-
Clinical Hemorheology and... 2023Resistance exercise induces thrombocytosis and increases platelet activation and function. These changes might be related to exercise variables including exercise...
BACKGROUND
Resistance exercise induces thrombocytosis and increases platelet activation and function. These changes might be related to exercise variables including exercise intensity and type.
OBJECTIVE
We compared the effects of traditional resistance exercise (TRE) and circuit resistance exercise (CRE) on cellular markers of platelet activation and function.
METHODS
In this crossover study ten healthy male (mean±SD: age, 25.6±2.4 years) subjects performed TRE encompassed 3 sets of 10 repetitions at 100% of 10-RM (10 repetition maximum) for 6 exercises, and CRE protocols included 3 sets of 10 repetitions at 100% of 10-RM for all 6 exercises consecutively, in two separate weeks. To measure platelet indices, PAC1, CD41a, CD42b and CD62P three blood samples were taken before, immediately after exercise, and after 30 min recovery.
RESULTS
Lactate concentration, blood pressure, platelet count (PLT), and mean platelet volume (MPV) were significantly (p < 0.05) increased following both resistance exercise trials. Significant increases in PAC1, and CD62P; and significant reductions for CD42b and CD41a were detected following both REs (p < 0.05). However, changes in PAC1 and CD62P were significantly different between the two protocols (p < 0.05), with higher increases detected following CRE.
CONCLUSIONS
Acute RE increases platelet indices and platelet activation; and that CRE results in higher platelet activation than TRE, probably due to exercise-induced increases in shear stress.
Topics: Humans; Male; Young Adult; Adult; Resistance Training; Cross-Over Studies; Platelet Activation; Blood Platelets; Lactic Acid
PubMed: 36565105
DOI: 10.3233/CH-221603 -
Critical Care Medicine Apr 2009
Topics: Acute Lung Injury; Animals; Inflammation; Platelet Activation
PubMed: 19318846
DOI: 10.1097/CCM.0b013e31819d2d45 -
Arquivos Brasileiros de Cardiologia Oct 2006
Topics: Coronary Artery Disease; Humans; Platelet Activation
PubMed: 17128306
DOI: 10.1590/s0066-782x2006001700001 -
Medical Science Monitor : International... Apr 2007Coronary heart disease is the major cause of death in the developed world. Platelet activation and aggregation are central processes in the pathophysiology of coronary...
BACKGROUND
Coronary heart disease is the major cause of death in the developed world. Platelet activation and aggregation are central processes in the pathophysiology of coronary heart disease. Mean platelet volume (MPV), a determinant of platelet function, is a newly emerging risk factor for atherothrombosis. The present study was designed to evaluate levels of MPV in subclinical hypothyroidic subjects compared with euthyroidic subjects in a cross-sectional study.
MATERIAL/METHODS
Thirty-six subclinical hypothyroidic subjects and 20 euthyroidic control subjects matched for age, gender, and body mass index were selected.
RESULTS
Metabolic parameters and platelet counts were not different among the study groups (p>0.05). The level of MPV was significantly higher in the subclinical hypothyroidic group than in the euthyroidic group (9.9+/-0.9 fl vs. 9.2+/-0.7 fl, p<0.001). The anti-TPO levels positively correlated to MPV levels in the subclinical hypothyroidic group (p<0.05).
CONCLUSIONS
These results suggest that subjects with subclinical hypothyroidism tend to have increased platelet activation. Increased platelet activity could contribute to increasing the risk of atherothrombotic complications in subclinical hypothyroidism.
Topics: Adult; Cross-Sectional Studies; Female; Humans; Hypothyroidism; Immunoassay; Male; Platelet Activation; Platelet Count
PubMed: 17392654
DOI: No ID Found -
BioMed Research International 2015As platelet activation is closely related to the liberation of growth factors and inflammatory mediators, platelets play a central role in the development of CVD.... (Review)
Review
As platelet activation is closely related to the liberation of growth factors and inflammatory mediators, platelets play a central role in the development of CVD. Virtually all cardiovascular risk factors favor platelet hyperreactivity and, accordingly, also physical (in)activity affects platelet function. Within this paper, we will summarize and discuss the current knowledge on the impact of acute and habitual exercise on platelet function. Although there are apparent discrepancies regarding the reported effects of acute, strenuous exercise on platelet activation, a deeper analysis of the available literature reveals that the applied exercise intensity and the subjects' cardiorespiratory fitness represent critical determinants for the observed effects. Consideration of these factors leads to the summary that (i) acute, strenuous exercise can lead to platelet activation, (ii) regular physical activity and/or physical fitness diminish or prevent platelet activation in response to acute exercise, and (iii) habitual physical activity and/or physical fitness also favorably modulate platelet function at physical rest. Notably, these effects of exercise on platelet function show obvious similarities to the well-recognized relation between exercise and the risk for cardiovascular events where vigorous exercise transiently increases the risk for myocardial infarction and a physically active lifestyle dramatically reduces cardiovascular mortality.
