			Home About us Contact

Platelet P-selectin Expression (platelet + p-selectin_expression)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Endothelin attenuates endothelium-dependent platelet inhibition in man

ACTA PHYSIOLOGICA, Issue 4 2010
R. E. Malmström
Abstract Aim:, The vascular endothelium produces several substances, including nitric oxide (NO) and endothelin-1 (ET-1), which participate in the regulation of vascular tone in humans. Both these substances may exert other actions of importance for cardiovascular disease, e.g. effects on vascular smooth muscle cell proliferation and inflammation, and NO inhibits platelet function. Experiments were designed to investigate the effect of ET-1 on endothelium-dependent vasodilatation and attenuation of platelet activation. Methods:, In 25 healthy male subjects (25 ± 1 years), forearm blood flow was measured by venous occlusion plethysmography, and platelet activity was assessed by whole blood flow cytometry (platelet fibrinogen binding and P-selectin expression) in unstimulated and adenosine diphosphate (ADP)-stimulated samples during administration of ET-1, the endothelium-dependent vasodilator acetylcholine and the NO synthase inhibitor l -NMMA. Results:, Acetylcholine increased forearm blood flow and significantly inhibited platelet activation in both unstimulated and ADP-stimulated samples. In samples stimulated with 0.3 ,m ADP, fibrinogen binding decreased from 41 ± 4% to 31 ± 3% (P < 0.01, n = 11) after acetylcholine administration. The vasodilator response to acetylcholine was significantly impaired during infusions of ET-1 and l -NMMA. ET-1 did not affect platelet activity per se, whereas l -NMMA increased platelet P-selectin expression. Both ET-1 and l -NMMA attenuated the acetylcholine-induced inhibition of platelet activity. Conclusions:, Our study indicates that, further to inhibiting endothelium-dependent vasodilatation, ET-1 may also attenuate endothelium-dependent inhibition of platelet activation induced by acetylcholine. An enhanced ET-1 activity, as suggested in endothelial dysfunction, may affect endothelium-dependent platelet modulation and thereby have pathophysiological implications. [source]

Elevated thrombopoietin in plasma of burned patients without and with sepsis enhances platelet activation

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2009
E. LUPIA
Summary.,Background:,Thrombopoietin (TPO) is a humoral growth factor that does not induce platelet aggregation per se, but enhances platelet activation in response to several agonists. Circulating levels of TPO are increased in patients with sepsis and are mainly related to sepsis severity. Objectives:,To investigate the potential contribution of elevated TPO levels in platelet activation during burn injury complicated or not by sepsis. Methods: We studied 22 burned patients, 10 without and 12 with sepsis, and 10 healthy subjects. We measured plasma levels of TPO, as well as leukocyte-platelet binding and P-selectin expression. The priming activity of plasma from burned patients or healthy subjects on platelet aggregation and leukocyte-platelet binding, and the role of TPO in these effects were also studied in vitro. Results:,Burned patients without and with sepsis showed higher circulating TPO levels and increased monocyte-platelet binding compared with healthy subjects. Moreover, TPO levels, monocyte-platelet binding and P-selectin expression were significantly higher in burned patients with sepsis than in burned patients without sepsis. In vitro, plasma from burned patients without and with sepsis, but not from healthy subjects, primed platelet aggregation, monocyte-platelet binding and platelet P-selectin expression. The effect of plasma from burned patients with sepsis was significantly higher than that of plasma from burned patients without sepsis. An inhibitor of TPO prevented the priming effect of plasma from burned patients. Conclusions:,Increased TPO levels may enhance platelet activation during burn injury and sepsis, potentially participating in the pathogenesis of multi-organ failure in these diseases. [source]

High glucose levels enhance platelet activation: involvement of multiple mechanisms

BRITISH JOURNAL OF HAEMATOLOGY, Issue 3 2006
Dzana Sudic
Summary Diabetes mellitus (DM) and hyperglycaemia are associated with platelet activation. The present study was designed to investigate how high glucose levels influence platelet function. Fasting human blood was incubated with different concentrations of d -glucose (5, 15 and 30 mmol/l) and other sugars without or with in vitro stimuli. Platelet activation was monitored by whole blood flow cytometry. High glucose levels enhanced adenosine diphosphate (ADP)- and thrombin receptor-activating peptide (TRAP)-induced platelet P-selectin expression, and TRAP-induced platelet fibrinogen binding. Similar effects were seen with 30 mmol/l l -glucose, sucrose and galactose. Hyperglycaemia also increased TRAP-induced platelet-leucocyte aggregation. Protein kinase C (PKC) blockade did not counteract the enhancement of platelet P-selectin expression, but abolished the enhancement of TRAP-induced platelet fibrinogen binding by hyperglycaemia. Superoxide anion scavenging by superoxide dismutase (SOD) attenuated the hyperglycaemic enhancement of platelet P-selectin expression, but did not counteract the enhancement of TRAP-induced platelet fibrinogen binding. Hyperglycaemia did not alter platelet intracellular calcium responses to agonist stimulation. Blockade of cyclo-oxygenase (COX), phosphotidylinositol-3 (PI3) kinase, or nitric oxide synthase, or the addition of insulin did not influence the effect of hyperglycaemia. In conclusion, high glucose levels enhanced platelet reactivity to agonist stimulation through elevated osmolality. This occurred via superoxide anion production, which enhanced platelet P-selectin expression (secretion), and PKC signalling, which enhanced TRAP-induced fibrinogen binding (aggregablity). [source]

Effects of stent coating on platelets and endothelial cells after intracoronary stent implantation

CLINICAL CARDIOLOGY, Issue 2 2001
Enver Atalar M.D.
Abstract Background: Adhesion molecules are known to be important in the regulation of endothelial cell and platelet functions. Increased platelets P-selectin expression is a marker of stent thrombosis after uncoated stent placement. Hypothesis: The aim of this study was to compare the effects of intracoronary placement of phosphorylcholine (PC)-coated, versus heparin-coated, versus uncoated stents on platelets and endothelial activity. Methods: Thirty patients (age 55 ± 10, 27 men) with significant proximal left anterior descending coronary artery stenoses were randomized to elective implantation of PC-coated. versus heparin-coated. versus uncoated stents. Following stent placement, intravenous heparin and aspirin plus ticlopidine were administered. Venous plasma soluble E-selectin, sP-sclectin, and intercellular adhesion molecule-1 levels were measured before the procedure and 24 and 48 h thereafter as markers of platelet and endothelial cell activation. Patients were excluded if they had a disease known to influence platelet and endothelial cell function. Results: Plasma sP-selectin levels decreased significantly after implantation of PC- and heparin-coated stents (p = 0.04), hut remained unchanged in patients randomized to uncoated stents. Plasma sE-selectin levels increased significantly after uncoated stent placement (p = 0.04) and remained unchanged after coated stent implantation. Conclusion: In patients treated with combined antiplatelet therapy, implantation of PC- and heparin-coated stents decreased platelet activity without activating endothelial cells, whereas placement of uncoated stents led to endothelial activation without changing platelet activity. These results suggest that PC-coated and heparin-coated stents may be advantageous in limiting thrombotic complications. [source]