Endotoxemia and blood coagulation-fibrinolysis systems

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
  • 内毒素血症と血液凝固・線溶系　　マウス系統と内毒素に対する感受性
  • マウス系統と内毒素に対する感受性

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Description

A single dose of endotoxin caused an increase in cytotoxic damages of bone marrow cells, an increase in procoagulant activity (p-activity) of the cells, decrease in nucleated cell counts in marrow due to the migration into circulation, and an increase in serum FDP levels. The increase in cytotoxicity of bone marrow cells correlated well with the increase in p-activity of the cells. Most of the p-activity was found in the membrane fragments in the cells and p-activity was thought to be tissue thromboplastin.<br>Endotoxin induced an increase in p-activity in monocytes (6.9-fold) and granulocytes (2.9-fold).<br>The ddY mice were more responsive than C3H/He mice as to increase in cytotoxicity and also a decrease in nucleated cell counts in marrow. In contrast, none of these reactions were induced in C3H/HeJ mice. Endotoxin caused strain-dependent production of p-activity in mice. ddY mice and C3H/He mice responded to endotoxin with 7.0 and 2.9-fold increase of p-activity in whole nucleated bone marrow cells. In contrast, C3H/HeJ mice did not respond to endotoxin. Endotoxin also caused strain-dependent increase in serum FDP levels. ddY mice were more responsive than C3H/He mice, however, no increase in FDP was found in C3H/HeJ mice even by injection of 500μg of endotoxin. In C3H/HeJ mice, none of three endotoxin preparations which contained different amounts of protein could increase in serum FDP levels.<br>In endotoxemia, bone marrow cells migrate to circulation, therefore, the cells with an enhanced p-activity would participate in the manifestation of DIC. This possibility is further supported from the findings that endotoxin induced strain-dependent responses as to all of the 4 parameters and that these parameters correlated well with each other.

Journal

  • Blood & Vessel

    Blood & Vessel 15 (4), 340-348, 1984

    The Japanese Society on Thrombosis and Hemostasis

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