Endotoxin-induced DIC and tissue thromboplastin activity of bone marrow cells.

DOI Open Access
  • HIRATA Michimasa
    Department of Bacteriology, School of Medicine, Iwate Medical University
  • TSUNODA Nobuko
    Department of Bacteriology, School of Medicine, Iwate Medical University
  • INADA Katsuya
    Department of Bacteriology, School of Medicine, Iwate Medical University
  • YOSHIDA Masao
    Department of Bacteriology, School of Medicine, Iwate Medical University

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Other Title
  • 内毒素性ＤＩＣと骨髄細胞の組織トロンボプラスチン活性

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Description

1. Endotoxin injection caused significant increase in procoagulant activity (PCA) of bone marrow cells. Endotoxin also caused an increase in PCA of supernatant (sup) obtained from bone marrow suspension.<br>2. Both activities were destroyed by heating at over 56°C. The activity of mouse brain thromboplastin used as reference preparation was destroyed at 60°C 'but stable at 80°C.<br>3. PCA of bone marrow cells decreased after incubation with Concanavalin A (Con A). The activity recovered by addition of α-methyl-D-glucoside.<br>4. Ploymyxin (PxB) inhibited the PCA of either cells (20%-inhibition) or sup (50%-inhibition).<br>5. Addition of phospholipid (PL) to the cells or sup caused enhancement of PCA.<br>6. Degrees of heat inactivation, Con A- or PxB-inhibition, and PL-enhancement of PCA were higher in sup than those in the bone marrow cells.<br>Procoagulants of the cells and sup were shown to be tissue thromboplastin (Tp) which consists of glycoprotein-phospholipid complex functioning as active sites. Membrane perturbation due to endotoxin would initiate the increase in exposure and/or contents of the active site (PL) on the membrane surface and would participate in the manifestation of Tp activity. As a result of membrane alteration, release of Tp from the cell surface into circulation may also be caused in endotoxemia.

Journal

  • Blood & Vessel

    Blood & Vessel 16 (5), 480-489, 1985

    The Japanese Society on Thrombosis and Hemostasis

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