribution of palmitoyl-CoA and arachidonoyl-CoA synthetase activities in human blood platelets.

Fractionation of human blood platelets showed that palmitoyl-CoA synthetase and arachidonoyl-CoA synthetase activities had an identical distribution among subcellular fractions. The activity was highest with arachidonic acid as substrate in all fractions, with an enzyme activity of 50 nmol/min per mg of protein, in a 'dense-tubular-system'-enriched fraction. The ratio activities with arachidonate and palmitate as substrates was about 1.5 in all fractions. Heat inactivation did not distinguish between arachidonoyl-CoA synthetase and a palmitoyl-CoA synthetase. On the other hand, heat inactivation indicated two pools of long-chain acyl-CoA synthetases: one in a mitochondria- and one in the dense-tubular-system-enriched fraction.

Blood Platelets↗
PubMedDate not supplied

Genetic factors underlying differential blood platelet sensitivity to inhibitors.

Blood platelets are not only the primary defence mechanism involved in physiological hemostasis, but also their disorders constitute a crucial risk factor in arterial thrombosis. As arterial thrombi are composed of predominantly platelets formed under conditions of elevated shear stress at sites of atherosclerotic vascular injury and disturbed blood flow, the prevention of arterial thrombosis has been for years the main target for antiplatelet therapy. Individual differences in the rate of platelet activation and reactivity markedly influence normal hemostasis and the pathological outcome of thrombosis. Such an individual variability is largely determined by environmental and genetic factors. These are known to either hamper platelets' response to agonists, and thereby mimic the pharmacological modulation of platelet function or mask therapy effect and sensitize platelets. Some clinical studies have indicated that platelet glycoprotein polymorphisms are genetic factors contributing to arterial thrombosis. In spite of some discrepancies between different studies, there is substantial evidence that the integrin beta3 P1(A2) allele, the variants GPIbalpha Met145 and GPIbalpha (-5C) haplotype or the integrin alpha2 haplotype 1 (807T) each contribute to the risk for and morbidity of thrombotic disease. In this article, we reviewed a role of the aforementioned polymorphisms in modulating platelet function and platelet response to inhibitors. The paper focuses on the association between Pl(A1/A2) polymorphism and sensitivity (or resistance) to aspirin and the inhibitory efficacy of GPIIb-IIIa antagonists. Additionally, a potential role of 807C/T polymorphism (GPIa), polymorphisms of GPIb and platelet purinoreceptor P2Y12 in affecting platelet sensitivity to blocking agents is discussed.

Blood Platelets↗
PubMed2002

Role of blood platelets in infection and inflammation.

Blood platelets are here presented as active players in antimicrobial host defense and the induction of inflammation and tissue repair in addition to their participation in hemostasis. Megakaryopoiesis is inhibited after acute infection with viruses or bacteria. In contrast, chronic inflammation is often associated with reactive thrombocytosis. Platelets can bind and internalize pathogens and release microbicidal proteins that kill certain bacteria and fungi. By making cell-cell contacts with leukocytes and endothelial cells, platelets assist white blood cells in rolling, arrest and transmigration. On stimulation by bacteria or thrombin, platelets release the content of their alpha-granules, which include an arsenal of bioactive peptides, such as CC-chemokines and CXC-chemokines and growth factors for endothelial cells, smooth muscle cells and fibroblasts. Thus, integral to innate immunity, the tiny little platelets may become bombshells when irritated by pathogens.

Animals↗
PubMed2001

Studies on pig blood platelet responses to peroxynitrite action.

The action of peroxynitrite (ONOO(-)) on pig blood platelet function was studied. Incubation of washed blood platelets with ONOO(-) (0.062-2 mM) caused strong, dose- and time-dependent inhibitory effects on adhesion of resting and thrombin-stimulated platelets to collagen and on platelet aggregation induced by thrombin. The platelet responses were measured 10 s after addition of peroxynitrite to platelets ('zero time') and after 60 min incubation of platelets with ONOO(-). Exposure of blood platelets to peroxynitrite (60 min) brought about platelet lipid peroxidation assessed by the thiobarbituric acid method but did not cause any changes in blood platelet proteins as determined by SDS-polyacrylamide gel electrophoresis.

