Platelets
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Platelet dysfunction plays a critical role in vascular complications of type 2 diabetes mellitus (T2DM). But the relationship between platelet hyperactivity and its energy metabolic process remains unclear. This study was designed to explore alterations of platelet mitochondrial ATP production and the possible mechanism. ⋯ For whole subjects, a stepwise regression showed that plasma glycated hemoglobin A1c (HbA1c) level positively correlated to platelet ATP content (beta = 0.552, 95% CI = 0.072-1.451), and fasting plasma glucose (FPG) level was negatively correlated to DeltaPsim (beta = -0.372, 95% CI = -0.471 to -0.089). These data support that hyperglycemia of T2DM promotes platelet mitochondria to generate more ATP, but decreases platelet mitochondrial potential. The discordance between them requires further researches to elucidate.
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Point-of-care platelet monitoring is increasingly used in cardiac patients treated with antiplatelet agents. The validity of a new assay needs to be evaluated not only for reproducible data in clinical samples, but also for other pre-analytical conditions that may influence measurements. The aim of this study was to evaluate the influence of a pneumatic tube system (PTS) for specimen transport on impedance platelet aggregometry. ⋯ In conclusion, PTS transport had a significant influence on platelet function testing by the Multiplate() analyzer. Significantly fewer test results indicated normal platelet function in TRAP test and reduced aspirin responsiveness in ASPI test after PTS transport. Therefore, clinical decisions regarding platelet function and aspirin responsiveness should not be based on blood specimens transported by a PTS system.
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Nitric oxide (NO)-mediated inhibition of platelet function occurs primarily through elevations in cGMP, although cGMP-independent mechanisms such as S-nitrosylation have been suggested as alternative NO-signaling pathways. In the present study we investigated the potential for S-nitrosylation to act as a NO-mediated cGMP-independent signaling mechanism in platelets. The NO-donor, S-nitrosoglutathione (GSNO), induced a concentration-dependent inhibition of platelet adhesion to immobilized collagen. ⋯ The extent of S-nitrosylation in response to exogenous NO was unaffected by platelet activation. Importantly, platelet activation in the absence of exogenous NO failed to increase S-nitrosylation beyond basal levels, indicating that platelet-derived NO was unable to induce this type of protein modification. Our data demonstrate that S-nitrosylation of platelet proteins in response to exogenous NO may act as a potentially important cGMP-independent signaling mechanism for controlling platelet adhesion.
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Several studies indicate that a biochemically reduced response to aspirin increases the risk of cardiovascular events. This study was designed to investigate the performance of Multiplate whole blood aggregometry as regards assessment of platelet function prior to and after aspirin treatment, and to compare it with light transmission aggregometry (LTA). We included 21 healthy individuals and 43 patients with documented coronary artery disease (CAD). ⋯ In conclusion, the repeatability of Multiplate aggregometry was good before aspirin treatment, whereas the CV was quite high during aspirin treatment in both healthy individuals and patients. However, the Multiplate device was fully capable of assessing platelet function prior to and after treatment with aspirin. Clinical studies are needed to investigate whether a high platelet aggregation level measured by Multiplate whole blood aggregometry during aspirin treatment is associated with a poor clinical outcome.
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Aspirin resistance continues to be a major challenge in patients after coronary artery bypass grafting (CABG). We investigated the impact of intravenous aspirin on platelet function in this clinical setting. Forty-two patients received 100 mg of oral aspirin once daily, beginning on day 1 after the operation. ⋯ Concomitantly, the number of patients with laboratory aspirin resistance as measured by CEPI-CT and TPA but not by IPA induced by AA or collagen dropped significantly. Agreement in the detection of aspirin responders and non-responders among platelet function tests was poor. Our findings indicate that the intravenous aspirin appears to be a promising approach for reducing laboratory aspirin resistance during the postoperative phase of CABG.