Effect of Huangzhi Oral Liquid on Platelet Aggregation
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OBJECTIVE: To explore the effect of Huangzhi oral liquid on platelet aggregation.METHODS: The platelet aggregation in rabbits was determined by turbidimetry and the bleeding time of mice was measured. RESULTS: Huangzhi oral liquid inhibited the platelet aggregation induced by adenosine diphosphate (ADP), arachidonic acid (AA) or PagVR (P0.01) and prolonged the bleeding time of mice.CONCLUSION: The platelet function can be inhibited by Huangzhi oral liquid.Keywords:
Adenosine diphosphate
Turbidimetry
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Ex vivo
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Summary The release of platelet factor 4 during platelet aggregation was investigated in diabetic patients. We observed an increased release of platelet factor 4 in diabetic patients. The authors suggest that the increased release of platelet factor 4 may play an essential role in pathogenesis of thromboembolic complications in diabetes mellitus.
Pathogenesis
Platelet adhesiveness
Beta-thromboglobulin
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Ex vivo
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11-Deoxymisoprostol demonstrates antiaggregant properties with respect to the adrenalin-, collagen-, and ADP-induced aggregation of thrombocytes, which is manifested by a decrease in the rate of blood platelet agglutination and their secretion, and by an increase in the time of thrombus formation.
Agglutination (biology)
Sodium salt
Prothrombin time
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Extracorporeal circulation
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The prolonged bleeding time in a 70- year-old man with a bleeding diathesis was attributed s to impaired platelet aggregation. This could be accounted for by the decrease of the platelet adhesiveness to collagen and the decreased release of adenosine diphosphate (ADP). The impaired availability of platelet factor 3 and acid phosphatase after induction by collagen was partly corrected by ADP or bovine fibrinogen. The total activity of platelet factor 3 and acid phosphatase was, however, normal in contrast to the lowered total activity of ADP and platelet factor 4, which showed even a disturbance of their release from platelets without any correction in the presence of ADP. Similarly, the total activity of β-glucuronidase was normal, though its release following collagen induction was impaired.
Adenosine diphosphate
Bleeding diathesis
Clot retraction
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Effects on platelet aggregation were examined of acetylsalicylic acid (ASA), indomethacin and a number of other agents including dipyridamole, phenylbutazone and sulfinpyrazone under standardized conditions. The Born turbidometric method of measuring platelet aggregation was used with collagen as the stimulus for aggregation. ASA and indomethacin were shown to be among the most potent inhibitors of aggregation, being active at minimal effective concentrations of 1–3 <i>μ</i>g/ml using a 10 min time of pre-incubation with the platelet-rich plasma (degree of aggregation inhibition was time dependent). Most of the other agents tested were also active <i>in vitro</i> and both prostaglandin El and adenosine were more potent than ASA or indomethacin. However, these agents were shown not to exert significant inhibitory effects when administered orally to rats (dose 10 and 30 mg/kg). ASA proved to be effective in doses as low as 3 mg/kg, and indomethacin in doses as low as 1 mg/kg orally. The inhibitory effects of ASA on aggregation remained for several days after a single oral dose, whereas the effects of indomethacin disappeared within 24 h.
Sulfinpyrazone
Dipyridamole
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S ummary . The plasma of two patients with heparin‐induced thrombocytopenia has been shown to cause platelet aggregation in the presence of heparin. The platelet aggregating factor was isolated in the IgG fraction of the patients’sera suggesting that it was an antibody. This heparin anti‐platelet antibody (HAP‐Ab) induced platelet aggregation and release but did not cause platelet lysis, although it fixed complement. Platelet aggregation was inhibited by EDTA and by inactivation of complement. There was a significant production of malondialdehyde (MDA) and thromboxane B 2 (TXB 2 ) implying a role of the prostaglandin synthesis pathway in HAP‐Ab induced aggregation. ADP release also appeared to be involved as apyrase blocked aggregation while hirudin, a thrombin inhibitor, had no effect. The thrombotic complications that have recently been reported in patients with heparin‐induced thrombocytopenia may be explained by some effects of HAP‐Ab on platelets, namely: the antibody mediated platelet factor 3 release, prostaglandin endoperoxides and thromboxane A 2 (TXA 2 ) production and platelet aggregation in vivo. These HAP‐Ab mediated effects could be inhibited by anti‐platelet drugs such as aspirin, indomethacin and dipyridamole and thus may have therapeutic implications.
Hirudin
Apyrase
Heparin-Induced Thrombocytopenia
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Temporarily improved platelet reactivity may reduce the bleeding in patients on antiplatelet therapy who have ongoing bleeding or who are in need of acute surgery. Adrenaline can bind to adrenergic α2A-receptors on platelets and potentially enhance platelet reactivity.To assess if adrenaline can improve adenosine diphosphate (ADP)-induced platelet aggregation and activation in blood samples from patients on dual antiplatelet therapy with acetylsalicylic acid (ASA) and the ADP-receptor antagonist ticagrelor.Blood samples were collected from a total of forty acute coronary syndrome patients on dual antiplatelet therapy with ASA and ticagrelor. ADP-induced platelet aggregation (by impedance aggregometry) and activation (by flow cytometry) were assessed before and after supplementation with adrenaline and/or platelet concentrate.Adrenaline supplementation (770 nmol L-1) increased median ADP-induced aggregation from 15 (25-75th percentiles: 10-20) to 26 (18-38) aggregation units. The effect was independent of concomitant platelet supplementation. Adrenaline also increased ADP-induced platelet activation: from 40% (36-54%) to 83% (74-88%) platelets with active fibrinogen receptor (binding PAC-1) and from 13% (7-21%) to 35% (18-50%) P-selectin-expressing platelets.Adrenaline potentiated ADP-induced platelet aggregation and activation in blood samples from ticagrelor-treated patients. Adrenaline infusion may be a new method to enhance platelet function in ticagrelor-treated patients who are in need of acute surgery or have ongoing bleeding. In vivo studies are needed to confirm the present results.
Adenosine diphosphate
Antiplatelet drug
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