Animals↗
PubMed1977

Effect of Corynebacterium parvum on peripheral blood platelets.

The level of peripheral blood platelets was determined after i.v. injection of Corynebacterium parvum in normal C57BL mice and in those bearing the Lewis lung carcinoma. Twenty minutes after injection of a formalin-killed active strain (CN6134, (CN6134, which inhibited tumour metastases) or a killed inactive strain (CN 5888, which did not inhibit metastases) the number of circulating blood platelets was reduced by 50%. The level of platelets returned to control values by 8 h after the active, and by approximately 3 days after the inactive strain. The active strain alone caused a second and prolonged fall in platelet numbers, from approximately 16 h to 21 days after injection. Heparin given 3 X weekly to these mice restored the platelet count to normal values by 10 days after injection of active-strain C. parvum. The level of platelets in tumour-bearing mice was essentially similar to that in normal mice. Possible causes of the thrombocytopenia and the significance of platelets in metastasis are discussed.

Animals↗
PubMed1991

Effect of bed rest on the adenine nucleotides concentration in human blood platelets.

The effect of immobilization in bed on metabolism and function of human blood platelet was studied. Blood platelets taken from patients with bone fractures after long term bed rest (14 days and 28 days) demonstrated significantly reduced concentration of total adenine nucleotides (after 28 days reduction about 30%). This decrease of total platelet adenine nucleotides after immobilization in bed is probably caused by stimulation of platelet secretory process. Thrombin which released from control platelets 58.2% +/- 1.5% of total adenine nucleotides liberated decreased amounts (only 23.1% +/- 3.3% of total) of nucleotides from patient platelets isolated after 28 days of immobilization in bed. Loss of nucleotides from platelets was accompanied by slightly increased extent of platelet aggregation. It is concluded that during bed rest the reactivity of blood platelets (aggregation and release reaction) is stimulated.

Adenine Nucleotides↗
PubMed1977

The effect of phospholipase C on platelet factor 3 in human blood platelets.

Intact human platelets isolated by gel filtration have been treated with purified phospholipase C. The effect of the enzyme on available and total platelet factor 3 has been tested. The available procoagulant platelet factor 3 was very low. A further small reduction was observed after incubation with phospholipase C when the enzyme was washed away before testing. External attack on platelets by phospholipase C led to a marked inactivation of total platelet factor 3.

Blood Coagulation Factors↗
PubMed1981

The role of arachidonate lipoxygenase and fatty acids during irreversible blood platelet aggregation in vitro.

Arachidonic acid is converted by blood platelets into thromboxane A2 (TXA2) and 12-hydroxyeicosatetraenoic acid (12-OH-C20:4). TXA2 causes platelet aggregation, but the physiological role of 12-OH-C20:4 on blood platelets is not known. The formation of 12-OH-C20:4 by washed platelets can be inhibited by eicosatetraynoic acid at a concentration of 0.7 mumol/l; TXA2-formation is not yet influenced at this low inhibitor concentration. Under these conditions, the irreversible 1-14C arachidonic acid-induced blood platelet aggregation is converted into a reversible type of aggregation. Similar results are obtained by addition of any long-chain fatty acid (20-30 mumol/l), including 12-OH-C20:4 and arachidonic acid, as well as by addition of sulfhydryl reagents. However, in these experiments no inhibition of the arachidonic acid conversion is observed. The results can be explained by a "sticking together" of the blood platelets caused by 12-OH-C20:4 generation. This effect is based on the same principle as that of the chemotactic effect of 12-OH-C20:4 on leucocytes as described by Turner et al. (Nature 257; 680-681, 1975). The explanation is supported by experiments with platelets obtained after ingestion of aspirin. ADP-induced reversible aggregation of three platelets becomes irreversible after addition of arachidonic acid. Irreversible platelet aggregation occurs only during endogenous 12-OH-C20:4 generation in consequence of a "sticking-together" process. This process coincides with a stimulation of the platelet guanylate cyclase.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1998

[Selected parameters of blood platelet function in patients with myeloproliferative syndrome].

