エンドトキシンのラット肝ミトコンドリアに及ぼす影響についての研究 II. エンドトキシン投与時のラット肝ミトコンドリア機能障害におけるフィブリン血栓の役割りについて
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Survival rate, hematologic changes, pathologic changes of liver, and liver mitochondrial function were investigated in heparinized and non-heparinized rats to study a role of disseminated intravascular coagulation (DIC) in the pathogenesis of hepatic mitochondrial dysfunction induced by endotoxin. The following results were obtained. 1) Pretreatment of rats with heparin (1,000U.) markedly alleviated lethality to shock induced by i. v.injection of E. coli endotoxin (Et). 2) At 3 hours after Et administration in non-heparinized rats, a decrease of platelet count and fibrnogen concentration and an increase of fibrin/fibrinogen degradation products (FDP) were observed, and bleeding and zonal necrosis were seen in the periportal area of hepatic lobules in which the formationof fibrin thrombi was remarkable. Hepatocytes and Kupffer cells in the periportal area showed considerable degeneration. Mitochondria in these hepatocytes were swollen. Respiratory control ratio and adenosine diphosphate/oxygen ratio (ADP/O) of liver mitochondria decreased at the same time. 3) At 3 hours after Et administration in pre-heparinized rats, a decrease of platelet count and fibrinogen concentration, together with bleeding in the periportal area were not seen, and the formation of fibrin thrombi was markedly prevented. The structure of hepatocytes, Kupffer cells and their intracellular organelles, and the function of mitochondria remained relatively intact. From these results, it may be considered that damming of blood in the portal system by thrombi inliver plays an important role in the pathogenesis of liver mitochondrial dysfunction caused by endotoxin.
- 札幌医科大学の論文
- 1981-02-02
札幌医科大学 | 論文
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