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    Please use this identifier to cite or link to this item: https://ir.fy.edu.tw:8080/ir/handle/987654321/13728

    Title: Lipopolysaccharide-stimulated Leukocytes Contribute to Platelet Aggregative Dysfunction, Which is Attenuated by Catalase in Rats
    Authors: Dong, Huei-Ping;Chunag, I-Chun;Wang, Dean-Chuan;Huang, Li-Ju;Lee, Chu-I;Tsai, Jen-Hsiang;Yang, Rei-Cheng
    Contributors: 輔英科技大學 物理治療系
    Keywords: catalase;lipopolysaccharide;platelet aggregation;polymorphonuclear leukocytes;sepsis
    Date: 2010-11-01
    Issue Date: 2011-08-30 22:48:23 (UTC+8)
    Abstract: Endotoxemia causes several hematological dysfunctions, including platelet degranulation or disseminated intravascular coagulation, which lead to thrombotic and hemorrhagic events. Here, we tested the hypothesis that bacterial lipopolysaccharide (LPS)-stimulated leukocytes contribute to platelet aggregative dysfunction, and this function is attenuated by antioxidants. Platelet-rich plasma (PRP) was prepared from whole blood of normal and endotoxemic rats. The ability of platelet aggregation was measured by an aggregometer. LPS (50-100 μg/mL) was incubated with PRP, whole blood and PRP with polymorphonuclear leukocytes (PMNs) for 30 minutes, 60 minutes and 90 minutes, and platelet aggregation was detected. LPS-induced platelet aggregative dysfunction was undetectable in intact PRP which was isolated from normal whole blood, whereas it was detected in PRP isolated from endotoxemic rats and LPS-treated whole blood. Moreover, the effect of LPS-induced platelet aggregative dysfunction on intact PRP was observed when the PMNs were added. LPS-induced platelet aggregative dysfunction was significantly attenuated by catalase alone and in combination with N(G)-nitro-L-arginine methyl ester, but not by N(G)-nitro-L-arginine methyl ester alone. These results indicate that LPS-stimulated PMNs modulate platelet aggregation during LPS treatment and the effects are reversed by antioxidants. PMNs serve as an approach to understand LPS-induced platelet aggregative dysfunction during endotoxemia. During this process, the generation of reactive oxygen species, hydrogen peroxide especially, from LPS-stimulated PMNs could be an important potential factor in LPS-induced platelet aggregative dysfunction. Catalase contributes to the prevention of platelet dysfunction during LPS-induced sepsis.
    Relation: Kaohsiung Journal of Medical Sciences 26(11),584-594
    Appears in Collections:[物理治療系] 期刊論文

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