No abstract available.
Platelet Aggregation Inhibitors* ; Thromboembolism

No abstract available.
Hemorrhage* ; Platelet Aggregation Inhibitors*

Acute Coronary Syndrome ; Humans ; Platelet Aggregation Inhibitors

OBJECTIVE: To analyze and compare the correlation of platelet aggregation rate measured by platelet analyzer, platelet aggregometer and thromboelastography. METHODS: The performance of platelet analyzer in platelet count and platelet aggregation function was evaluated. The platelet aggregation rate of 55 patients with type 2 diabetes mellitus (T2DM) before and after taking aspirin alone (32 cases) and clopidogrel alone (23 cases) was measured by thromboelastography, platelet aggregometer and platelet analyzer respectively, and the analytical results were compared. The correlation between the results measured by different instruments and equipment were further analyzed and the data were included in the statistical analysis. RESULTS: The precision of platelet analyzer in day and in batch was 1/3 lower than the total error (7%). The contamination rate was 0.30%. The slope of regression equation was 1.02 and R was 0.99 in the linear range of 4.15×10/L to 1379.95×10/L. The coincidence rate of platelet count and platelet reference method was 85%, which met the requirements of industry standards. The platelet aggregation rates of patients with T2DM after clopidogrel or aspirin by using thromboelastography, platelet aggregometer and platelet analyzer respectively was significantly lower than those whom before clopidogrel administration (P<0.01). CONCLUSION Platelet analyzer can provide reliable, objective and accurate information for clinical detection of platelet count and aggregation function, which is meet the requirements of industry standards, and its results are similar to those of platelet aggregometer and thromboelastography.
Diabetes Mellitus, Type 2 ; Humans ; Platelet Aggregation ; Platelet Aggregation Inhibitors ; Platelet Function Tests ; Thrombelastography

Snake venom proteins,particularly from the viper and elapid families, have been known to contain a number of platelet active components including what cause platelet aggregation or inhibit platelet aggregation. Some of them have potential clinical usefulness for the treatment of human hemorrhagic or thrombotic disease. Agkistrodon halys pallas belonging to viper family is only growing in China. The aim of this study was to purify a human platelet aggregation inhibitor from venom of Agkistrodon halys pallas and determine its biochemical character. Whether a component could inhibit human platelet aggregation was act as a method to follow the tracks of the protein. Crude venom of Agkistrodon halys pallas was loaded onto a DEAE-Sepharose CL-6B chromatography column could gain 6 peaks. A platelet inhibitor with molecular mass of 65 kD on SDS-PAGE, was purified from peak 2 by Sephadex G-75 gel filtration and SP-Sepharose, Mono Q on FPLC. It could inhibit human platelet aggregation induced by ADP, collagen without activities of phospholipase A2, esterase, fibrinogenolytic. It is concluded that a platelet inhibitor can be isolated and purified from venom of Agkistrodon halys pallas and its inhibition of platelet aggregation is does-dependent.
Crotalid Venoms ; analysis ; Humans ; Oligopeptides ; chemistry ; Platelet Aggregation ; drug effects ; Platelet Aggregation Inhibitors ; isolation & purification

OBJECTIVE: To investigate the effect of protein kinase A (PKA) activation on aggregation funetion of platelets in vitro. METHODS: The peripheral blood of healthy adults were collected, and the washed platelets were gained from collected peripheral blood. The washed platelets were treated with PKA activator Forskolin, then the platelet aggregation was induced by using Ristocetin, Thrombin, Collagen and ADP respectively, the platelet aggregation level was detected by the platelet aggregator. RESULTS: Compared with the controls, 5 μmol/L forskolin significantly inhibited ADP and collagen-induced platelet aggregation (P＜0.001), and showed mild inhibiting effect on Thrombin-induced platelet aggregation (P＜0.05). 2.5-10 μmol/L forskolin significantly inhibited ADP and Collagen -induced platelet aggregation (P＜0.001); but not showed significantly inhibitory effects on Ristocetin-induced platelet aggregation (P＞0.05). CONCLUSION PKA activation inhibits agonists-induced platelet aggregation.
Blood Platelets ; Cyclic AMP-Dependent Protein Kinases ; Humans ; Platelet Aggregation ; Platelet Aggregation Inhibitors ; Ristocetin ; Thrombin