Topics: Blood Platelets; Cardiovascular Diseases; Humans; Motor Activity; Platelet Activation; Platelet Aggregation; Risk Factors; Sedentary Behavior
PubMed: 26557653
DOI: 10.1155/2015/165078 -
Current Opinion in Hematology Sep 2011The story of platelet activation is complex, involving many intertwined and overlapping pathways and processes that continue to expand in complexity. This review will... (Review)
Review
PURPOSE OF REVIEW
The story of platelet activation is complex, involving many intertwined and overlapping pathways and processes that continue to expand in complexity. This review will cover some of the recent novel mediators and receptors identified to be important in platelet activation.
RECENT FINDINGS
Many newly discovered platelet activators and receptors are not strong platelet agonists, but rather are important modifiers of platelet activation, and thus represent potentially novel targets to blunt, but not totally prevent, platelet activation and thrombus formation. The diversity of platelet activation mediators and receptors also expands as we learn more about the disease processes that are either initiated or accelerated by platelets. Although platelets are a unique cell type with a unique role in thrombosis, they share a surprising amount in common with the molecules and machinery present in synaptic termini and immune cells. Many of these secreted molecules have important roles in platelet activation.
SUMMARY
Many newly identified platelet activators are weak agonists. These represent intriguing targets for platelet inhibitor development or shed light on the overlap between inflammation and thrombosis.
Topics: Animals; Blood Platelets; Communicable Diseases; Glutamic Acid; Humans; Inflammation Mediators; Lectins, C-Type; Platelet Activation; Signal Transduction
PubMed: 21730836
DOI: 10.1097/MOH.0b013e3283497dfb -
Platelets Jan 2022During cardiopulmonary bypass (CPB), platelet activation and dysfunction are associated with adverse outcomes. Remote ischemic preconditioning (RIPC) has been shown to... (Randomized Controlled Trial)
Randomized Controlled Trial
Effects of remote ischemic preconditioning on platelet activation and reactivity in patients undergoing cardiac surgery using cardiopulmonary bypass: a randomized controlled trial.
During cardiopulmonary bypass (CPB), platelet activation and dysfunction are associated with adverse outcomes. Remote ischemic preconditioning (RIPC) has been shown to attenuate platelet activation. We evaluated the effects of RIPC on platelet activation during CPB in patients undergoing cardiac surgery. Among 58 randomized patients, 26 in the RIPC group and 28 in the sham-RIPC group were analyzed. RIPC consisted of 4 cycles of 5-min ischemia induced by inflation of pneumatic cuff pressure to 200 mmHg, followed by 5-min reperfusion comprising deflation of the cuff on the upper arm. Platelet activation was assessed using flow cytometry analysis of platelet activation markers. The primary endpoint was the AUC of CD62P expression during the first 3 h after initiation of CPB. Secondary outcomes were the AUC of PAC-1 expression and monocyte-platelet aggregates (MPA) during 3 h of CPB. The AUCs of CD62P expression during 3 h after initiation of CPB were 219.4 ± 43.9 and 211.0 ± 41.2 MFI in the RIPC and sham-RIPC groups, respectively (mean difference, 8.42; 95% CI, -14.8 and 31.7 MFI; =.471). The AUCs of PAC-1 expression and MPA did not differ between groups. RIPC did not alter platelet activation and reactivity during CPB in patients undergoing cardiac surgery.
Topics: Blood Platelets; Cardiac Surgical Procedures; Coronary Artery Bypass; Humans; Ischemic Preconditioning; Platelet Activation
PubMed: 33307907
DOI: 10.1080/09537104.2020.1856362 -
Thrombosis Research Feb 2018Cystic fibrosis (CF) is an inflammatory lung disease. Platelets have an emerging role in inflammation, however previous studies of platelet activation in CF have...