Symptoms of hemorrhagic diathesis and/or thrombotic complications are observed in patients with myeloproliferative syndrome (m-p.s.). It is emphasized that there is a meaningful direct and indirect share of blood platelets in the mentioned disturbances of hemostasis. Therefore in own investigations an attempt was made to evaluate the morphology and function of blood platelets in patients with various forms of m-p.s., as well as to find an answer to the question: do any differences in morphology and function (activation) of blood platelets appear in patients with m-p.s.?, and is activation of blood platelets always accompanied by the symptom of hemorrhagic diathesis or past thrombotic episodes (the second ones evidenced in the patients anamneses)?, do the blood platelets in idiopathic thrombocytopenia (one of the forms of m-p.s.), differ morphologically and functionally from platelets in other forms of m-p.s. The investigation comprised 45 patients, in whom m-p.s. was diagnosed at Department of Hematology PAM (28 women, 17 men) aged from 36 to 82 years (mean age 58.10 + 10.61). The diagnosis of m-p.s. in each patient was established on the basis of clinical picture and laboratory examinations (blood morphology, hematocrit, FAG score, histopathological examination of bone marrow). In patients the accomplished determination concerned blood platelets count, mean blood platelet volume, platelocrit, volume range of blood platelets, coagulation time by Duke's method. The function of platelets was estimated with the help of the following studies: aggregation of blood platelets under the influence of ADP according to Born's method, concentration of beta-thromboglobulin (beta-TG) and platelet factor--4 (PF-4) in plasma by ELISA method. In order to pay due consideration to the effect of blood platelets count exerted on the concentration of beta-TG and PF-4, a supplementary parameter was introduced, the so-called beta-TG and PF-4 standardized. That allowed for studying the platelets in all patients under the same conditions. The results of own investigations have shown that most of the patients with m-p.s. had disturbances involving the morphology of blood platelets (Tab. 2) and increased activity of platelets, being expressed by a rise in concentrations of beta-TG and PF-4 in plasma (Fig. 1, 2) and by abnormal aggregation of platelets due to ADP influence. Moreover, the determination of beta-TG and PF-4 concentration in plasma in thrombocytopenia states, particularly in patients with idiopathic thrombocytopenia ought to be performed after the standardization of platelets count, the finding being also supported by the results of own investigations (Tab. 3). There may be compliance with the viewpoint expressed in the literature that the results of studying the morphological parameters of blood platelets and their function (activation) in m-p.s. are not a prognostic factor for the appearance of thrombotic complications and/or hemorrhages.

Adult↗
PubMed1990

Effect of retinoic acid on adenosine diphosphate and collagen-induced alterations in enzymes of GSH-linked antioxidant defence system of human blood platelets in vitro.

Collagen stimulation of blood platelets resulted in significant increases in malondialdehyde (MDA) formation and activity of glucose-6-phosphate dehydrogenase (G6PDH) and a decrease in catalase and glutathione peroxidase (GPx). Retinoic acid (RA) pretreatment did not show any appreciable changes except for a decrease in G6PDH activity as compared with collagen alone. RA pretreatment of human blood platelets resulted in an increase in the activities of catalase and GPx, two important radical scavenging enzymes, with significant decrease in MDA formation when compared with ADP alone. It is suggested that RA has a significant effect on the antioxidant defence system in ADP stimulated platelets but not in the collagen stimulated platelets.

Adenosine Diphosphate↗
PubMed1980

Similar kinetic characteristics of 5-hydroxytryptamine binding in blood platelets and brain membranes of rats.

Blood platelets and brain membranes of SIV and Lewis rats both exhibited two saturable binding sites for 5-hydroxytryptamine (5-HT) in the concentration range 1-100 nM. The Kd values for the high-affinity sites were 4-6 nM and for the low-affinity sites 20-40 nM in both tissues of both rat strains. Blood platelets had 100-200 times more binding sites per mg protein (Bmax) than brain membranes. Thus, 5-HT receptors of platelets may be used as models for those of cerebral 5-HT-neurons.

Animals↗