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KMID : 0378019780210040069
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New Medical Journal
1978 Volume.21 No. 4 p.69 ~ p.79
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Pathologic Findings in the Experimental Diffuse Intravascular Coagulation
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Abstract
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To study the experimental diffuse intravascular coagulation histologically, total 78 white rats (of which 45 were Fisher strain), weighing 120-200 gm, were given either thrombin (Bovine Thrombin ®), Thromboplastin(Dade ®) or Escherichia coli endotoxin (lipoplysaccharide 0127:Ba) in several different amounts and situations. Thrombin and thromboplastin were infused continuously over 2 hours using infusion pump via tail vein and sacrificed 24 hours later, if not died during or soon after the infusion. Also the rats given endotoxin were examined 24 hours after the last injection of endotoxin. Tissues including pituitary gland, kidneys, liver, lungs, adrenals, intestine and spleen, were examined under the microscope after hematoxylin-eosin stain. Followings were the results; 1. The amount of thrombin which can produce the diffuse intravascular coagulation in rabbit failed to produce the diffuse intravascular coagulation in the rat. 2. Infusion of 50-400mg per hour of thromboplastin in the rats failed to produce the typical pathologic findings of diffuse intravascular coagulation, but there were severe congestion on all organs examined, suggesting probable presence of diffuse intravascular coagulation process during the experiments. 3. Of total 33 Fisher rats given 0.5-3.0 mg of E. coli lipopolysaccharide intravenously, twice, 24 hours apart, the thrombosis present in 12 (36.3%) rats suggesting the diffuse intravascular coagulation. But the specific lesion of diffuse intravascular coagulation, fibrin thrombi, was suggested to be present in only 4 rats and the renal cortical necrosis was not found. Main pathologic picture of this group of rats was the severe congestion, hemorrhage, thrombosis and necrosis of the organs, and of which lungs, liver and adrenals showed most prominent alterations. 4. In the Fisher rats, pregnant for 17-18 days, endotoxin just for one time, of same dose as above, produced marked thrombosis, hemorrhage, congestion and (cortical) necrosis in the adrenals and less severely in liver, lungs and spleen. 5. The response to the endotoxin were more marked in pregnant rats. The estrogen treatment failed to enhance the reaction to the endotoxin in female rats, suggesting the possibility that the above phenomenon was not due to hyperlipemia induced by estrogens during pregnancy.
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