内毒素性DIC与幼兔多发性骨坏死关系的实验研究

The Relationship of EndotoxinInduced DIC with MultiOsteonecrosis in Young Rabbits

本研究用２０只纯种日本大耳白幼兔，实验组连续二次、间隔２４ｈ经静脉注入纯制大肠杆菌内毒素（１００μｇ／ｋｇ），建立革兰氏阴性菌败血症休克模型，二周末处死，以９９ｍＴｃ－ＭＤＰ骨显像法及病理学检查观察模型动物骨骼系统改变情况，评价ＤＩＣ过程对骨骼系统的影响。结果发现，在第二次静脉注射内毒素一周后，实验组动物长骨骨端血流量计数对比值显著下降，二周末病理检查，证明出现了多发性骨坏死，并集中地发生在长管状骨骨端，分别为股骨髁、肱骨头、胫骨上端、股骨头及尺骨近端。病理表现为骺及干骺端侧髓腔内骨髓细胞坏死，以及骺板干骺端侧的软骨细胞柱、新生及成熟骨小梁的坏死崩解。部分动物有整块骺板的变性及坏死。实验发现，骨坏死的发生和分布，与骨微循环结构的破坏密切相关。这表明，内毒素及其引发的ＤＩＣ反应可以破坏骺区的骨微循环系统，引起幼兔全身多发的以骺板为中心的骨坏死。本研究提示，内毒素及其引发的ＤＩＣ过程可能是严重革兰氏阴性菌败血症后。

In our experiment, E. Coli Lipopoly saccharides (LPS) was twice injected intravenously in young rabbits in a time interval of 24 hours, to make disseminated intravascular coagulation (DIC) model, and our main focus of observation was on pathological changes in the skeletonal system. 20 young Japanese white rabbits were devided into one control group and one experimental group. In the experiment group, purified E.Coli LPS was twice injected intravenously (100g/kg) with a 24hours interval. All the rabbits were sacrified 2 weeks after injection. We used 99m TcMDP scientigraphy and pathological methods to detect the occurance of osteonecrosis. 1 week after the second injection, ischemia was detected by scientigraphy in epimetaphyseal regions of long bones, including femoral condyle, femoral head, humeral head, proximal part of tibia, and proximal part of ulna. The pathological detection confirmed osteonecrosis in these regions, including bone marrow hemorrhage, marrow necrosis as well as trabecular bone necrosis represented by amorphous eosinphilic debris. In some cases, osteonecrotic changes occupied the whole depth of the growth plate. We found that the disruption of microcirculation structures correlated with the occurrence and distribution very firmly. DIC caused by LPS can destroy the microcirculation structures in epimetaphyseal region and bring out multicentered osteonecrosis around the centre of growth plate. Endotoxininduced DIC may play an important role in children who survived from late skeleton sequlae of severe meningococcemia.