Dale J, Ohlsson K, Nordstoga K, Aasen A O
Eur Surg Res. 1980;12(1):39-51. doi: 10.1159/000128108.
Intravascular hemolysis and ultrastructure of erythrocytes from liver sinusoids were studied during and after infusion of Escherichia coli endotoxin in Labrador retriever dogs. Endotoxin infusion caused hemoconcentration, and induced disseminated intravascular coagulation (DIC), characterized by a rapid drop of platelet numbers, a gradual consumption of coagulation factors and activation of fibrinolysis. Advanced DIC and circulatory shock gradually developed, and the animals died after 7-15 h. Plasma hemoglobin concentrations did not rise for several hours, but late in the experimental period a significant intravascular hemolysis was constantly found. Circulating adenosine diphosphate (ADP) did not appear. During shock, liver biopsies revealed accumulation of erythrocytes often disintegrated within distended sinusoidal lumina. In advanced shock the fragmented erythrocyte seemed to form occlusive masses within the vessels. A fibrin-like material frequently appeared adjacent to the red cells. However, it did not have the periodicity characteristic for fibrin, and the ultrastructure of the material was very similar to that inside the erythrocytes. None of these changes were induced by saline infusion in control animals. The lack of fibrin formation and the late development of intravascular hemolysis indicate that red cell breakdown was of little importance for the initiation and progress of DIC.
在给拉布拉多猎犬输注大肠杆菌内毒素期间及之后,对肝血窦内的血管内溶血和红细胞超微结构进行了研究。内毒素输注导致血液浓缩,并诱发弥散性血管内凝血(DIC),其特征为血小板数量迅速下降、凝血因子逐渐消耗以及纤维蛋白溶解激活。严重的DIC和循环性休克逐渐发展,动物在7 - 15小时后死亡。血浆血红蛋白浓度在数小时内未升高,但在实验后期持续发现明显的血管内溶血。循环中的二磷酸腺苷(ADP)未出现。休克期间,肝脏活检显示红细胞积聚,这些红细胞常在扩张的血窦腔内崩解。在严重休克时,破碎的红细胞似乎在血管内形成阻塞性团块。一种纤维蛋白样物质经常出现在红细胞附近。然而,它不具有纤维蛋白的周期性特征,且该物质的超微结构与红细胞内的非常相似。对照动物输注生理盐水未诱发这些变化。缺乏纤维蛋白形成以及血管内溶血的晚期出现表明红细胞破裂对DIC的启动和进展影响不大。