Objective To examine the antiplatelet effect of ticagrelor by microfluidic chip and flow cytometry under shear stress in vitro. Methods Microfluidic chip was used to examine the effect of ticagrelor on platelet aggregation at the shear rates of 300/s and 1500/s.We adopted the surface coverage of platelet aggregation to calculate the half inhibition rate of ticagrelor.The inhibitory effect of ticagrelor on ADP-induced platelet aggregation was verified by optical turbidimetry.Microfluidic chip was used to construct an in vitro vascular stenosis model,with which the platelet reactivity under high shear rate was determined.Furthermore,the effect of ticagrelor on the expression of fibrinogen receptor (PAC-1) and P-selectin (CD62P) on platelet membrane activated by high shear rate was analyzed by flow cytometry. Results At the shear rates of 300/s and 1500/s,ticagrelor inhibited platelet aggregation in a concentration-dependent manner,and the inhibition at 300/s was stronger than that at 1500/s (both P<0.001).Ticagrelor at a concentration ≥4 μmol/L almost completely inhibited platelet aggregation.The inhibition of ADP-induced platelet aggregation by ticagrelor was similar to the results under flow conditions and also in a concentration-dependent manner.Ticagrelor inhibited the expression of PAC-1 and CD62P. Conclusion We employed microfluidic chip to analyze platelet aggregation and flow cytometry to detect platelet activation,which can reveal the responses of different patients to ticagrelor.
Humans ; Ticagrelor/pharmacology* ; Platelet Aggregation Inhibitors/pharmacology* ; Flow Cytometry/methods* ; Microfluidics ; Platelet Aggregation

OBJECTIVE: To study the effect of gradient shear stress on platelet aggregation by microfluidic chip Technology. METHODS: Microfluidic chip was used to simulate 80% fixed stenotic microchannel, and the hydrodynamic behavior of the stenotic microchannel model was analyzed by the finite element analysis module of sollidwork software. Microfluidic chip was used to analyze the adhesion and aggregation behavior of platelets in patients with different diseases, and flow cytometry was used to detect expression of the platelet activation marker CD62p. Aspirin, Tirofiban and protocatechuic acid were used to treat the blood, and the adhesion and aggregation of platelets were observed by fluorescence microscope. RESULTS: The gradient fluid shear rate produced by the stenosis model of microfluidic chip could induce platelet aggregation, and the degree of platelet adhesion and aggregation increased with the increase of shear rate within a certain range of shear rate. The effect of platelet aggregation in patients with arterial thrombotic diseases were significantly higher than normal group (P<0.05), and the effect of platelet aggregation in patients with myelodysplastic disease was lower than normal group (P<0.05). CONCLUSION The microfluidic chip analysis technology can accurately analyze and evaluate the platelet adhesion and aggregation effects of various thrombotic diseases unde the environment of the shear rate, and is helpful for auxiliary diagnosis of clinical thrombotic diseases.
Humans ; Microfluidics ; Platelet Adhesiveness ; Platelet Aggregation ; Blood Platelets/metabolism* ; Platelet Aggregation Inhibitors/pharmacology* ; Platelet Activation/physiology* ; Thrombosis

The aim of this update of Korean clinical practice guidelines for stroke is to provide timely evidence-based recommendations on the antiplatelet therapy in secondary prevention of stroke. Evidence-based recommendations are included for the use of antiplatelet agents for noncardioembolic stroke. Changes in the guidelines necessitated by new evidence will be continuously reflected in the new guideline.
Aspirin ; Platelet Aggregation Inhibitors ; Secondary Prevention ; Stroke ; Ticlopidine

Current stroke guidelines recommend the administration of non-vitamin-K-antagonist oral anticoagulant (NOAC) for the prevention of cardioembolic stroke induced by nonvalvular atrial fibrillation. We report a patient who suffered from recurrent posterior circulation strokes-occurring eight times in 4 months-even under adequate antiplatelet medication. Changing the medication from antiplatelet agents to NOAC stopped the stroke recurrence. We suggest that NOAC has a role in the prevention of recurrent stroke of undetermined etiology in the posterior circulation.
Atrial Fibrillation ; Humans ; Platelet Aggregation Inhibitors ; Recurrence ; Stroke*