Cystic fibrosis (CF) is an inflammatory lung disease. Platelets have an emerging role in inflammation, however previous studies of platelet activation in CF have generated conflicting results. In this study, we determined platelet function in CF patients and correlated platelet activation to establish clinical and laboratory parameters. Twenty-two patients, aged 20.7 to 54.4 (mean 34.0, SD 9.45) years and with a mean FEV1%pred (forced expiratory volume in one second, % of predicted) of 72 (SD 21.4, range 32-110) were recruited. A combination of platelet assays was used: platelet aggregation, platelet activation and platelet-leukocyte complex formation. Platelets from CF patients exhibited significantly increased aggregation when stimulated ex-vivo, a tendency towards increased platelet upregulation of CD62P, but no increase of GPIIb/IIIa activation (PAC-1). Platelet-monocyte complex (PMC) formation was significantly increased in CF patients compared to controls, while platelet-neutrophil complex formation was not. In the CF group, platelet aggregation correlates with levels of anti-neutrophil cytoplasmic antibodies (ANCA) with specificity for bactericidal/permeability-increasing protein (BPI), BPI-ANCA (r=0.56). The formation of PMCs correlates with lung function decline (1-FEV1%), CRP and BPI-ANCA (r=0.61, 0.55, 0.5). We therefore confirm the presence of increased platelet activation in CF patients, and determine that further evaluation of platelet activation in relation to prognostic factors in CF is warranted.
Topics: Adult; Cystic Fibrosis; Female; Humans; Male; Middle Aged; Platelet Activation; Platelet Aggregation; Young Adult
PubMed: 29274562
DOI: 10.1016/j.thromres.2017.12.012 -
Current Drug Targets 2015Platelets play a crucial role in immune responses. Impaired platelet activation may cause persistent mucosal inflammation through P-selectin, CD40-CD40L and other... (Review)
Review
Platelets play a crucial role in immune responses. Impaired platelet activation may cause persistent mucosal inflammation through P-selectin, CD40-CD40L and other systems influencing granulocytes, macrophages or endothelial cells. Pharmacological regulation of platelet activation may reduce thromboembolism and limit the interaction of platelets with endothelial and inflammatory cells, in turn weakening the inflammatory responses. In this review we focus on pathophysiological activities of platelets in inflammatory bowel diseases and discuss the studies on currently available anti-platelet therapies in the treatment of gastrointestinal inflammation. Finally, we provide a prospective view to new anti-platelet agents currently under development.
Topics: Animals; Blood Platelets; Humans; Inflammatory Bowel Diseases; Platelet Activation; Platelet Aggregation Inhibitors
PubMed: 25585124
DOI: 10.2174/1389450116666150113122229 -
Oncotarget May 2017Increased risk of thromboembolism and platelet hyperreactivity has been reported in patients receiving thalidomide therapy. Whether thalidomide induces platelet...
Increased risk of thromboembolism and platelet hyperreactivity has been reported in patients receiving thalidomide therapy. Whether thalidomide induces platelet activation directly or through other factors remains unclear. The aim of this study was to evaluate the effect of thalidomide on platelet activation under resting conditions in vitro and in vivo. Isolated human or mouse platelets were treated with different concentrations of thalidomide (10, 50 and 100 μg/ml) for 60 min at 37°C followed by analysis of platelet surface expression of platelet receptors GPIbα, GPVI, αIIbβ3 and P-selectin, and PAC-1 or fibrinogen binding, by flow cytometry and collagen- or ADP-induced platelet aggregation. In addition, thalidomide (200 mg/kg) was intraperitoneally injected into mice for analysis of the effect of thalidomide on platelet activation in vivo. No increased expression of P-selectin, PAC-1 or fibrinogen binding was observed in either human and mouse platelets after thalidomide treatment in vitro for 60 min at 37oC. Thalidomide treatment also did not affect expression of GPIbα, GPVI or αIIbβ3, nor did it affect collagen- or ADP-induced platelet aggregation at threshold concentrations. However, while mice injected with thalidomide displayed no increased surface expression of platelet P-selectin or αIIbβ3, there was a significantly shortened tail bleeding time, thrombin time, prothrombin time together with higher levels of Factor IX and fibrinogen. In conclusion, thalidomide at therapeutic doses does not directly induce platelet activation under resting conditions in vitro or in vivo, but results in increased procoagulant activity, which could explain the thalidomide-dependent prothrombotic tendency in patients.
Topics: Animals; Biomarkers; Blood Platelets; Gene Expression; Humans; Mice; Platelet Activation; Platelet Aggregation; Platelet Membrane Glycoproteins; Thalidomide
PubMed: 28415757
DOI: 10.18632/oncotarget.16205