Activation of intravascular coagulation induced by endotoxin administration An ultrastructural study

• Published in: Blood & Vessel Vol. 10; no. 1; pp. 28 - 33
• Main Authors: ASANO, Goro, HOSHINO, Masazumi, OHKUBO, Kenji, FUKUSHI, Katsunari
• Format: Journal Article
• Language: English; Japanese
• Published: The Japanese Society on Thrombosis and Hemostasis 01.03.1979
• Subjects: endotoxin; intravascular coagulation
• ISSN: 0386-9717; 1884-2372
• DOI: 10.2491/jjsth1970.10.28

It is noticed that the decreased peripheral leukocyte and platelet and activation of intravascular coagulation are induced by direct effect of endotoxin to the vascular system. But its mechanism is still uncertain. We used E-coli 0-26 endotoxin injected into the Donryu rats by intraperitoneal injection, 20mg per kg. and observed the vascular changes of lung, liver, kidney and adrenal, chronologically 30min. 1, 3 and 5hrs. by light and electron microscope. And we also studied the vascular permeability using fesin and horseradish peroxidase as tracers. By electron microscopic examination, we noted the increased pinocytotic vesicle, swelling of mitochondria, widening of intercellular spaces and vacuolization of endothelium and medial cells in the arterial system of lung, liver, adrenal and kidney. These findings were prominent in kidney in the early stage. And the destruction of polymorphonuclear leukocyte and platelet, deposition of fibrin were observed in sinusoids of the liver, in capillaries of the adrenal and kidney. And, especially, the kidney showed early prominent changes compared with other organs. The degenerative leukocytes were encountered strikingly in pulmonary vessels. According to the vascular clearance methods, the electron dense tracers and reaction products of peroxidase are also seen in the pinocytotic vesicles and cytosomes of the endothelium through the endothelial intercellular spaces. The extent of increased permeability depends upon the qualitative difference of properties of vesicles and the vesicular system in the endothelium, medial cell and other mesenchymal cells. The effects of the accumulation and disintegration of polymorphonuclear leukocytes and the break down of their lysosomes in blood vessels may a result of the direct cytotoxic effect of the endotoxin. The authors believe that the endotoxin installed shock may have resulted from the above mentioned vascular changes and the increased vascular permeability which is distinctly substantiated from the investigation of tracer methodology. We conclude that the activated coagulability, as the direct effect of endotoxin administration is a very important factor in accelerating the pathologic changes of the vessels.